Cellular stress increases RGS2 mRNA and decreases RGS4 mRNA levels in SH-SY5Y cells

Ling Song, Richard S Jope

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Modulation of the expression of regulator of G-protein signaling (RGS) proteins is a major mechanism used to modulate their actions. Besides control by second messengers, the expression of RGS proteins, particularly RGS2, can be regulated by cell stress. Because RGS2 and RGS4 expression can be regulated by the cell cycle, we examined if cell cycle signals are involved in their regulation following stress. Treatment of SH-SY5Y cells with camptothecin increased RGS2 mRNA and decreased RGS4 mRNA levels. This effect on RGS2 mRNA was blocked by the cyclin-dependent kinase-2 (cdk2) inhibitors roscovitine and purvalanol. Cell cycle arrest was further implicated in regulating RGS mRNA levels because geldanamycin, which causes cell cycle arrest by inhibiting the actions of heat shock protein 90, caused changes in the mRNA levels of RGS2 and RGS4 similar to, and additive with, the effects of camptothecin. Overall, these results indicate that cell cycle arrest regulates the expression of RGS2 and RGS4, and that the expression of these two RGS family members is oppositely regulated by stress that causes cell cycle arrest.

Original languageEnglish
Pages (from-to)205-209
Number of pages5
JournalNeuroscience Letters
Volume402
Issue number3
DOIs
StatePublished - Jul 24 2006
Externally publishedYes

Fingerprint

Cell Cycle Checkpoints
Messenger RNA
RGS Proteins
GTP-Binding Protein Regulators
Camptothecin
Cell Cycle
Cyclin-Dependent Kinase 2
HSP90 Heat-Shock Proteins
Second Messenger Systems

Keywords

  • Camptothecin
  • cdk2
  • Cell cycle arrest
  • Geldanamycin
  • RGS2
  • RGS4
  • Roscovitine

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Cellular stress increases RGS2 mRNA and decreases RGS4 mRNA levels in SH-SY5Y cells. / Song, Ling; Jope, Richard S.

In: Neuroscience Letters, Vol. 402, No. 3, 24.07.2006, p. 205-209.

Research output: Contribution to journalArticle

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