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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...
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Related Experiment Video

Updated: Jun 3, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Published on: July 17, 2019

RASD2 Drives Renal Clear Cell Carcinoma Progression via RAF1 (Ser338) Phosphorylation.

Jingxuan Yu1,2, Gang Yu3, Yuan Liu4

  • 1Department of Urology, Postgraduate Union Training Base of General Hospital of Central Theater Command, School of Medicine, Wuhan University of Science and Technology, Wuhan, Hubei, China.

Cancer Science
|June 2, 2026
PubMed
Summary

RASD2 is overexpressed in kidney cancer, promoting tumor growth and spread by activating the P38/ERK-MAPK pathway via RAF1. Inhibiting RAF1 shows promise for treating clear cell renal cell carcinoma (ccRCC).

Keywords:
P38/ERK–MAPK signalingRAF1RASD2ccRCC

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The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers
12:22

The Use of Reverse Phase Protein Arrays (RPPA) to Explore Protein Expression Variation within Individual Renal Cell Cancers

Published on: January 22, 2013

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Clear cell renal cell carcinoma (ccRCC) is an aggressive cancer with few treatments.
  • The role of RASD2 in ccRCC tumorigenesis is currently unknown.
  • RASD2, a Ras-related GTP-binding protein, is implicated in melanoma progression.

Purpose of the Study:

  • To investigate the oncogenic functions and molecular mechanisms of RASD2 in ccRCC.
  • To determine if RASD2 plays a role in ccRCC progression and patient prognosis.
  • To explore potential therapeutic strategies targeting RASD2-mediated pathways.

Main Methods:

  • Analysis of RASD2 expression in ccRCC tissues and correlation with patient prognosis.
  • In vitro functional assays (proliferation, migration, invasion) and in vivo xenograft models.
  • Mechanistic studies involving pathway activation (P38/ERK-MAPK), protein interaction (co-immunoprecipitation, LC-MS/MS), and drug inhibition (BAY43-9006).

Main Results:

  • RASD2 is significantly overexpressed in ccRCC tumors and linked to poor prognosis.
  • RASD2 promotes ccRCC cell proliferation, migration, and invasion in vitro and in vivo.
  • RASD2 activates the P38/ERK-MAPK pathway by enhancing RAF1 phosphorylation at Ser338, which is critical for ccRCC growth.
  • RAF1 inhibition suppressed ccRCC progression and tumor growth.

Conclusions:

  • RASD2 acts as an oncoprotein in ccRCC, driving tumorigenesis through RAF1-mediated P38/ERK-MAPK pathway activation.
  • Targeting RAF1 represents a potential therapeutic strategy for ccRCC patients.
  • RASD2 is a novel therapeutic target for clear cell renal cell carcinoma.