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Somatostatin type V receptor activates c-Jun N-terminal kinases via Galpha(12) family G proteins

K Komatsuzaki1, K Terashita, T B Kinane

  • 1Department of Pediatrics, Pediatric Pulmonary Service, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USA.

Biochemical and Biophysical Research Communications
|December 14, 2001
PubMed

Insights

Somatostatin binding to its receptor SSTR5 activates stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK). This pathway involves Galpha(12) and Galpha(13) proteins, revealing a novel signaling mechanism.

Area of Science:

  • Neuroendocrinology
  • Cell Signaling
  • Molecular Biology

Background:

  • Somatostatin exhibits varied cellular effects, including anti-proliferation and growth stimulation.
  • Stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) pathways are implicated in cell growth regulation.
  • The precise interaction between somatostatin and SAPK/JNK signaling remains incompletely understood.

Purpose of the Study:

  • To elucidate the relationship between somatostatin receptor activation and SAPK/JNK pathway modulation.
  • To identify the specific somatostatin receptor subtype involved in SAPK/JNK regulation.
  • To determine the intracellular signaling molecules mediating this cross-talk.

Main Methods:

  • Utilized cell-based assays to investigate somatostatin receptor signaling.
  • Employed Western blotting and kinase assays to measure SAPK/JNK activity.
  • Investigated the role of G proteins, specifically Galpha(12) and Galpha(13), in the signaling cascade.

Main Results:

  • Somatostatin binding to somatostatin receptor type V (SSTR5) leads to a significant upregulation of SAPK/JNK activity.
  • This SAPK/JNK activation is dependent on the involvement of Galpha(12) and Galpha(13) proteins.
  • SSTR5 acts as the heptahelical receptor initiating SAPK/JNK activation through the G(12) family of G proteins.

Conclusions:

  • Somatostatin receptor type V (SSTR5) is a key mediator in activating the SAPK/JNK signaling pathway.
  • The G(12) family of G proteins (Galpha(12)/Galpha(13)) plays a crucial role in transducing the signal from SSTR5 to SAPK/JNK.
  • This finding establishes a novel signaling axis linking somatostatin receptor activation to stress-activated kinase pathways.

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