Related Experiment Video

Updated: Aug 7, 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

Inducible transcription factor expression in a cell culture model of apoptosis

A Woodgate1, M Walton, G A MacGibbon

  • 1The Department of Pharmacology and Clinical Pharmacology, Faculty of Medicine and Health Science, University of Auckland, Private Bag 92019, Auckland, New Zealand.

Brain Research. Molecular Brain Research
|March 30, 1999
PubMed

Insights

Okadaic acid induces nerve cell death (apoptosis) in PC12 cells, involving Jun and Fos proteins and increased AP-1 activity. This model aids research into inducible transcription factors in apoptosis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Neuroscience

Background:

  • Apoptosis, or programmed cell death, is crucial for development and homeostasis.
  • The role of inducible transcription factors (ITFs) in apoptosis is not fully understood.
  • Okadaic acid is a known inducer of cellular stress and apoptosis.

Purpose of the Study:

  • To develop and characterize a model of nerve cell death using okadaic acid.
  • To investigate the involvement of Jun and Fos proteins in okadaic acid-induced apoptosis.
  • To explore the role of AP-1 transcriptional activity in this cell death pathway.

Main Methods:

  • Utilized PC12 cells as a model system for nerve cell death.
  • Administered okadaic acid to induce apoptosis.
  • Employed phosphorylation-specific antibodies to detect c-Jun phosphorylation.
  • Performed electrophoretic gel mobility shift and luciferase assays to assess AP-1 binding and activity.

Main Results:

  • Okadaic acid triggered apoptosis in PC12 cells via a protein synthesis-dependent pathway.
  • Apoptosis was associated with the induction of JunB, c-Jun, JunD, and Fos proteins.
  • c-Jun was phosphorylated at serine 63 and serine 73.
  • Increased AP-1 binding and transcriptional activity were observed, correlating with Fos and Jun protein expression.

Conclusions:

  • The okadaic acid-induced PC12 cell death model effectively demonstrates the involvement of inducible transcription factors in apoptosis.
  • Fos and Jun proteins play a significant role in the apoptotic cascade.
  • This model system is valuable for further investigating the mechanisms of ITFs in programmed cell death.

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

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

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...
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.
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...