Related Experiment Video

Updated: Aug 7, 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

Role of Bid-induced mitochondrial outer membrane permeabilization in granzyme B-induced apoptosis

Nigel J Waterhouse1, Karin A Sedelies, Joseph A Trapani

  • 1Cancer Cell Death Laboratory, Cancer Immunology Program, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia. nigel.waterhouse@petermac.org

Immunology and Cell Biology
|January 13, 2006
PubMed

Insights

Cytotoxic lymphocytes induce target cell death via granzyme release. This study explores granzyme B

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Cytotoxic lymphocytes (CL) eliminate target cells through granule exocytosis.
  • Granzymes delivered by CL induce target cell death by cleaving substrates.
  • Granzyme B is implicated in apoptosis, but its precise mechanism and role in CL-mediated killing remain debated.

Purpose of the Study:

  • To elucidate the mechanism of granzyme B-induced cell death.
  • To clarify the contribution of granzyme B to cytotoxic lymphocyte-mediated cell death.
  • To assess the relevance of granzyme B pathways in viral-infected and transformed cells.

Main Methods:

  • Analysis of granzyme B-mediated cell death pathways.
  • Investigation of granzyme B's role in cytotoxic lymphocyte function.
  • Examination of granzyme B's relevance in specific cellular contexts (viral infection, transformation).

Main Results:

  • Recent findings on granzyme B-induced cell death mechanisms are discussed.
  • The specific contribution of granzyme B to overall CL-induced cell death is evaluated.
  • Potential implications for CL-mediated killing of infected and cancerous cells are explored.

Conclusions:

  • Granzyme B plays a significant role in cytotoxic lymphocyte-mediated cell death.
  • Understanding granzyme B pathways is crucial for comprehending immune responses against viral infections and cancer.
  • Further research is needed to fully delineate granzyme B's function and therapeutic potential.

More Related Videos

A Colorimetric Assay that Specifically Measures Granzyme B Proteolytic Activity: Hydrolysis of Boc-Ala-Ala-Asp-S-Bzl05:20

A Colorimetric Assay that Specifically Measures Granzyme B Proteolytic Activity: Hydrolysis of Boc-Ala-Ala-Asp-S-Bzl

Published on: November 28, 2014

A High Yield and Cost-efficient Expression System of Human Granzymes in Mammalian Cells09:16

A High Yield and Cost-efficient Expression System of Human Granzymes in Mammalian Cells

Published on: June 10, 2015

Related Concept Videos

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.
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...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
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...