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.
InteractionsTRIB3 has been shown to interact with:
- SIAH1, and
TGFB1-induced anti-apoptotic factor 1 is a protein that in humans is encoded by the TIAF1 gene.
InteractionsTIAF1 has been shown to interact with Janus kinase 3 and TRIB3.wikipedia
(watch this in Promyelocytic leukemia)
CRBCM is coming!