CHOP is implicated in programmed cell death in response to impaired function of the endoplasmic reticulum

Article Abstract:

The transcription factor CHOP plays a role in cell death in cases of malfunction of the endoplasmic reticulum. It may also contribute to cell regeneration. The experiment involved injecting mice recognized as having chop genotypes with a sublethal dose of tunicamycin. The chop-/- mice did not experience cellular death despite problems with renal function.

Genetic aspects, Cell death

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p53 and stress in the ER.

Article Abstract:

The potent effects of p53 including inducing apoptosis and senescence are discussed. The physiological significance of inhibiting p53 in response to endoplasmic reticulum (ER) stress is elaborated

Psychological aspects, Aging, Aging (Biology), Apoptosis

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Endoplasmic reticulum stress induces p53 cytoplasmic localization and prevents p53-dependent apoptosis by a pathway involving glycogen synthase kinase-3 beta

Article Abstract:

Inhibition of p53-mediated apoptosis by endoplasmic reticulum (ER) stress is demonstrated. Findings suggest that inactivation of p53 is a protective mechanism used by cells to adapt to ER stress.

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