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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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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...
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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...
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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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Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans
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Pumping the brakes on RAS - negative regulators and death effectors of RAS.

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|February 12, 2020
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Summary
This summary is machine-generated.

Aberrant RAS signaling drives cancer, often via defects in RAS regulators like Ras GTPase-activating proteins (RasGAPs). These proteins, including the RASSF family, suppress tumors through RAS-dependent and independent pathways.

Keywords:
DAB2IPGAPNF1RASRASA1RASAL2RASSF

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Activating mutations in RAS oncoproteins are frequent drivers of cancer.
  • RAS signaling can be aberrantly upregulated without RAS gene mutations, due to defects in RAS regulators.
  • Loss of function in Ras GTPase-activating proteins (RasGAPs) is common in tumors, with germline mutations causing clinical syndromes.

Purpose of the Study:

  • To examine the role of RAS effectors in tumor suppression.
  • To elucidate the mechanisms by which RasGAPs and the RASSF family contribute to tumor suppression.
  • To investigate both RAS-dependent and RAS-independent contributions to oncogenesis.

Main Methods:

  • Review of existing literature on RAS signaling pathways.
  • Analysis of the diverse binding partners and signaling mechanisms of RasGAPs.
  • Examination of the RASSF family's role in apoptosis, senescence, and RAS-mediated transformation.

Main Results:

  • RasGAPs regulate RAS activity but also impact signaling through RAS-independent mechanisms.
  • The RASSF family of tumor suppressors are critical for RAS-induced apoptosis and senescence.
  • Suppression of RASSF protein expression can lead to excessive RAS signaling by disrupting growth inhibitory pathways.

Conclusions:

  • RAS regulators, particularly RasGAPs and RASSF proteins, are crucial tumor suppressors.
  • These effectors contribute to tumor suppression via both direct RAS regulation and independent signaling pathways.
  • Understanding these mechanisms offers potential therapeutic targets for cancers with aberrant RAS activity.