Related Experiment Video

Updated: Aug 31, 2026

Examining BCL-2 Family Function with Large Unilamellar Vesicles
08:35

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

Ins(1,4,5)P3-mediated calcium signals and apoptosis: is there a role for Bcl-2?

C W Distelhorst1, H L Roderick

  • 1Department of Medicine, Comprehensive Cancer Center, Case Western Reserve University, Cleveland, OH 44106, USA. cwd@po.cwru.edu

Biochemical Society Transactions
|September 25, 2003
PubMed

Insights

The anti-apoptotic protein Bcl-2 may control calcium signals that influence cell death. This review explores how Bcl-2 might interact with inositol trisphosphate receptors to regulate calcium release and cell fate decisions.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Background:

  • Apoptosis, or programmed cell death, is a critical cellular process.
  • Calcium ions (Ca2+) play a crucial role in regulating cellular functions, including apoptosis.
  • The inositol 1,4,5-trisphosphate receptor (Ins(1,4,5)P3R) is a key mediator of calcium release from the endoplasmic reticulum.

Purpose of the Study:

  • To review the evidence linking the anti-apoptotic protein Bcl-2 to calcium signaling.
  • To explore the potential role of Bcl-2 in modulating Ins(1,4,5)P3R-mediated calcium release.
  • To speculate on the functional or physical interactions between Bcl-2 and Ins(1,4,5)P3R in cell death decisions.

Main Methods:

  • Literature review and synthesis of existing research.
  • Analysis of experimental data on Bcl-2 function and calcium signaling.
  • Speculative modeling of protein-receptor interactions.

Main Results:

  • Evidence suggests that Ins(1,4,5)P3-mediated calcium release from the endoplasmic reticulum triggers apoptosis.
  • Bcl-2 has been shown to regulate calcium release from the endoplasmic reticulum.
  • The anti-apoptotic protein Bcl-2 may modulate calcium signals that determine cell survival or death.

Conclusions:

  • Bcl-2 may regulate calcium signals involved in cell death.
  • Bcl-2 might interact with Ins(1,4,5)P3 receptors to control calcium release.
  • These interactions could be critical in determining cell fate decisions.

More Related Videos

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling08:51

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

Published on: June 25, 2015

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

Related Concept Videos

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...
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...
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...
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.
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.
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...