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Apoptosis

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.

Cellular Injury V: Apoptosis and Autophagy

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

The Extrinsic Apoptotic Pathway

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

Caspases

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.

Regulation of the Unfolded Protein Response

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...

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Related Experiment Video

Updated: Jun 5, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Resveratrol and apoptosis.

Hung-Yun Lin¹, Heng-Yuan Tang, Faith B Davis

¹Ordway Research Institute, Albany, New York 12208, USA. hlin@ordwayresearch.org

Annals of the New York Academy of Sciences

|January 26, 2011

Summary

This summary is machine-generated.

Resveratrol induces cancer cell death by activating ERK1/2 and p53, leading to nuclear COX-2 accumulation. This pathway, involving integrin α(v)β₃, is crucial for resveratrol

Related Experiment Videos

Last Updated: Jun 5, 2026

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Area of Science:

Molecular biology
Cellular biology
Cancer research

Background:

Resveratrol, a natural stilbene, exhibits cardioprotective and anti-cancer effects.
Integrin α(v)β₃ and its arginine-glycine-aspartate (RGD) recognition site are implicated in cellular signaling.
Mitogen-activated protein kinase (ERK1/2) and p53 are key regulators of apoptosis.

Purpose of the Study:

To elucidate the molecular mechanism of resveratrol-induced apoptosis in cancer cells.
To identify the role of integrin α(v)β₃ and downstream signaling pathways in resveratrol's anti-cancer activity.

Main Methods:

In vitro cell treatment with resveratrol and specific inhibitors (RGD peptide, PD98059, NS-398).
Analysis of protein activation and nuclear translocation (ERK1/2, p53, COX-2).
Chromatin immunoprecipitation to assess gene promoter binding.

Main Results:

Resveratrol activates ERK1/2, leading to p53 phosphorylation and apoptosis, blocked by an RGD peptide.
Resveratrol induces nuclear accumulation of COX-2, which complexes with pERK1/2 and p53.
Nuclear COX-2 binds to promoters of p53-responsive genes; its inhibition prevents apoptosis.

Conclusions:

Resveratrol triggers cancer cell apoptosis via a mechanism involving integrin α(v)β₃, ERK1/2, p53, and nuclear COX-2.
The anti-apoptotic effect is mediated by COX-2's nuclear role in gene regulation, independent of its enzymatic activity.
Growth factors like EGF, estrogen, and thyroid hormone can counteract resveratrol-induced apoptosis downstream of ERK1/2.