It is by now quite clear that Senescence is clearly linked to the health of your eyes (given the frequency of cataract in elderly) and intrinsic deterioration of the heart muscle and muscles in general. Elderly's muscles seem to become hypothrophic without control. Kidney deterioration seem to follow closely as if an organ shutdown is in the work. Indeed some genes seems to be at work in a very discrete way indicating to the eyes, the heart, the muscles, and peripherally the kidney that it is time to shut this thing down. The proof is that keeping exercising seems to fool this message keeping people "young".
At cellular or gene level, the genes that form the muscles must be implicated! The Myb, MyoD,Myogenein, Myf5, MEF2, GNA12 ...some of which interacts with MDFI (watch out because it is an gene inhibitor): (look at the leukemias'story when it comes to interacting with inhibitors (our eyes is square and fare in the SIX1)) six1 talks to PAX (Melanoma) (how this is liked to Breast cancer...well? did you see E2A? It's here though!)
MDFI (don't say we at CRBCM did not warned you) AND IF YOUR EYES ARE RIVETED ON THIS ONE, DON'T FORGET MDFIC AS A TARGET! OH! BY THE WAY LOOK-UP ECRG2 (esophageal cancer ) AND RBEL1 WHILE ON THIS! (Why? because it is a rebel gene! think about that!)
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UniProtKB/Swiss-Prot: MDFI_HUMAN, Q99750
Function: Inhibits the transactivation activity of the Myod family of myogenic factors and represses myogenesis. Actsby associating with Myod family members and retaining them in the cytoplasm by masking their nuclear localizationsignals. Can also interfere with the DNA-binding activity of Myod family members. Plays an important role introphoblast and chondrogenic differentiation. Regulates the transcriptional activity of TCF7L1/TCF3 by interactingdirectly with TCF7L1/TCF3 and preventing it from binding DNA. Binds to the axin complex, resulting in an increase inthe level of free beta-catenin. Affects axin regulation of the WNT and JNK signaling pathways (By similarity) |
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