Reviewer #1 (Public Review):

Summary:

Extracellular ATP represents a danger-associated molecular pattern associated to tissue damage and can act also in an autocrine fashion in macrophages to promote proinflammatory responses, as observed in a previous paper by the authors in abdominal sepsis. The present study addresses an important aspect possibly conditioning the outcome of sepsis that is the release of ATP by bacteria. The authors show that sepsis-associated bacteria do in fact release ATP in a growth dependent and strain-specific manner. However, whether this bacterial derived ATP play a role in the pathogenesis of abdominal sepsis has not been determined. To address this question, a number of mutant strains of E. coli has been used first to correlate bacterial ATP release with growth and then, with outer membrane integrity and bacterial death. By using E. coli transformants expressing the ATP-degrading enzyme apyrase in the periplasmic space, the paper nicely shows that abdominal sepsis by these transformants results in significantly improved survival. This effect was associated with a reduction of peritoneal macrophages and CX3CR1+ monocytes, and an increase in neutrophils. To extrapolate the function of bacterial ATP from the systemic response to microorganisms, the authors exploited bacterial OMVs either loaded or not with ATP to investigate the systemic effects devoid of living microorganisms. This approach showed that ATP-loaded OMVs induced degranulation of neutrophils after lysosomal uptake, suggesting that this mechanism could contribute to sepsis severity.

Strengths:

A strong part of the study is the analysis of E. coli mutants to address different aspects of bacterial release of ATP that could be relevant during systemic dissemination of bacteria in the host.

Weaknesses:

As pointed out in the limitations of the study whether ATP-loaded OMVs provide a mechanistic proof of the pathogenetic role of bacteria-derived ATP independently of live microorganisms in sepsis is interesting but not definitively convincing. It could be useful to see whether degranulation of neutrophils is differentially induced by apyrase-expressing vs control E. coli transformants. Also, the increase of neutrophils in bacterial ATP-depleted abdominal sepsis, which has better outcomes than "ATP-proficient" sepsis, seems difficult to correlate to the hypothesized tissue damage induced by ATP delivered via non-infectious OMVs. Are the neutrophils counts affected by ATP delivered via OMVs? A comparison of cytokine profiles in the abdominal fluids of E. coli and OMV treated animals could be helpful in defining the different responses induced by OMV-delivered vs bacterial-released ATP. The analyses performed on OMV treated versus E. coli infected mice are not closely related and difficult to combine when trying to draw a hypothesis for bacterial ATP in sepsis. Also it was not clear why lung neutrophils were used for the RNAseq data generation and analysis.

Reviewer #2 (Public Review):

Summary:

In their manuscript "Released Bacterial ATP Shapes Local and Systemic Inflammation during Abdominal Sepsis", Daniel Spari et al. explored the dual role of ATP in exacerbating sepsis, revealing that ATP from both host and bacteria significantly impacts immune responses and disease progression.

Strengths:<br /> The study meticulously examines the complex relationship between ATP release and bacterial growth, membrane integrity, and how bacterial ATP potentially dampens inflammatory responses, thereby impairing survival in sepsis models. Additionally, this compelling paper implies a concept that bacterial OMVs act as vehicles for the systemic distribution of ATP, influencing neutrophil activity and exacerbating sepsis severity.

Weaknesses:

(1) The researchers extracted and cultivated abdominal fluid on LB agar plates, then randomly picked 25 colonies for analysis. However, they did not conduct 16S rRNA gene amplicon sequencing on the fluid itself. It is worth noting that the bacterial species present may vary depending on the individual patients. It would be beneficial if the authors could specify whether they've verified the existence of unculturable species capable of secreting high levels of Extracellular ATP.

(2) Do mice lacking commensal bacteria show a lack of extracellular ATP following cecal ligation puncture?

(3) The authors isolated various bacteria from abdominal fluid, encompassing both Gram-negative and Gram-positive types. Nevertheless, their emphasis appeared to be primarily on the Gram-negative E. coli. It would be beneficial to ascertain whether the mechanisms of Extracellular ATP release differ between Gram-positive and Gram-negative bacteria. This is particularly relevant given that the Gram-positive bacterium E. faecalis, also isolated from the abdominal fluid, is recognized for its propensity to release substantial amounts of Extracellular ATP.

(4) The authors observed changes in the levels of LPM, SPM, and neutrophils in vivo. However, it remains uncertain whether the proliferation or migration of these cells is modulated or inhibited by ATP receptors like P2Y receptors. This aspect requires further investigation to establish a convincing connection.

(5) Additionally, is it possible that the observed in vivo changes could be triggered by bacterial components other than Extracellular ATP? In this research field, a comprehensive collection of inhibitors is available, so it is desirable to utilize them to demonstrate clearer results.

(6) Have the authors considered the role of host-derived Extracellular ATP in the context of inflammation?

(7) The authors mention that Extracellular ATP is rapidly hydrolyzed by ectonucleotases in vivo. Are the changes of immune cells within the peritoneal cavity caused by Extracellular ATP released from bacterial death or by OMVs?

(8) In the manuscript, the sample size (n) for the data consistently remains at 2. I would suggest expanding the sample size to enhance the robustness and rigor of the results.

eLife assessment

This important study investigates, from Drosophila to mammals, the role of the Forkhead box O (FoxO) transcription factors in airway epithelial cells' response to stressors including hypoxia, temperature variations, and oxidative stress. The findings suggest a conserved role of FoxO in maintaining airway homeostasis across species. However, limitations in the specificity and concerns with the loss-of-function experiments render the evidence presented incomplete. Nonetheless, this study highlights FoxO's potential relevance in respiratory diseases like asthma and offers insights into potential therapeutic targets for conditions affecting airway health.

Joint Public Review

This work investigates the evolutionary conservation and functional significance of FoxO transcription factors in the response of airway epithelia to diverse stressors, ranging from hypoxia to temperature fluctuations and oxidative stress. Utilizing a comprehensive approach encompassing Drosophila, murine models, and human samples, the study investigates FoxO's role across species. The authors demonstrate that hypoxia triggers a dFOXO-dependent immune response in Drosophila airways, with subsequent nuclear localization of dFOXO in response to various stressors. Transcriptomic analysis reveals differential regulation of crucial gene categories in respiratory tissues, highlighting FoxO's involvement in metabolic pathways, DNA replication, and stress resistance mechanisms.

The study underscores FoxO's importance in maintaining homeostasis by revealing reduced stress resistance in dFOXO Drosophila mutants, shedding light on its protective role against stressors. In mammalian airway cells, FoxO exhibits nuclear translocation in response to hypoxia, accompanied by upregulation of cytokines with antimicrobial activities. Intriguingly, mouse models of asthma show FoxO downregulation, which is also observed in sputum samples from human asthma patients, implicating FoxO dysregulation in respiratory pathologies.

Overall, the manuscript suggests that FoxO signaling plays a critical role in preserving airway epithelial cell homeostasis under stress conditions, with implications for understanding and potentially treating respiratory diseases like asthma. By providing compelling evidence of FoxO's involvement across species and its correlation with disease states, the study underscores the importance of further exploration into FoxO-mediated mechanisms in respiratory health.

Strengths

(1) This study shows that FoxO transcription factors are critical for regulating immune and inflammatory responses across species, and for orchestrating responses to various stressors encountered by airway epithelial cells, including hypoxia, temperature changes, and oxidative stress. Understanding the intricate regulation of FoxO transcription factors provides insights into modulating immune and inflammatory pathways, offering potential avenues for therapeutic interventions against respiratory diseases and other illnesses.

(2) The work employs diverse model systems, including Drosophila, murine models, and human samples, thereby establishing a conserved role for FoxOs in airway epithelium and aiding translational relevance to human health.

(3) The manuscript establishes a strong correlation between FoxO expression levels and respiratory diseases such as asthma. Through analyses of both murine models of asthma and asthmatic human samples, the study demonstrates a consistent reduction in FoxO expression, indicating its potential involvement in the pathogenesis of respiratory disorders. This correlation underscores the clinical relevance of FoxO dysregulation and opens avenues for developing treatments for respiratory conditions like asthma, COPD, and pulmonary fibrosis, addressing significant unmet clinical needs.

(4) The study unveils intriguing mechanistic details regarding FoxO regulation and function. Particularly noteworthy is the observation of distinct regulatory mechanisms governing dFOXO translocation in response to different stressors. The independence of hypoxia-induced dFOXO translocation from JNK signaling adds complexity to our understanding of FoxO-mediated stress responses. Such mechanistic insights deepen our understanding of FoxO biology and pave the way for future investigations into the intricacies of FoxO signaling pathways in airway epithelial cells.

Weaknesses

(1) The manuscript does not distinguish between FoxO expression levels and FoxO activation status. While FoxO nuclear localization is observed in Drosophila and murine models, it remains unclear whether this reflects active FoxO signaling or merely FoxO expression, limiting the mechanistic understanding of FoxO regulation.

(2) The manuscript utilizes various stressors across different experiments without providing a clear rationale for their selection. This lack of coherence in stressor choice complicates the interpretation of results and diminishes the ability to draw meaningful comparisons across experiments.

(3) The manuscript frequently refers to "FoxO signaling" without providing specific signaling readouts. This ambiguity undermines the clarity of the conclusions drawn from the data and hinders the establishment of clear cause-and-effect relationships between FoxO activation and cellular responses to stress.

(4) Many conclusions drawn in the manuscript rely heavily on the quantification of immunostaining images for FoxO nuclear localization. While this is an important observation, it does not provide a sufficient mechanistic understanding of FoxO expression or activation regulation.

(5) The primary weakness in the Drosophila experiments is the analysis of dFoxO in homozygous dFoxO mutant animals, which precludes determining the specific role of dFoxO in airway cells. Despite available tools for tissue-specific gene manipulation, such as tissue-specific RNAi and CRISPR techniques, these approaches were not employed, limiting the precision of the findings.

(6) In mammalian experiments, the results are primarily correlative, lacking causal evidence. While changes in FoxO expression are observed under pathological conditions, the absence of experiments on FoxO-deficient cells or tissues precludes establishing a causal relationship between FoxO dysregulation and respiratory pathologies.

(7) Although the evidence suggests a critical role for FoxO in airway tissues, the precise nature of this role remains unclear. With gene expression changes analyzed only in Drosophila, the extent of conservation in downstream FoxO-mediated pathways between mammals and Drosophila remains uncertain. Additionally, the functional consequences of FoxO deficiency in airway cells were not determined, hindering comparisons between species and limiting insights into FoxO's functional roles in different contexts.

eLife assessment

This fundamental study provides insights into how pathogens respond, on a systemic level including several gene targets and clusters, to selected antimicrobial molecules. Compelling evidence is provided, through multi-omics and functional approaches, that very similar molecules originally designed to target the same bacterial protein act differently within the context of the whole set of cellular transcripts, expressed proteins, and pre-lethal metabolic changes. Given the incredibly fast accumulation of omics data to date and the much slower capacity of extracting biologically relevant insights from big data, this work exemplifies how the development of sensitive data analysis is still a major necessity in modern research.

Reviewer #1 (Public Review):

In this manuscript, entitled " Merging Multi-OMICs with Proteome Integral Solubility Alteration Unveils Antibiotic Mode of Action", Dr. Maity and colleagues aim to elucidate the mechanisms of action of antibiotics through combined approaches of omics and the PISA tool to discover new targets of five drugs developed against Helicobacter pylori.

Strengths:

Using transcriptomics, proteomic analysis, protein stability (PISA), and integrative analysis, Dr. Maity and colleagues have identified pathways targeted by five compounds initially discovered as inhibitors against H. pylori flavodoxin. This study underscores the necessity of a global approach to comprehensively understanding the mechanisms of drug action. The experiments conducted in this paper are well-designed and the obtained results support the authors' conclusions.

Weaknesses:

This manuscript describes several interesting findings. A few points listed below require further clarification:

(1) Compounds IVk exhibits markedly different behavior compared to the other compounds. The authors are encouraged to discuss these findings in the context of existing literature or chemical principles.

(2) The incubation time for treating H. pylori with the drugs was set at 4 hours for transcriptomic and proteomic analyses, compared to 20 min for PISA analysis. The authors need to explain the reason for these differences in treatment duration.

(3) The PISA method facilitates the identification of proteins stabilized by drug treatment. DnaJ and Trigger factor (tig), well-known molecular chaperones, prevent protein aggregation under stress. Their enrichment in the soluble fraction is expected and does not necessarily indicate direct stabilization by the drugs. The possibility that their stabilization results from binding to other proteins destabilized by the drugs should be considered. To prevent any misunderstanding, the authors should clarify that their methodology does not solely identify direct targets. Instead, the combination of their findings sheds light on various pathways affected by the treatment.

(4) At the end of the manuscript, the authors conclude that four compounds "strongly interact with CagA". However, detailed molecule/protein interaction studies are necessary to definitively support this claim. The authors should exercise caution in their statement. As the authors mentioned, additional research (not mandated in the scope of this current paper) is necessary to determine the drug's binding affinity to the proposed targets.

(5) The authors should clarify the PISA-Express approach over standard PISA. A detailed explanation of the differences between both methods in the main text is important.

Reviewer #2 (Public Review):

Summary:

This work has an important and ambitious goal: understanding the effects of drugs, in this case antimicrobial molecules, from a holistic perspective. This means that the effect of drugs on a group of genes and whole metabolic pathways is unveiled, rather than its immediate effect on a protein target only. To achieve this goal the authors successfully implement the PISA-Express method (Protein Integral Solubility Alteration), using combined transcriptomics, proteomics, and drug-induced changes in protein stability to retrieve a large number of genes and proteins affected by the used compounds. The compounds used in the study (compound IVa, IVb, IVj, and IVk) were all derived from the precursors compound IV, they are effective against Helicobacter pylori, and their mode of action on clusters of genes and proteins has been compared to the one of the known pylori drug metronidazole (MNZ). Due to this comparison, and confirmed by the diversity of responses induced by these very similar compounds, it can be understood that the approach used is reliable and very informative. Notably, although all compound IV derivatives were designed to target pylori Flavodoxin (Fld), only one showed a statistically significant shift of Fld solubility (compound IVj, FIG S11). For most other compounds, instead, the involvement of other possible targets affecting diverse metabolic pathways was also observed, notably concerning a series of genes with other important functions: CagA (virulence factor), FtsY/FtsA (cell division), AtpD (ATP-synthase complex), the essential GTPase ObgE, Tig (protein export), as well as other proteins involved in ribosomal synthesis, chemotaxis/motility and DNA replication/repairs. Finally, for all tested molecules, in vivo functional data have been collected that parallel the omics predictions, comforting them and showing that compound IV derivatives differently affect cellular generation of reactive oxygen species (ROS), oxygen consumption rates (OCR), DNA damage, and ATP synthesis.

Strengths:

The approach used is very potent in retrieving the effects of chemically active molecules (in this case antimicrobial ones) on whole cells, evidencing protein and gene networks that are involved in cell sensitivity to the studied molecules. The choice of these compounds against H. pylori is perfect, showcasing how different the real biological response is, compared to the hypothetical one. In fact, although all molecules were retrieved based on their activity on Fld, the authors unambiguously show that large unexpected gene clusters may, and in fact are, affected by these compounds, and each of them in different manners.

Impact:

The present work is the first report relying on PISA-Express performed on living bacterial cells. Because of its findings, this work will certainly have a high impact on the way we design research to develop effective drugs, allowing us to understand the fine effects of a drug on gene clusters, drive molecule design towards specific metabolic pathways, and eventually better plan the combination of multiple active molecules for drug formulation. Beyond this, however, we expect this article to impact other related and unrelated fields of research as well. The same holistic approaches might also allow gaining deep, and sometimes unexpected, insight into the cellular targets involved in drug side effects, drug resistance, toxicity, and cellular adaptation, in fields beyond the medicinal one, such as cellular biology and environmental studies on pollutants.

eLife assessment

This important study reveals how Drosophila may be used to investigate the role of missense variants in the gene PLCG1 related to human disease in case studies. The evidence that most of these variants have a gain-of-function effect in the fly is convincing and supportive of their pathogenic effect. With some additional control experiments to assess overexpression toxicity, this work would be of relevance to human and Drosophila geneticists alike.

Reviewer #1 (Public Review):

Summary:

This manuscript provides an initial characterization of three new missense variants of the PLCG1 gene associated with diverse disease phenotypes, utilizing a Drosophila model to investigate their molecular effects in vivo. Through the meticulous creation of genetic tools, the study assesses the small wing (sl) phenotype - the fly's ortholog of PLCG1 - across an array of phenotypes from longevity to behavior in both sl null mutants and variants. The findings indicate that the Drosophila PLCG1 ortholog displays aberrant functions. Notably, it is demonstrated that overexpression of both human and Drosophila PLCG1 variants in fly tissue leads to toxicity, underscoring their pathogenic potential in vivo.

Strengths:

The research effectively highlights the physiological significance of sl in Drosophila. In addition, the study establishes the in vivo toxicity of disease-associated variants of both human PLCG1 and Drosophila sl.

Weaknesses:

The study's limitations include the human PLCG1 transgene's inability to compensate for the Drosophila sl null mutant phenotype, suggesting potential functional divergence between the species. This discrepancy signals the need for additional exploration into the mechanistic nuances of PLCG1 variant pathogenesis, especially regarding their gain-of-function effects in vivo.

Overall:

The study offers compelling evidence for the pathogenicity of newly discovered disease-related PLCG1 variants, manifesting as toxicity in a Drosophila in vivo model, which substantiates the main claim by the authors. Nevertheless, a deeper inquiry into the specific in vivo mechanisms driving the toxicity caused by these variants in Drosophila could significantly enhance the study's impact.

Reviewer #2 (Public Review):

The manuscript by Ma et al. reports the identification of three unrelated people who are heterozygous for de novo missense variants in PLCG1, which encodes phospholipase C-gamma 1, a key signaling protein. These individuals present with partially overlapping phenotypes including hearing loss, ocular pathology, cardiac defects, abnormal brain imaging results, and immune defects. None of the patients present with all of the above phenotypes. PLCG1 has also been implicated as a possible driver for cell proliferation in cancer.

The three missense variants found in the patients result in the following amino acid substitutions: His380Arg, Asp1019Gly, and Asp1165Gly. PLCG1 (and the closely related PLCG2) have a single Drosophila ortholog called small wing (sl). sl-null flies are viable but have small wings with ectopic wing veins and supernumerary photoreceptors in the eye. As all three amino acids affected in the patients are conserved in the fly protein, in this work Ma et al. tested whether they are pathogenic by expressing either reference or patient variant fly or human genes in Drosophila and determining the phenotypes produced by doing so.

Expression in Drosophila of the variant forms of PLCG1 found in these three patients is toxic; highly so for Asp1019Gly and Asp1165Gly, much more modestly for His380Arg. Another variant, Asp1165His which was identified in lymphoma samples and shown by others to be hyperactive, was also found to be toxic in the Drosophila assays. However, a final variant, Ser1021Phe, identified by others in an individual with severe immune dysregulation, produced no phenotype upon expression in flies.

Based on these results, the authors conclude that the PLCG1 variants found in patients are pathogenic, producing gain-of-function phenotypes through hyperactivity. In my view, the data supporting this conclusion are robust, despite the lack of a detectable phenotype with Ser1021Phe, and I have no concerns about the core experiments that comprise the paper.

Figure 6, the last in the paper, provides information about PLCG1 structure and how the different variants would affect it. It shows that the His380, Asp1019, and Asp1165 all lie within catalytic domains or intramolecular interfaces and that variants in the latter two affect residues essential for autoinhibition. It also shows that Ser1021 falls outside the key interface occupied by Asp1019, but more could have been said about the potential effects of Ser1021Phe.

Overall, I believe the authors fully achieved the aims of their study. The work will have a substantial impact because it reports the identification of novel disease-linked genes, and because it further demonstrates the high value of the Drosophila model for finding and understanding gene-disease linkages.

Reviewer #3 (Public Review):

Summary:

The paper attempts to model the functional significance of variants of PLCG2 in a set of patients with variable clinical manifestations.

Strengths:

A study attempting to use the Drosophila system to test the function of variants reported from human patients.

Weaknesses:

Additional experiments are needed to shore up the claims in the paper. These are listed below.

Major Comments:

(1) Does the pLI/ missense constraint Z score prediction algorithm take into consideration whether the gene exhibits monoallelic or biallelic expression?

(2) Figure 1B: Include human PLCG2 in the alignment that displays the species-wide conserved variant residues.

(3) Figure 4A:<br /> Given that<br /> (i) sl is predicted to be the fly ortholog for both mammalian PLCγ isozymes: PLCG1 and PLCG2 [Line 62]<br /> (ii) they are shown to have non-redundant roles in mammals [Line 71] and<br /> (iii) reconstituting PLCG1 is highly toxic in flies, leading to increased lethality.<br /> This raises questions about whether sl mutant phenotypes are specifically caused by the absence of PLG1 or PLCG2 functions in flies. Can hPLCG2 reconstitution in sl mutants be used as a negative control to rule out the possibility of the same?

(4) Do slT2A/Y; UAS-PLCG1Reference flies survive when grown at 22{degree sign}C? Since transgenic fly expressing PLCG1 cDNA when driven under ubiquitous gal4s, Tubulin and Da, can result in viable progeny at 22{degree sign}C, the survival of slT2A/Y; UAS-PLCG1Reference should be possible.<br /> and similarly<br /> Does slT2A flies exhibit the phenotypes of (i) reduced eclosion rate (ii) reduced wing size and ectopic wing veins and (iii) extra R7 photoreceptor in the fly eye at 22{degree sign}C?<br /> If so, will it be possible to get a complete rescue of the slT2A mutant phenotypes with the hPLCG1 cDNA at 22{degree sign}C? This dataset is essential to establish Drosophila as an ideal model to study the PLCG1 de novo variants.

(5) Localisation and western blot assays to check if the introduction of the de novo mutations can have an impact on the sub-cellular targeting of the protein or protein stability respectively.

(6) Analysing the nature of the reported gain of function (experimental proof for the same is missing in the manuscript) variants:<br /> Instead of directly showing the effect of introducing the de novo variant transgenes in the Drosophila model especially when the full-length PLCG1 is not able to completely rescue the slT2A phenotype;<br /> (i) Show that the gain-of-function variants can have an impact on the protein function or signalling via one of the three signalling outputs in the mammalian cell culture system: (i) inositol-1,4,5-trisphosphate production, (ii) intracellular Ca2+ release or (iii) increased phosphorylation of extracellular signal-related kinase, p65, and p38.<br /> OR<br /> (ii) Run a molecular simulation to demonstrate how the protein's auto-inhibited state can be disrupted and basal lipase activity increased by introducing D1019G and D1165G, which destabilise the association between the C2 and cSH2 domains. The H380R variant may also exhibit characteristics similar to the previously documented H335A mutation which leaves the protein catalytically inactive as the residue is important to coordinate the incoming water molecule required for PIP2 hydrolysis.

(7) Clarify the reason for carrying out the wing-specific and eye-specific experiments using nub-gal4 and eyless-gal4 at 29˚C despite the high gal4 toxicity at this temperature.

(8) For the sake of completeness the authors should also report other variants identified in the genomes of these patients that could also contribute to the clinical features.

įjungtas RA ON ir mažinu srovę iki 1,2W. Labai svarbu tai padaryti dabar, nes vėliau apertūros užstos ir nežinorime kokia galia šviečia.

سلام اینجا داره افراق میکنه

The descriptions of how racial harassment is often met with silence and the inadequate responses from educational systems are particularly striking. This resonates with me because it underscores the pervasive nature of racial discrimination and the complicity of silence in perpetuating oppression. Josh’s and his sister’s reactions, along with the historical context of African Americans being taught to suppress their reactions to racism, highlight a harmful cycle where non-confrontation leads to unresolved trauma and mental health issues. It’s disheartening to see that despite more attention to mental health in schools, there remains a significant gap in culturally competent counseling.

The passage discussing Eve’s school experiences as a multiethnic individual caught my attention due to its nuanced depiction of identity and isolation in predominantly white educational settings. It illustrates the complexity of racial identity and how individuals often internalize societal perceptions, attributing social difficulties to personal quirks rather than racial dynamics. This reflection deepens my understanding of the subtle ways racism can manifest and influence self-perception, highlighting the importance of addressing racial issues openly in educational environments to foster a more inclusive atmosphere.

This passage sheds light on the dual-edged sword of the model minority stereotype and its impact on Asian American students. It piques my interest because it reveals how positive stereotypes can mask the underlying racial discrimination and social isolation experienced by Asian American students. The narrative challenges the notion that racial teasing is just a part of growing up, emphasizing its damaging effect on students’ social interactions and self-perception. This discourse prompts me to reflect on the deeper societal changes needed to address such ingrained prejudices in educational institutions.

The incident at South Philadelphia High School, where Asian American students were targeted and bullied, is deeply troubling and highlights systemic racism’s pervasive influence in educational settings. It underscores the urgent need for schools to understand and actively address the dynamics of racial tensions. The media’s failure to delve into how the “model minority” stereotype may have contributed to misunderstandings and hostility in this environment is particularly disconcerting. This situation reminds us that stereotypes can have dangerous implications and stresses the importance of fostering a culturally aware and inclusive school climate.

시민왕 파리에 적게 개입

시민왕

지구. 외곽이려나? 팽창? 이거는 확인 필요하다

1930년대 인구 80만 찍고, 비위생적인 곳에는 노동자가 개인 주도의 현대적 구획 -> 중산층

• 루이18세 때는 토목건축보다는 개조에 초점
• 아케이드 증가

루이18세 시기의 센 지사 - 시 재정 회복과 부채 청산이 목표

.

.왕정복고에서 할 수 있던 일

왕정복고 후 지출 제한

.

제1제정 몰락, 루이18세 왕정복고

1802 공공 위생에 대한 관심과 보건 관련 기관의 설립. 나무의 중요성이 부각되는 기초

(이후) 19세기 후반 서구의 위생 및 공중보건학 발달. 상하수도 체계 확립(안전한 식수 공급, 콜레라, 이질 등 예방), 주택 청결, 해충 박멸 등 목표

동전의 양면 - 회복과 안정 - 인구의 증가

1809년 나폴레옹1세 시기에 나중에 나폴레옹 4세와 오스만이 구현할 도시개조에 대한 요구가 있었음. 이미 -> 하지만 제국의 몰락

튈르리의 입구이자 전망 닫기

중요 나폴레옹 1세의 도시 건설 프로젝트 "파리의 장식" embellishment

기존 시스템 시장, 지역구에도 대표가 있고, 경찰청장이 있어 충돌

중요. 센 강 지사의 권력이 컸다. 총리에 버금가나? 일종의 장관

시장? 센 강 지사 -> 정확한 표현 확인 - 제정과 행정시스템의 출범

.

.

확장하는 제국 프랑스의 수도로서 파리, 유럽의 수도로

혼란에 지친 시민들에 대한 증언

이전 왕실의 장소들이 입법부, 상원, 황제 등등 자리를 내줌

중요 혁명은 파괴했지만 건설한 것은 별로 없었따. 인용하기 너무 좋다. 좋은 문장

• 1789-1799 내전, 외부전쟁을 동반한 경제 및 식량 위기로 인구 10만 줄은 듯 원문확인

왕정주의 진압한 장군 나폴레옹 보나파르트 , 그는 황제가 된다. 제정으로

왕실의 재산은 어떻게 되었나? 샹젤리제, 쿠르라헨 등

오 명칭의 변화. 시민!

튈르리 침공의 상징성. 샹젤리제까지도 민중의 승리를 의미하는 공간이 될 수 있겠다.

튈르리 공원? park? 입법부는 로열에게 충성햇으나 파리의 민중들이 왕을 몰락시켰다

산책로? 프롬미나드?

루이 16세 참수 전 튈르리/파리로 소환

혁명 후 첫 파리 시장

청산

경제위기와 새로운 정치 사상의 결부

정치적 변혁

건설의 재정과 여유 없었음 -> 나폴레옹 3세 오스만 대에 경제적 , 정치적 여건이 가능했을 것

18세기 말엽과 19세기 -> 혁명의 세기로서 파리가 중세의 외피를 잃음. 지금까지 이어지는 "빛의 도시"의 외피

This passage captivates me due to its exploration of the internalization and questioning of the “Asian” cultural script within education. Both Gary Wong and Paul Pham’s experiences highlight a complex interaction between cultural expectations and individual experiences in academic achievement. It’s enlightening to see examples of Asian Americans who recognize and deviate from the stereotypical educational pressures often associated with their communities. This deviation challenges the monolithic view of Asian American educational values and shows the diversity of experiences and expectations within the community.

The discussion around the model minority stereotype and its implications for Asian American students at Alhambra High is deeply engaging because it exposes how cultural stereotypes can shape educational expectations and experiences. It resonates with me as it highlights the pressure and unrealistic standards that can arise from essentializing cultural traits, such as hard work and academic excellence, to an entire ethnic group. This reinforces the need for a more nuanced understanding of individual and community dynamics that go beyond simplistic and often harmful stereotypes.

The discussion on the racialization of academic achievement, especially in light of historical and ongoing legislative efforts like the No Child Left Behind Act, strikes a chord with me because it underscores the complexity of addressing educational disparities. The fact that older racial biases are often veiled under cultural explanations today highlights the subtle ways systemic racism perpetuates. This prompts me to think critically about how societal structures shape educational outcomes and the importance of addressing these issues from a systemic rather than an individualistic perspective. It’s essential to explore more profound, structural changes that go beyond mere symptom treatment.

The transition from ethnically mixed groups in junior high to more racially homogeneous groups in high school at Alhambra highlights a troubling yet significant trend in educational environments. The divide becomes particularly stark with the separation into different academic tracks, exacerbating the racialized “achievement gap.” This segregation in schooling interests me because it reflects broader societal issues and challenges the ideal of educational equity. It is concerning how institutional structures, such as tracking, can reinforce and perpetuate these divisions, impacting students’ academic and social lives.

The dynamic at Alhambra High, as described by Nancy and Paul, where ethnic identity deeply influences social categorization and interaction, provides a clear example of how racial and ethnic perceptions shape student experiences in diverse settings. This portrayal is intriguing because it reveals the nuanced ways students navigate their identities in a predominantly Asian and Latina/o environment, challenging the simplistic racial binaries often prevalent in less diverse areas. It emphasizes the complexity of identity in multicultural settings and the role of schools as spaces where these identities are continuously negotiated and redefined.

This passage captivates me with its deep dive into the complex role schools play in shaping societal norms and structures. It emphasizes how schools not only reflect but actively construct social realities, perpetuating hierarchies under the guise of neutrality. The idea that schools are arenas for both maintaining and challenging societal norms is particularly compelling, illustrating the dual role of education as both a tool for social reproduction and a potential catalyst for change. This dual role suggests that while schools can reinforce inequalities, they also hold the power to dismantle them, making education a critical field for social justice efforts.

The incident at Alhambra High, spurred by Robin’s column, caught my attention because it highlights the powerful role schools play in reflecting and challenging societal norms, particularly around issues of race and achievement. The controversy not only exposed underlying racial tensions but also prompted a broader conversation about equality, meritocracy, and the complex ways in which race influences educational outcomes. It is a vivid example of how educational settings can become battlegrounds for larger societal debates, revealing the deep-seated ideologies that shape our understanding of race and success.

The passage reflects on the profound role schools play in shaping societal norms under the guise of neutrality, which intrigues me due to the dual nature of educational institutions as both upholders and challengers of societal structures. Schools not only propagate certain social and racial orders but also provide a platform for challenging these hegemonies. This perspective is vital as it prompts a deeper examination of educational practices and their impact on societal inequalities. It emphasizes the need for critical awareness in educational settings to foster a more equitable society.

Version 2 of this preprint has been peer-reviewed and recommended by Peer Community in Ecology.<br /> See the peer reviews and the recommendation.

2 116 586

Eine extreme Hitzewelle hat in der Sahelzone Hunderte, wahrscheinlich Tausende Menschenleben gefordert. World Weather Attribution zufolge ist die Höhe der Temperaturen eindeutig auf die globale Erhitzung durch Treibhausgase zurückzuführen. https://www.theguardian.com/environment/2024/apr/18/lethal-heatwave-in-sahel-worsened-by-fossil-fuel-burning-study-finds

Zur Studie: https://www.worldweatherattribution.org/extreme-sahel-heatwave-that-hit-highly-vulnerable-population-at-the-end-of-ramadan-would-not-have-occurred-without-climate-change/

This passage highlights the critical issue of misunderstanding and misjudging parental actions based on cultural and socioeconomic differences. The story of David’s mother, who despite her unconventional appearance, demonstrated her deep care and commitment by organizing a birthday party, illustrates the quick judgments educators often make. This resonates with me because it underscores the importance of empathy and understanding in education, especially towards parents from diverse backgrounds. Recognizing the intent behind actions, rather than just the actions themselves, could foster a more supportive and inclusive school environment.

The cultural nuances affecting educational assessments, particularly in Latino and Native American communities, captivate me due to their profound implications on equitable teaching practices. The Latino girls’ hesitance to showcase their knowledge in mixed-gender settings and the Native American students’ struggle with traditional academic tasks like summarizing, due to cultural norms against speaking for others, underline the necessity for culturally responsive education. These examples drive home the importance of educators understanding and adapting to the diverse cultural backgrounds of their students to foster an inclusive and effective learning environment.

The segment discussing the interaction between the cultural backgrounds of students and teachers caught my attention because it highlights how easily a student’s capabilities can be misunderstood due to cultural differences. Marti’s example, where her use of language was misinterpreted by her teacher, showcases the need for educators to have a deeper understanding and appreciation of linguistic diversity. This resonates with me as it underlines the importance of cultural competence in education, where recognizing and valuing diverse forms of expression can enrich the learning experience and better support all students.

This passage on the dynamics of teacher-student interaction across different cultural and ethnic backgrounds highlights the significant impact of communication styles in education. The differentiation in how teachers from diverse backgrounds express authority and set expectations resonates with me because it showcases how cultural misunderstandings can hinder effective teaching and learning. It emphasizes the need for culturally responsive teaching strategies that acknowledge and adapt to the varied backgrounds of students to enhance educational outcomes and mutual respect.

This is interesting because it's about more than just cultural differences. It includes how societal expectations and norms influence behavior, not just for boys more than girls, but for everyone.

I didn't realize before that the way people talk can influence who they become friends with. But it makes sense that if people speak similarly, they're more likely to connect and become friends.

I agree with this idea. Every child is unique and should be seen as their own person. It's difficult to shape them or tell them how to behave when they are still learning everything.

是打击打击的成都市

https://shopgoodwill.com/item/196139225

Nebo is a Mac app for handwritten notes. Its OCR claims to do English plus one of 66 other languages both. First time I've seen that. Q remains: does it do so simultaneously in a single note, or as selected per note? My e-ink device allows a range of languages but not at the same time, I need to switch the setting, and applies one language to one note. This clashes with the fact that multilingual users will use multiple languages inside their notes at the same time. n:: [[Multilingual is not multiple monolingual 20191019072010]] obv https://www.zylstra.org/blog/2019/10/adding-better-language-support-ii/

The discussion of “educación” in this text strongly resonates with me as it broadens the conventional definition of education beyond mere academic achievement to include moral and ethical development. It challenges the impersonal, test-driven approach prevalent in many educational systems today and emphasizes the importance of nurturing a holistic sense of responsibility and care towards others. This approach aligns with my belief that education should foster not only intellectual but also personal growth, encouraging students to become compassionate and responsible citizens.

The concept of “subtractive schooling” is a powerful lens through which to view the impact of educational policies on minority students. It effectively captures how assimilationist approaches can strip students of their linguistic and cultural identities, rather than enriching their educational experience with their native heritage. This resonates with me as it challenges the conventional perspective on bilingual education and emphasizes the need for more inclusive and affirming educational practices that recognize and build upon the diverse backgrounds of students.

The dynamics within Seguin High School, where educational challenges are compounded by high dropout rates and low parental education levels, are reflective of broader systemic issues in education. It’s concerning to see how the blame for educational failures often falls on students and their families rather than addressing systemic inadequacies. This reinforces my belief in the need for a holistic approach to educational reform that includes community engagement and reevaluation of educational policies and practices. The entrenched nature of these issues at Seguin highlights the difficulty of effecting meaningful change in such settings.

address and phone numbers for Henry Dreyfuss, the industrial designer responsible for the The Western Electric model 500 telephone series and the later princess phone.

South Pasadena City Directory, 1961-1962<br /> by California Directory Publishing Co. https://archive.org/details/csp_000062/page/n21/mode/2up?view=theater

this extra factor of E^(3/2) should not be here. it is carried through the next few equations but then rightly disappears in the equations after Figure 2.

Такое ощущение, что тут фрагмент текста потерялся. Типа находим ещё один адрес (домен?) analytical.htb, идём смотреть.

addresses challenge of isolating the selection

Parasitic because feeding on feathers means disruption of warm and movement. More energy needs to be expended, lower fitness cost.

Transmission usually direct contact, could also happen by hitchhiking on parasitic flies. Selection via preening. Countered by camo

question: Is adaptive radiation occurring in these parasites and what is driving it?

name of lice

Selection being traced. Usually host defense is hard to manipulate/isolate but in this case its pretty straight forward.

herbivorous plant eaters (aka not animal parasites)

Islands or host islands; regardless both have that gene flow restriction that is imperfect

basically camouflage, ability to blend in with surroundings aka host

closely related

Wide range of adaptions occuring rapdily as a response to coming into a new area with lots of unfilled niches

For exam

Las pedagogías decoloniales desempeñan un papel fundamental en la enseñanza por diversas razones. En primer lugar, ofrecen una perspectiva crítica sobre el impacto del colonialismo en la educación, lo que permite identificar y cuestionar las estructuras de poder y conocimiento impuestas por dicho legado. Esto resulta esencial para impulsar una educación que sea más inclusiva y justa, al reconocer y valorar las diversas perspectivas y saberes presentes en diferentes culturas y comunes, además, estas pedagogías estimulan una reflexión profunda sobre cómo el colonialismo ha influido en la creación y difusión del conocimiento, lo que posibilita cuestionar las narrativas dominantes, en resumen, puedo aportar diciendo que las pedagogías decoloniales representan herramientas poderosas en la actualidad.

https://typewriterdatabase.com/royal.72.typewriter-serial-number-database

Henry Dreyfuss, Noted Designer, Is Found Dead With His Wife by The New York Times

Henry Dreyfuss: Designer for Humanity | The South Pasadenan by [[Rick Thomas]] of South Pasadena News

the progressivism we need in modern christianity

don't conform for people who don't deserve you

DOI: 10.1016/j.celrep.2021.108889

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DOI: 10.1016/j.celrep.2021.108883

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DOI: 10.1016/j.celrep.2024.114115

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DOI: 10.1016/j.celrep.2024.114115

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DOI: 10.1016/j.celrep.2024.114115

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DOI: 10.1016/j.celrep.2024.114115

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DOI: 10.1016/j.celrep.2024.114115

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DOI: 10.1016/j.celrep.2024.114115

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DOI: 10.1016/j.celrep.2024.114126

Resource: (CCLV Cat# CCLV-RIE 1018, RRID:CVCL_0063)

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DOI: 10.1016/j.celrep.2024.114123

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DOI: 10.1016/j.celrep.2024.114119

Resource: RRID:Addgene_12259

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DOI: 10.1016/j.celrep.2024.114119

Resource: (BCRJ Cat# 0263, RRID:CVCL_1239)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (BCRC Cat# 60094, RRID:CVCL_0224)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (IZSLER Cat# BS CL 188, RRID:CVCL_0075)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (KCB Cat# KCB 200706YJ, RRID:CVCL_0291)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (CCLV Cat# CCLV-RIE 1018, RRID:CVCL_0063)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (RCB Cat# RCB1872, RRID:CVCL_0037)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (ATCC Cat# CRM-HTB-26, RRID:CVCL_0062)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (Santa Cruz Biotechnology Cat# sc-711, RRID:AB_631835)

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DOI: 10.1016/j.celrep.2024.114119

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DOI: 10.1016/j.celrep.2024.114119

Resource: (Santa Cruz Biotechnology Cat# sc-7974, RRID:AB_628187)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (Santa Cruz Biotechnology Cat# sc-120, RRID:AB_627492)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (Thermo Fisher Scientific Cat# 26181, RRID:AB_2537081)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (Abcam Cat# ab126811, RRID:AB_11128060)

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DOI: 10.1016/j.celrep.2024.114119

Resource: (Abcam Cat# ab191606, RRID:AB_2891324)

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DOI: 10.1016/j.celrep.2024.114119

Resource: AB_777253

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What is this?

DOI: 10.1038/s44318-024-00047-y

Resource: (ABclonal Cat# A12802, RRID:AB_2759641)

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DOI: 10.1038/s44318-024-00047-y

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DOI: 10.1038/s44318-024-00045-0

Resource: (R and D Systems Cat# AF357, RRID:AB_355320)

Curator: @abever99

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What is this?

DOI: 10.1038/s44318-024-00045-0

Resource: (Abcam Cat# ab211777, RRID:AB_2895604)

Curator: @abever99

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What is this?

DOI: 10.1038/s44318-024-00045-0

Resource: (R and D Systems Cat# AF349, RRID:AB_355314)

Curator: @abever99

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What is this?

DOI: 10.1038/s44318-024-00045-0

Resource: (Abcam Cat# ab14917, RRID:AB_301509)

Curator: @abever99

SciCrunch record: RRID:AB_301509

What is this?

DOI: 10.1038/s44318-024-00045-0

Resource: (R and D Systems Cat# AF2727, RRID:AB_2170716)

Curator: @abever99

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What is this?

DOI: 10.1038/s44318-024-00045-0

Resource: (AngioBio Cat# 11-002, RRID:AB_10013720)

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DOI: 10.1038/s44318-024-00043-2

Resource: (Agilent Cat# P0447, RRID:AB_2617137)

Curator: @abever99

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What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (Agilent Cat# P0448, RRID:AB_2617138)

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DOI: 10.1038/s44318-024-00043-2

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DOI: 10.1038/s44318-024-00043-2

Resource: (BD Biosciences Cat# 347580, RRID:AB_10015219)

Curator: @abever99

SciCrunch record: RRID:AB_10015219

What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (Abcam Cat# ab6326, RRID:AB_305426)

Curator: @abever99

SciCrunch record: RRID:AB_305426

What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (Santa Cruz Biotechnology Cat# sc-56, RRID:AB_628110)

Curator: @abever99

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What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (Bethyl Cat# A700-009, RRID:AB_2891810)

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DOI: 10.1038/s44318-024-00043-2

Resource: (Millipore Cat# 05-636, RRID:AB_309864)

Curator: @abever99

SciCrunch record: RRID:AB_309864

What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (Cell Signaling Technology Cat# 2577, RRID:AB_2118010)

Curator: @abever99

SciCrunch record: RRID:AB_2118010

What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (Cell Signaling Technology Cat# 9542, RRID:AB_2160739)

Curator: @abever99

SciCrunch record: RRID:AB_2160739

What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (Cell Signaling Technology Cat# 83732, RRID:AB_2749858)

Curator: @abever99

SciCrunch record: RRID:AB_2749858

What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: FlowJo (RRID:SCR_008520)

Curator: @abever99

SciCrunch record: RRID:SCR_008520

What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (RRID:CVCL_HD57)

Curator: @abever99

SciCrunch record: RRID:CVCL_HD57

What is this?

DOI: 10.1038/s44318-024-00043-2

Resource: (ATCC Cat# PTA-5077, RRID:CVCL_6911)

Curator: @abever99

SciCrunch record: RRID:CVCL_6911

What is this?

DOI: 10.1038/s44318-024-00038-z

Resource: (CLS Cat# 300364/p489_U-2_OS, RRID:CVCL_0042)

Curator: @abever99

SciCrunch record: RRID:CVCL_0042

What is this?

DOI: 10.1038/s44318-024-00038-z

Resource: (KCB Cat# KCB 200706YJ, RRID:CVCL_0291)

Curator: @abever99

SciCrunch record: RRID:CVCL_0291

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Jackson ImmunoResearch Labs Cat# 711-585-152, RRID:AB_2340621)

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SciCrunch record: RRID:AB_2340621

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (LI-COR Biosciences Cat# 925-32211, RRID:AB_2651127)

Curator: @abever99

SciCrunch record: RRID:AB_2651127

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (LI-COR Biosciences Cat# 925-68020, RRID:AB_2687826)

Curator: @abever99

SciCrunch record: RRID:AB_2687826

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: AB_209584

Curator: @abever99

SciCrunch record: RRID: AB_209584

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: AB_2277617

Curator: @abever99

SciCrunch record: RRID: AB_2277617

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Thermo Fisher Scientific Cat# 44-668G, RRID:AB_2533716)

Curator: @abever99

SciCrunch record: RRID:AB_2533716

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Santa Cruz Biotechnology Cat# sc-6282, RRID:AB_628150)

Curator: @abever99

SciCrunch record: RRID:AB_628150

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Abcam Cat# ab209483, RRID:AB_2722676)

Curator: @abever99

SciCrunch record: RRID:AB_2722676

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Abcam Cat# ab207434, RRID:AB_2734728)

Curator: @abever99

SciCrunch record: RRID:AB_2734728

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: AB_47669

Curator: @abever99

SciCrunch record: RRID:AB_47669

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Abcam Cat# ab131205, RRID:AB_11156121)

Curator: @abever99

SciCrunch record: RRID:AB_11156121

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Abcam Cat# ab171941, RRID:AB_2629460)

Curator: @abever99

SciCrunch record: RRID:AB_2629460

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Abcam Cat# ab154856, RRID:AB_2687466)

Curator: @abever99

SciCrunch record: RRID:AB_2687466

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Cell Signaling Technology Cat# 3455, RRID:AB_2085352)

Curator: @abever99

SciCrunch record: RRID:AB_2085352

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Cell Signaling Technology Cat# 9722, RRID:AB_2230924)

Curator: @abever99

SciCrunch record: RRID:AB_2230924

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Cell Signaling Technology Cat# 3398, RRID:AB_2096481)

Curator: @abever99

SciCrunch record: RRID:AB_2096481

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Cell Signaling Technology Cat# 11815, RRID:AB_2616025)

Curator: @abever99

SciCrunch record: RRID:AB_2616025

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Abcam Cat# ab184247, RRID:AB_2895215)

Curator: @abever99

SciCrunch record: RRID:AB_2895215

What is this?

DOI: 10.1038/s44318-023-00008-x

Resource: (Cell Signaling Technology Cat# 72298, RRID:AB_2936479)

Curator: @abever99

SciCrunch record: RRID:AB_2936479

What is this?

DOI: 10.1172/JCI163145

Resource: (IMSR Cat# JAX_032536,RRID:IMSR_JAX:032536)

Curator: @bandrow

SciCrunch record: RRID:IMSR_JAX:032536

What is this?

DOI: 10.1172/JCI163145

Resource: (MMRRC Cat# 015499-UNC,RRID:MMRRC_015499-UNC)

Curator: @bandrow

SciCrunch record: RRID:MMRRC_015499-UNC

What is this?

DOI: 10.1021/jacs.3c09918

Resource: RRID:Addgene_161738

Curator: @evieth

SciCrunch record: RRID:Addgene_161738

What is this?

DOI: 10.1016/j.celrep.2024.114117

Resource: RRID:IMSR_JAX:037063

Curator: @abever99

SciCrunch record: RRID:IMSR_JAX:037063

What is this?

DOI: 10.1016/j.celrep.2024.114117

Resource: (CCLV Cat# CCLV-RIE 1018, RRID:CVCL_0063)

Curator: @abever99

SciCrunch record: RRID:CVCL_0063

What is this?

DOI: 10.1016/j.celrep.2024.114117

Resource: (BCRC Cat# 60005, RRID:CVCL_0030)

Curator: @abever99

SciCrunch record: RRID:CVCL_0030

What is this?

DOI: 10.1021/acs.jmedchem.3c01549

Resource: FlowJo (RRID:SCR_008520)

Curator: @evieth

SciCrunch record: RRID:SCR_008520

What is this?

DOI: 10.1021/acs.jmedchem.3c01549

Resource: (Cell Signaling Technology Cat# 2118, RRID:AB_561053)

Curator: @evieth

SciCrunch record: RRID:AB_561053

What is this?

DOI: 10.1021/acs.jmedchem.3c01549

Resource: (Proteintech Cat# 17168-1-AP, RRID:AB_2716755)

Curator: @evieth

SciCrunch record: RRID:AB_2716755

What is this?

DOI: 10.1021/acs.jmedchem.3c01549

Resource: (Abcam Cat# ab32356, RRID:AB_732924)

Curator: @evieth

SciCrunch record: RRID:AB_732924

What is this?

DOI: 10.1021/acs.jmedchem.3c01549

Resource: (Abcam Cat# ab8895, RRID:AB_306847)

Curator: @evieth

SciCrunch record: RRID:AB_306847

What is this?

DOI: 10.1021/acs.jmedchem.3c01549

Resource: (Abcam Cat# ab17721, RRID:AB_443964)

Curator: @evieth

SciCrunch record: RRID:AB_443964

What is this?

DOI: 10.1021/acs.jmedchem.3c01549

Resource: GraphPad Prism (RRID:SCR_002798)

Curator: @evieth

SciCrunch record: RRID:SCR_002798

What is this?

DOI: 10.1016/j.celrep.2024.114102

Resource: (Jackson ImmunoResearch Labs Cat# 711-605-152, RRID:AB_2492288)

Curator: @abever99

SciCrunch record: RRID:AB_2492288

What is this?

DOI: 10.1016/j.celrep.2024.114102

Resource: (Jackson ImmunoResearch Labs Cat# 713-545-147, RRID:AB_2340745)

Curator: @abever99

SciCrunch record: RRID:AB_2340745

What is this?

DOI: 10.1016/j.celrep.2024.114102

Resource: (Jackson ImmunoResearch Labs Cat# 712-605-153, RRID:AB_2340694)

Curator: @abever99

SciCrunch record: RRID:AB_2340694

What is this?

DOI: 10.1016/j.celrep.2024.114099

Resource: (RCB Cat# RCB2767, RRID:CVCL_0594)

Curator: @abever99

SciCrunch record: RRID:CVCL_0594

What is this?

DOI: 10.1016/j.celrep.2024.114099

Resource: (CCLV Cat# CCLV-RIE 1018, RRID:CVCL_0063)

Curator: @abever99

SciCrunch record: RRID:CVCL_0063

What is this?

DOI: 10.1016/j.celrep.2024.114099

Resource: RRID:IMSR_TAC:B6

Curator: @abever99

SciCrunch record: RRID:IMSR_TAC:B6

What is this?

DOI: 10.1021/acschembio.3c00493

Resource: Colorado State University Analytical Resources Core Facility (RRID:SCR_021758)

Curator: @evieth

SciCrunch record: RRID:SCR_021758

What is this?

DOI: 10.1016/j.celrep.2024.114016

Resource: (BCRJ Cat# 0278, RRID:CVCL_0132)

Curator: @abever99

SciCrunch record: RRID:CVCL_0132

What is this?

DOI: 10.1016/j.celrep.2024.114016

Resource: (ECACC Cat# 91061233, RRID:CVCL_2765)

Curator: @abever99

SciCrunch record: RRID:CVCL_2765

What is this?

DOI: 10.1016/j.immuni.2024.03.020

Resource: RRID:IMSR_ENV:HSD-044

Curator: @abever99

SciCrunch record: RRID:IMSR_ENV:HSD-044

What is this?

DOI: 10.1016/j.immuni.2024.03.020

Resource: (Abcam Cat# ab487, RRID:AB_304696)

Curator: @abever99

SciCrunch record: RRID:AB_304696

What is this?

DOI: 10.1016/j.cub.2024.03.053

Resource: RRID:Addgene_50459

Curator: @abever99

SciCrunch record: RRID:Addgene_50459

What is this?

DOI: 10.1016/j.cub.2024.03.053

Resource: RRID:Addgene_50475

Curator: @abever99

SciCrunch record: RRID:Addgene_50475

What is this?

DOI: 10.1016/j.cub.2024.03.053

Resource: RRID:Addgene_44361

Curator: @abever99

SciCrunch record: RRID:Addgene_44361

What is this?

DOI: 10.1016/j.cub.2024.03.053

Resource: RRID:Addgene_100834

Curator: @abever99

SciCrunch record: RRID:Addgene_100834

What is this?

DOI: 10.1016/j.neuron.2024.03.019

Resource: (IMSR Cat# JAX_012706,RRID:IMSR_JAX:012706)

Curator: @abever99

SciCrunch record: RRID:IMSR_JAX:012706

What is this?

DOI: 10.1016/j.neuron.2024.03.019

Resource: IMSR_JAX: 012706

Curator: @abever99

SciCrunch record: RRID:IMSR_JAX: 012706

What is this?

DOI: 10.1016/j.neuron.2024.03.019

Resource: (IMSR Cat# JAX_010815,RRID:IMSR_JAX:010815)

Curator: @abever99

SciCrunch record: RRID:IMSR_JAX:010815

What is this?

DOI: 10.1021/acscatal.3c03632

Resource: Texas A and M University Materials Characterization Core Facility (RRID:SCR_022202)

Curator: @evieth

SciCrunch record: RRID:SCR_022202

What is this?

DOI: 10.1021/acsbiomaterials.3c01393

Resource: Colorado University Boulder BioFrontiers Advanced Light Microscopy Core Facility (RRID:SCR_018302)

Curator: @evieth

SciCrunch record: RRID:SCR_018302

What is this?

DOI: 10.1021/acs.biomac.3c00982

Resource: RRID:Addgene_71461

Curator: @evieth

SciCrunch record: RRID:Addgene_71461

What is this?