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.

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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

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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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