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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.
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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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...
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...

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Updated: Jul 22, 2026

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

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

Published on: December 27, 2016

Specific TrkA survival signals interfere with different apoptotic pathways

E Ulrich1, A Duwel, A Kauffmann-Zeh

  • 1Imperial Cancer Research Fund Laboratories, London, UK.

Oncogene
|March 4, 1998
PubMed
Summary

Nerve growth factor receptor TrkA delays apoptosis by activating distinct pathways. The Akt/PKB pathway is crucial for U.V.-induced apoptosis, while c-Myc-induced apoptosis involves a novel, Akt/PKB-independent pathway.

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Area of Science:

  • Cell biology
  • Molecular biology
  • Signal transduction

Background:

  • Tyrosine kinase receptors, like TrkA, are vital for cell survival by balancing cell viability and apoptosis.
  • Understanding the specific domains and pathways involved in TrkA-mediated survival signaling is crucial for deciphering cellular fate decisions.

Purpose of the Study:

  • To investigate the role of specific TrkA receptor domains in mediating survival signaling against different apoptotic stimuli.
  • To elucidate the downstream signaling pathways, including Akt/PKB and MAPK, activated by TrkA in response to various apoptotic triggers.

Main Methods:

  • Expression of wild-type (wt) and mutant TrkA receptors (Y490F, Y785F, YY490/785FF) in Rat-1/MycER fibroblasts.
  • Assessment of TrkA's ability to delay apoptosis induced by c-Myc, U.V. irradiation, and Cycloheximide.
  • Analysis of downstream signaling pathway activation (MAPK Erk2, Akt/PKB) and inhibition using specific kinase inhibitors (LY294002, Wortmannin).

Main Results:

  • wt-TrkA delays apoptosis induced by c-Myc, U.V., and Cycloheximide, activating Erk2 and Akt/PKB.
  • TrkA Y490F mutant delays c-Myc-induced apoptosis but not U.V.-induced apoptosis, and does not activate Akt/PKB.
  • TrkA Y785F mutant protects against both c-Myc and U.V.-induced apoptosis, while the double mutant YY490/785FF loses this protective ability.
  • PI3-kinase inhibitors block U.V.-induced survival but not c-Myc-induced survival mediated by TrkA.
  • U.V.-induced apoptosis relies on the Akt/PKB pathway, whereas c-Myc-induced apoptosis is inhibited via a novel, Akt/PKB-independent pathway.

Conclusions:

  • TrkA employs distinct signaling pathways to counteract specific apoptotic stimuli.
  • The Akt/PKB pathway is essential for TrkA-mediated survival against U.V. damage.
  • A novel, Akt/PKB-independent pathway activated by TrkA contributes to survival against c-Myc-induced apoptosis.
  • These findings highlight the adaptability of TrkA signaling in regulating cell survival through multiple mechanisms.