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Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations
10:54

Studying Proteolysis of Cyclin B at the Single Cell Level in Whole Cell Populations

Published on: September 17, 2012

P38SAPK2 phosphorylates cyclin D3 at Thr-283 and targets it for proteasomal degradation

Oriol Casanovas1, Montserrat Jaumot, Ana-Belén Paules

  • 1Departament de Biologia Cel lular i Anatomia Patològica, Facultat de Medicina, Institut d'Investigacions Biomèdiques August Pi i Sunyer, University of Barcelona, Casanova 143, 08036, Spain.

Oncogene
|August 25, 2004
PubMed

Insights

Cyclin D3 degradation is essential for T-cell maturation and is regulated by p38SAPK kinases phosphorylating Thr-283. Dysregulation of this pathway may contribute to lymphoid cancers.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Cyclin D3 is crucial for precursor T-cell maturation.
  • Its tightly regulated levels are implicated in lymphoid malignancies.

Purpose of the Study:

  • To investigate the mechanisms regulating cyclin D3 levels.
  • To identify kinases involved in cyclin D3 regulation.

Main Methods:

  • Proteasome inhibition assays.
  • Analysis of ubiquitylation and degradation.
  • Kinase activity assays using p38SAPK family members.

Main Results:

  • Cyclin D3 degradation occurs via the proteasome, dependent on Thr-283 phosphorylation.
  • Stress conditions induce Thr-283-dependent cyclin D3 degradation.
  • p38SAPK kinases, including p38alphaSAPK2, phosphorylate cyclin D3 at Thr-283, leading to decreased cyclin D3 levels.

Conclusions:

  • p38SAPK-mediated phosphorylation of cyclin D3 at Thr-283 regulates its degradation.
  • This mechanism is vital for T-cell maturation.
  • Aberrations in this pathway may play a role in oncogenesis.

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