Gβγ counteracts Gαq signaling upon α1-adrenergic receptor stimulation

Motohiro Nishida, Shuichi Takagahara, Yoshiko Maruyama, Yoshiyuki Sugimoto, Taku Nagao, Hitoshi Kurose

研究成果: ジャーナルへの寄稿学術誌査読

7 被引用数 (Scopus)


In rat neonatal myocytes, a constitutively active Gαq causes cellular injury and apoptosis. However, stimulation of the α1-adrenergic receptor, one of the Gq protein-coupled receptors, with phenylephrine for 48 h causes little cellular injury and apoptosis. Expression of the Gβγ-sequestering peptide βARK-ct increases the phenylephrine-induced cardiac injury, indicating that Gβγ released from Gq counteracts the Gαq-mediated cellular injury. Stimulation with phenylephrine activates extracellular signal-regulated kinase (ERK) and Akt, and activation is significantly blunted by βARK-ct. Inhibition of Akt by inhibitors of phosphatidylinositol 3-kinase increases the cellular injury induced by phenylephrine stimulation. In contrast to the inhibition of Akt, inhibition of ERK does not affect the phenylephrine-induced cardiac injury. These results suggest that Gβγ released from Gq upon α1-adrenergic receptor stimulation activates ERK and Akt. However, activation of Akt but not ERK plays an important role in the protection against the Gαq-induced cellular injury and apoptosis.

ジャーナルBiochemical and Biophysical Research Communications
出版ステータス出版済み - 3月 8 2002

!!!All Science Journal Classification (ASJC) codes

  • 生物理学
  • 生化学
  • 分子生物学
  • 細胞生物学


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