Related Experiment Video

Updated: Jul 20, 2026

Analysis of Apoptosis in Zebrafish Embryos by Whole-mount Immunofluorescence to Detect Activated Caspase 3
08:20

Analysis of Apoptosis in Zebrafish Embryos by Whole-mount Immunofluorescence to Detect Activated Caspase 3

Published on: December 20, 2013

p41 as a possible marker for cell death is generated by caspase cleavage of p42/SETbeta in irradiated MOLT-4 cells

A Morita1, N Suzuki, Y Matsumoto

  • 1Department of Radiation Oncology, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.

Biochemical and Biophysical Research Communications
|November 30, 2000
PubMed

Insights

Radiation exposure induces a protein fragment, p41, from SETbeta (p42) via caspase-7 cleavage during apoptosis. This p41 protein may serve as a novel biomarker for cell death.

Area of Science:

  • Molecular Biology
  • Cell Death Research
  • Biochemistry

Background:

  • Previous work identified a novel protein, p41, in X-irradiated MOLT-4 cells undergoing rapid cell death.
  • An antibody (AM-1) detected both p41 and p42, with sequence analysis suggesting homology between p41 and the oncogene SET.

Purpose of the Study:

  • To elucidate the relationship between p41 and p42.
  • To identify the molecular mechanisms and caspases responsible for p42 cleavage.
  • To develop a simpler method for detecting p41 as a potential apoptosis marker.

Main Methods:

  • N-terminal amino acid sequencing of p41 and p42.
  • Preparation of polyclonal antibodies against peptide sequences.
  • In vitro cleavage assays using recombinant proteins and caspases.
  • Inhibition studies with caspase-specific inhibitors (Ac-DEVD-CHO, Ac-YVAD-CHO).
  • Detection methods including two-dimensional polyacrylamide gel electrophoresis (2-D PAGE) and one-dimensional PAGE (1-D PAGE).

Main Results:

  • p41 was identified as an N-terminal truncation of p42, with cleavage occurring at the carboxyl end of SNHD 18.
  • p42 was identified as SETbeta.
  • Radiation-induced cleavage of p42 and apoptosis were inhibited by Ac-DEVD-CHO, implicating caspases, particularly caspase-7.
  • A new antibody (AM-4) enabled simple 1-D PAGE detection of p41.

Conclusions:

  • p42 (SETbeta) is cleaved into p41 by caspases, primarily caspase-7, during radiation-induced apoptosis.
  • p41 can be detected using a specific antibody (AM-4) via 1-D PAGE, offering a simpler alternative to 2-D PAGE.
  • p41 shows potential as a reliable biomarker for apoptotic cell death.

More Related Videos

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis12:55

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

Published on: February 16, 2015

Evaluation of Caspase Activation to Assess Innate Immune Cell Death10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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...