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Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

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 Pathway01:31

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...
Apoptosis01:30

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.
Caspases01:24

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.
Cellular Injury V: Apoptosis and Autophagy01:22

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...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...

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Related Experiment Video

Updated: May 15, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Foxa2 may modulate hepatic apoptosis through the cIAP1 pathway.

Kewei Wang1, John J Brems, Richard L Gamelli

  • 1Departments of Surgery, University of Illinois College of Medicine at Peoria, IL 61605, USA. kewang@uic.edu

Cellular Signalling
|January 1, 2013
PubMed
Summary

The liver transcription factor Foxa2 (forkhead box A2) protects against liver injury by inhibiting hepatocyte apoptosis. Foxa2 regulates the anti-apoptotic gene cIAP1, offering a therapeutic target for liver diseases.

More Related Videos

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Related Experiment Videos

Last Updated: May 15, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Area of Science:

  • Hepatology
  • Molecular Biology
  • Cell Death Research

Background:

  • Hepatocyte apoptosis is a key feature of chronic liver injury.
  • The precise molecular mechanisms driving this apoptosis are not fully understood.
  • The liver-enriched transcription factor Foxa2 (forkhead box A2) is linked to inflammation and neoplasia and may regulate apoptosis.

Purpose of the Study:

  • To investigate the relationship between Foxa2 and hepatic apoptosis.
  • To elucidate the molecular mechanisms by which Foxa2 influences liver cell death.

Main Methods:

  • Induction of apoptosis in liver cells using various factors.
  • Measurement of caspase activity and TUNEL assay to quantify apoptosis.
  • Analysis of Foxa2 expression, gene silencing (siRNA), and overexpression (vectors) in HepG2 cells.
  • Correlation of Foxa2 levels with anti-apoptotic gene expression (cIAP1, cIAP2, XIAP, survivin).
  • Electrophoretic mobility shift assay (EMSA), gel supershift assay, and chromatin immunoprecipitation (ChIP) assay to assess Foxa2 binding to the cIAP1 promoter.

Main Results:

  • Apoptotic liver injury correlated with decreased Foxa2 expression.
  • Foxa2 overexpression reduced apoptosis, while Foxa2 silencing increased apoptosis in HepG2 cells.
  • Foxa2 expression levels were associated with anti-apoptotic genes, notably cIAP1.
  • Foxa2 directly binds to the cIAP1 promoter, regulating its activity and expression.

Conclusions:

  • Foxa2 transcription factor modulates hepatic apoptosis potentially via the cIAP1 signaling pathway.
  • Foxa2 represents a potential therapeutic target for treating liver diseases characterized by apoptosis.