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Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...
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.
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...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
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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

Granzymes and cell death.

Denis Martinvalet1, Jerome Thiery, Dipanjan Chowdhury

  • 1Immune Disease Institute and Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.

Methods in Enzymology
|July 30, 2008
PubMed
Summary
This summary is machine-generated.

Granzymes induce cell death and require perforin for entry into target cells. This work details in vitro methods to study granzyme function, overcoming challenges posed by functional redundancy in animal models.

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

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Granzymes are serine proteases crucial for immune surveillance, inducing apoptosis in target cells.
  • Cytotoxic T lymphocytes and natural killer cells release granzymes via granule exocytosis.
  • Perforin is essential for granzyme delivery into target cells, initiating programmed cell death.

Purpose of the Study:

  • To present methods for studying granzyme function in vitro.
  • To address the challenge of granzyme functional redundancy in animal models.
  • To enable research under physiologically relevant conditions.

Main Methods:

  • Detailed description of in vitro experimental systems.
  • Focus on methods mimicking physiological conditions.
  • Techniques to overcome limitations of animal models.

Main Results:

  • Established experimental conditions for studying granzyme activity.
  • Provided a framework for dissecting individual granzyme functions.
  • Facilitated the study of granzyme-mediated apoptosis pathways.

Conclusions:

  • In vitro systems are essential for understanding granzyme biology due to functional redundancy.
  • The discussed methods allow for precise investigation of granzyme functions.
  • This work supports further research into targeted cell death pathways.