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Related Experiment Video

Updated: May 20, 2026

Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
15:43

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Published on: January 7, 2013

CD98 increases renal epithelial cell proliferation by activating MAPKs.

Nada Bulus1, Chloe Feral, Ambra Pozzi

  • 1Department of Medicine (Division of Nephrology), Vanderbilt University Medical Center, Tennessee, United States of America.

Plos One
|July 7, 2012
PubMed
Summary
This summary is machine-generated.

CD98 heavy chain (CD98hc) regulates kidney cell proliferation through distinct mechanisms involving its cytoplasmic tail and amino acid transport. Both pathways activate MAPK signaling, impacting cell survival and growth.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Renal Physiology

Background:

  • CD98 heavy chain (CD98hc) is a scaffolding protein involved in cell survival and growth.
  • CD98hc interacts with amino acid transporters (Lats) and integrins.
  • The precise role of CD98hc in cell proliferation and its signaling pathways remain incompletely understood.

Purpose of the Study:

  • To investigate the role of CD98hc in murine renal inner medullary collecting duct (IMCD) cell proliferation.
  • To elucidate the signaling pathways mediating CD98hc-dependent cell proliferation.
  • To determine if CD98hc-dependent amino acid transport influences cell proliferation.

Main Methods:

  • Downregulation of CD98hc expression using genetic manipulation.
  • Overexpression studies of CD98hc mutants lacking cytoplasmic tails or Lats-binding domains.
  • Analysis of MAPK (Erk, p38) and mTor signaling pathways.
  • Assessment of IMCD cell viability and proliferation.

Main Results:

  • Downregulating CD98hc expression led to IMCD cell death.
  • CD98hc's cytoplasmic tail is essential for serum-dependent cell proliferation.
  • CD98hc-dependent amino acid transport promotes proliferation independently of the cytoplasmic tail.
  • Both CD98hc-mediated proliferation mechanisms are regulated by Erk and p38 MAPK signaling.
  • mTor signaling activation by amino acid transport did not affect cell proliferation.

Conclusions:

  • CD98hc plays a critical role in IMCD cell survival and proliferation.
  • Distinct domains of CD98hc regulate cell proliferation through separate mechanisms.
  • MAPK signaling pathways are central mediators of CD98hc-dependent renal cell proliferation.
  • CD98hc's functions in cell proliferation are partially independent of mTor signaling.