Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
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.
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...
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...
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...
Phagocytosis of Apoptotic Cells01:17

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or  immature dendritic cells. Non-professional phagocytes such as  epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes. 
Normal cells contain receptors that prevent them from being recognized by phagocytes.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Interaction of Human Peripheral NK Cells with Bacterial Polysaccharides.

Doklady. Biochemistry and biophysics·2026
Same author

Clinical and Morphological Features of gPALB2-Associated Breast Cancer in the Russian Population.

Bulletin of experimental biology and medicine·2025
Same author

The Antigen-Specific Response of NK Cells to SARS-CoV-2 Correlates With KIR2DS4 Expression.

Journal of medical virology·2024
Same author

Subpopulation Heterogeneity of NK Cells during the Genetic Modification for Subsequent Use in Targeted Therapy.

Doklady. Biochemistry and biophysics·2023
Same author

Heat Shock Protein 70 kDa as a Target for Diagnostics and Therapy of Cardiovascular and Cerebrovascular Diseases.

Current pharmaceutical design·2019
Same author

Tumor-Infiltrating Lymphocytes in Breast Cancer. Association with Clinical and Pathological Parameters.

Bulletin of experimental biology and medicine·2018

Related Experiment Video

Updated: Jun 27, 2026

A Colorimetric Assay that Specifically Measures Granzyme B Proteolytic Activity: Hydrolysis of Boc-Ala-Ala-Asp-S-Bzl
05:20

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

Published on: November 28, 2014

[Apoptosis induced by granzyme B].

A V Sintsov1, E I Kovalenko, M A Khanin

  • 1Center for Theoretical Problems of Physicochemical Pharmacology, Russian Academy of Sciences, ul. Kosygina 4, Moscow, 119991 Russia.

Bioorganicheskaia Khimiia
|December 18, 2008
PubMed
Summary
This summary is machine-generated.

This study summarizes biochemical research on granzyme B-induced apoptosis, focusing on procaspase activation and target proteolysis. Kinetic constants for these granzyme B enzymatic reactions are detailed.

More Related Videos

A High Yield and Cost-efficient Expression System of Human Granzymes in Mammalian Cells
09:16

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

Published on: June 10, 2015

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

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

Published on: February 16, 2015

Related Experiment Videos

Last Updated: Jun 27, 2026

A Colorimetric Assay that Specifically Measures Granzyme B Proteolytic Activity: Hydrolysis of Boc-Ala-Ala-Asp-S-Bzl
05:20

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 Cells
09:16

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

Published on: June 10, 2015

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
12:55

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

Published on: February 16, 2015

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cellular Biology

Context:

  • Granzyme B is a key serine protease involved in immune responses and programmed cell death.
  • Apoptosis, or programmed cell death, is a crucial process for development and tissue homeostasis.
  • Understanding granzyme B's enzymatic activity is vital for dissecting apoptotic pathways.

Purpose:

  • To review and synthesize biochemical findings on granzyme B-mediated apoptosis.
  • To highlight the mechanisms of procaspase activation and substrate cleavage by granzyme B.
  • To present quantitative kinetic data for granzyme B's enzymatic reactions.

Summary:

  • Biochemical studies on granzyme B-induced apoptosis are summarized, detailing its role in activating caspases and cleaving cellular targets.
  • The review focuses on the enzymatic mechanisms underlying granzyme B's function in initiating apoptosis.
  • Kinetic constants for key granzyme B-catalyzed reactions are compiled, providing quantitative insights into its catalytic efficiency.

Impact:

  • Provides a consolidated resource for researchers studying granzyme B and apoptosis.
  • Facilitates a deeper understanding of the molecular mechanisms driving programmed cell death.
  • Offers valuable kinetic parameters for computational modeling and drug development targeting apoptotic pathways.