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Regulation of cyclin D1 expression and cell cycle progression by mitogen-activated protein kinase cascade

Y Terada1, S Inoshita, O Nakashima

  • 1Second Department of Internal Medicine, Tokyo Medical and Dental University, Japan. yterada.med2@med.tmd.ac.jp

Kidney International
|October 3, 1999
PubMed

Insights

The transforming growth factor-beta-activating kinase-1 (TAK1) pathway regulates cell cycle progression. This study shows TAK1 influences cyclin D1 levels and cell proliferation via the MKK6-p38K pathway.

Area of Science:

  • Cellular Biology
  • Signal Transduction

Background:

  • Mitogen-activated protein kinases (MAPKs) are crucial for signal transduction and cell proliferation.
  • Transforming growth factor-beta-activating kinase-1 (TAK1) is a MAPK kinase kinase linked to the MKK6-p38K pathway.

Purpose of the Study:

  • To investigate the functional roles of the TAK1 pathway in regulating cell cycle progression and cyclin D1 expression.
  • To elucidate the involvement of the MKK6-p38K pathway in TAK1-mediated cellular responses.

Main Methods:

  • Transfection of constitutive active (TAKdN) and negative (TAKK63W) forms of TAK1 into LLC-PK1 cells.
  • Assessment of MKK6 phosphorylation, p38K activity, and cell cycle phase distribution (S and G2/M phases).
  • Analysis of cyclin D1 protein levels and promoter-luciferase activity.

Main Results:

  • Constitutively active TAK1 (TAKdN) enhanced MKK6 phosphorylation and p38K activity, inhibiting S and G2/M phases.
  • The negative form of TAK1 (TAKK63W) reduced TGF-beta-stimulated MKK6 phosphorylation and p38K activity, increasing S and G2/M phases.
  • The TAK1 pathway decreased cyclin D1 protein levels and promoter activity, whereas MKK1 activation increased them.

Conclusions:

  • The TAK1 pathway, through MKK6-p38K, plays a significant role in inhibiting cell proliferation by downregulating cyclin D1.
  • TAK1 acts as a negative regulator of cell cycle progression, contrasting with the positive role of the classic MAPK pathway activator MKK1.

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