For starters, TA-65 does NOT increase the transcription of the hTERT or telomerase gene. That can be shown from this Affymetrix Gene Chip data performed by Sierra Sciences *(unpublished poster by Tim Wang)
Secondly, it appears to have only a limited gene activation profile of these select genes:
What this means is that there is no direct 1:1 upregulation of one gene (like more cowbell) but rather there is an upstream ‘conductor’ of sorts, or cell signaling mechanism, that is charged with enhancing these multiple gene activations by signaling.
The key discovery was by Molgora et al in 2013 with this paper indicating the MAPK pathway was the mechanism by which TA-65 increased telomerase activity.
In other words, there is a suite of behaviors that is kicked up a notch, like a musical ensemble that is conducted by a small band leader. It is not one instrument but a set of evolutionary behaviors that have telomerase activation as one of their features although as the above slide shows, there are many behaviors related to cell copying that are enhanced.
So in conclusion, the MAPK pathways are (from Wikipedia)
MAPKs are involved in directing cellular responses to a diverse array of stimuli, such as mitogens, osmotic stress, heat shock and proinflammatory cytokines. They regulate cell functions including proliferation, gene expression, differentiation, mitosis, cell survival, and apoptosis.
In other words, TA-65 is an adaptogen that uses the MAPK pathways to help the cells improve cell proliferation, efficiency, and even, paradoxically, cell suicide.
This is consistent with my clinical observations and if you would like to know more about telomerase activation medicine, or perhaps more properly, adaptogenic medicine, read my book, Telomere Timebombs: Defusing the Terror of Aging
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