7 Matching Annotations
  1. Jul 2019
  2. Jun 2019
    1. KMO is located in the outer mitochondrial membrane.

      So, this entire pathway, or segment, is dependent on mitochondria

    2. targets is PPARγ, presumably being a major signalling pathway involved in neuroinflammation

      All of the above is great info and there are many suspects, the main current is PPARgamma. TheNrf pathways hold quite a bit of niftiness in the translation regulation, cap dependent, independent proteins and folding. Seeking some connection to, causative agent to the age related and stress related cascade hinges on mitochodria in some, (it certainly has its finger in the pie-- but so do many root level processes) Part of my diligence in the mito domain is the Anti-Streetlight effect. That is, we have looked everywhere else and, yes, tehre are constantly new revelations, but these areas of mitochondria gentics, translational regulation and defects(both-not all "errors" are errors), and ribosomal and tRNA changes have been excluded from research and thought to be mechanistis and stable non-changing variables.And now, that they are known to be ariable...muchwill have to be reevaluated

    1. In 99.3% of the time under unstressed conditions,

      Danism: A cell in a diseased state does not respond the same way as a cell in a non-diseased state. This is essential and has many roots. Translation Regulation being the most controversial.

    2. PRDX5 being present in the mitochondrion,
    3. CysP sulfhydryl

      keep track of this sulfur molecule. It has turned up in other areas.

  3. Nov 2013