Related Experiment Video

Updated: Aug 29, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Role of Gab1 in UV-induced c-Jun NH2-terminal kinase activation and cell apoptosis

Yingqing Sun1, Jing Yuan, Houqi Liu

  • 1Cancer Research Center, The Burnham Institute, La Jolla, California 92037, USA.

Molecular and Cellular Biology
|January 30, 2004
PubMed

Insights

The Gab1 adapter protein is crucial for activating the c-Jun NH(2)-terminal protein kinase (JNK) pathway in response to UV irradiation, a process linked to cell apoptosis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • UV irradiation triggers the JNK pathway, leading to apoptosis in mammalian cells.
  • The precise molecular mechanisms of UV-induced JNK activation remain incompletely understood.

Purpose of the Study:

  • To elucidate the role of the Gab1 adapter protein in the UV-induced JNK signaling cascade.
  • To investigate Gab1's involvement in UV-induced apoptosis.

Main Methods:

  • Utilized Gab1-deficient mouse fibroblast cells and control cells.
  • Assessed JNK activity, caspase 3 induction, and apoptotic cell death.
  • Performed genetic rescue experiments and analyzed protein-protein interactions.
  • Investigated the involvement of c-Met and Src family kinases.

Main Results:

  • Gab1-deficient cells showed impaired JNK activation and reduced apoptosis after UV or heat shock.
  • Reintroducing Gab1 restored JNK activity and UV-induced apoptosis.
  • Gab1 forms a complex with JNK and undergoes tyrosine phosphorylation upon UV exposure.
  • c-Met and Src family kinases mediate UV-induced Gab1 phosphorylation and JNK activation.

Conclusions:

  • Gab1 plays an essential role in the UV-induced JNK pathway activation.
  • Gab1 functions as a key mediator in the cellular response to UV light, influencing apoptosis.

More Related Videos

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

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...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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...
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.
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...
Amplifying Signals via Enzymatic Cascade01:22

Amplifying Signals via Enzymatic Cascade

When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze the...