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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.
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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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Functional and structural insights into RAS effector proteins.

Alessandro M Mozzarelli1, Dhirendra K Simanshu2, Pau Castel1

  • 1Department of Biochemistry and Molecular Pharmacology, NYU Grossman School of Medicine, New York, NY, USA; Laura and Isaac Perlmutter NYU Cancer Center, NYU Langone Health, New York, NY, USA.

Molecular Cell
|July 18, 2024
PubMed
Summary
This summary is machine-generated.

RAS proteins are molecular switches crucial for cell processes. This review details RAS effector proteins, their interactions, and therapeutic potential in RAS-mediated signaling.

Keywords:
GTPaseRASRAS-binding domainRBDeffector

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Area of Science:

  • Molecular biology
  • Cellular signaling
  • Biochemistry

Background:

  • RAS proteins function as guanosine triphosphate (GTP) hydrolases, acting as molecular switches in cellular processes.
  • Activated RAS GTPases interact with specific RAS effector proteins, initiating downstream signaling pathways.
  • Over 50 human RAS effector proteins are known, with many implicated in RAS-dependent signaling.

Purpose of the Study:

  • To review the mechanisms and functions of known RAS effector proteins.
  • To provide structural insights into RAS-effector interactions.
  • To explore the significance of RAS-effector complexes in signaling and their therapeutic potential.

Main Methods:

  • Literature review of biochemical and structural analyses of RAS effectors.
  • Examination of studies using model organisms to understand RAS-effector roles.
  • Analysis of existing data on RAS-mediated signaling pathways.

Main Results:

  • Detailed discussion of identified RAS effector proteins and their functions.
  • Structural perspectives on the dynamics of RAS-effector complex formation.
  • Evaluation of the significance of these interactions in cellular signaling and disease.

Conclusions:

  • While much is known, critical aspects of RAS-effector complex dynamics and biological functions require further elucidation.
  • Understanding RAS-effector interactions is vital for deciphering RAS-mediated signaling.
  • RAS effector proteins represent promising therapeutic targets for diseases involving RAS signaling.