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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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The RAS/MAPK Axis Gets Stressed Out.

Scott A Foster1, Shiva Malek1

  • 1Department of Discovery Oncology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA.

Molecular Cell
|December 3, 2016
PubMed
Summary
This summary is machine-generated.

A novel stress-induced checkpoint suppresses RAS-MAPK signaling. This pathway, triggered by agents like Rigosertib, inhibits RAS-MAPK components SOS and RAF via JNK signaling, impacting cell growth and stress response.

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Area of Science:

  • Cellular biology
  • Molecular signaling pathways
  • Cancer research

Background:

  • RAS-MAPK signaling is crucial for cell proliferation and survival.
  • Dysregulation of RAS-MAPK is implicated in various cancers.
  • Understanding stress-induced regulation of this pathway is vital.

Purpose of the Study:

  • To identify and characterize a stress-induced checkpoint that regulates RAS-MAPK signaling.
  • To elucidate the molecular mechanisms underlying this stress response.
  • To explore the potential of targeting this pathway with agents like Rigosertib.

Main Methods:

  • Investigated cellular responses to mitotic and oxidative stress.
  • Utilized molecular biology techniques to analyze protein interactions and signaling cascades.
  • Examined the role of c-Jun N-terminal kinase (JNK) in mediating the checkpoint.

Main Results:

  • Identified a stress-induced checkpoint that suppresses RAS-MAPK activity.
  • Demonstrated that agents like Rigosertib activate this checkpoint.
  • Showed JNK-mediated inhibition of RAS-MAPK pathway components SOS and RAF.

Conclusions:

  • A novel stress-induced checkpoint effectively suppresses RAS-MAPK signaling.
  • This pathway offers a potential therapeutic target for cancers driven by RAS-MAPK.
  • Further research into Rigosertib and related compounds is warranted.