Cell survival
Cell Survival
You want it protecting the sound, not shielding the damaged — survival for healthy cells, not a refuge for faulty ones.
In depth
Pro-survival signaling — the machinery that decides a stressed cell repairs rather than dies. Not uniformly good: the same signaling that rescues a healthy neuron protects a damaged cell that should have been cleared.
What drives it
Growth & survival signaling increases it.
Datta 1997, Cell 91:231 — PI3K/Akt phosphorylates the bcl-2-family member bad, inactivating it to suppress apoptosis and promote cell survival. PMID 9346240. Akt directly regulates cell survival by inhibiting pro-apoptotic signals — named specifically as bad and the FOXO transcription factors. The survival effect is therefore de-repression: Akt does not switch on a survival program so much as remove two death signals. this is the arm that makes Akt an oncogenic node — the same review frames it as a cancer therapy target, so 'more Akt signaling' is not straightforwardly desirable. Akt is not one switch — its two activating phosphosites govern different substrates: selectively inhibiting Ser473 weakened FOXO1/2a and FOXO3 but did not affect GSK3-beta or TSC2, while it is THR308 phosphorylation that tracks p-eNOS Ser1177 — Ser473 exerts rare effects on eNOS (PMC8255840). Which Akt site is engaged decides which downstream arm moves. PMID 9346240 · PMC8255840
Damage checkpoint reduces it.
p53 suppresses transformation by removing the proliferative OR survival capacity of cells carrying DNA damage or driving inappropriate cell-cycle progression — it is the switch that decides a damaged cell should not continue (PMC5287062). Loss or mutation of TP53 inhibits senescence, apoptosis and DNA repair, promoting self-renewal while impairing elimination of damaged cells (PMC7422622). Survival is not always the desirable direction: this pathway is why. PMC5287062
Metal-binding protein increases it.
Metallothionein induction is cytoprotective, raising cell survival under metal and oxidant stress. doi 10.1590/S0004-282X2011000100020
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.