Saturday, September 28, 2013

OVEREXPRESSION OF TRIB3 AMD SUPPRESSION OF TIAF1,NEW TARGETS IN THERAPY!

Based on our current understanding most receptor failure will go on to induce the stress related pathways which ultimately will go on to produce epigenetic events which will include not only transcription factors production but also significant cytokines production.  Some of these Cytokines includes growth factors which not only have the role of inducing growth of the cell, but also blocking Apoptosis.
The activation of NF-kB, one of our stress coping pathway, happens to induce TRIB3 but this elevation has a negative regulator effect on the NF-kB therefore decreasing the intensity of one of the most significant trigger (in chronic exposure to irritant stimuli) or amplifier  of specific cancers, and driver of cytokine production.   Activating  this TRIB3 could have significant effect in autoimmune diseases and have a significant effect in supportive cancer treatment and maintenance settings.

TIAF1, however, needs to be suppressed because it is the mechanism by the TGF to block death of cells.
In diseases where growth factors are the drivers , block the hell out of this TIAF1 please.     At CRBCM we are trying to see if these 2 interventions may help IL-2 effect in melanoma and Renal cancers.  FUNDS are missing so please help if you can!
What we keep as a secret is the work on anti-granulin (because here Cyclin T is involved, and with it TRIB3)!(HIV is not far a target!)


"The protein encoded by this gene is a putative protein kinase that is induced by the transcription factor NF-kappaB. The encoded protein is a negative regulator of NF-kappaB, and can also sensitize cells to TNF- and TRAIL-induced apoptosis. In addition, this protein can negatively regulate the cell survival serine-threonine kinase AKT1.[3]

Interactions

TRIB3 has been shown to interact with:
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