wild4nano, after reading thru this several times, here's the part that helps me:
"p53 has many mechanisms of anticancer function, and plays a role in apoptosis, genomic stability, and inhibition of angiogenesis. In its anti-cancer role, p53 works through several mechanisms:
• It can activate DNA repair proteins when DNA has sustained damage.
• It can arrest growth by holding the cell cycle at the G1/S regulation point on DNA damage recognition (if it holds the cell here for long enough, the DNA repair proteins will have time to fix the damage and the cell will be allowed to continue the cell cycle).
• It can initiate apoptosis, the programmed cell death, if DNA damage proves to be irreparable.
p53 pathway: In a normal cell p53 is inactivated by its negative regulator, mdm2. Upon DNA damage or other stresses, various pathways will lead to the dissociation of the p53 and mdm2 complex. Once activated, p53 will induce a cell cycle arrest to allow either repair and survival of the cell or apoptosis to discard the damaged cell. How p53 makes this choice is currently unknown.
Activated p53 binds DNA and activates expression of several genes including microRNA miR-34a,[27] WAF1/CIP1 encoding for p21 and hundreds of other down-stream genes. p21 (WAF1) binds to the G1-S/CDK (CDK2) and S/CDK complexes (molecules important for the G1/S transition in the cell cycle) inhibiting their activity.
When p21(WAF1) is complexed with CDK2 the cell cannot continue to the next stage of cell division. A mutant p53 will no longer bind DNA in an effective way, and, as a consequence, the p21 protein will not be available to act as the "stop signal" for cell division."
So the activation of wild p53 or the repair of mutant p53 (by Kevitrin) would then trigger the expression of p21 and thereby stop the replication of tumor cells.
Very cool!!
Thanks wild, doc, JB, etc. I think I understand now.
Magic
Opportunities always look bigger going than coming!
