Induction of the PAC1-R (PACAP-type I receptor) gene by p53 and Zac

Brain Res Mol Brain Res. 1999 Jun 8;69(2):290-4. doi: 10.1016/s0169-328x(99)00116-3.

Abstract

Pituitary adenylate cyclase-activating polypeptides and PAC1-R are expressed during early embryogenesis and PACAP's neurotrophic action supports a role in neuronal development. In the adult brain PACAP functions as a neuroprotective factor that attenuates the neuronal damage resulting from various insults. The tumor suppressor gene p53 and the new zinc finger protein Zac regulate apoptosis and cell cycle arrest through unrelated pathways and both genes are up-regulated under cerebral ischemia. We report here that p53 and Zac induce expression of the PAC1-R gene. By this mechanism p53 and Zac could fine-tune the balance between death promoting and protective signals and may thus fulfil a dual role in ischemia.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Brain Ischemia / metabolism
  • Cell Cycle / physiology
  • Cell Differentiation / physiology
  • Genes, p53*
  • Humans
  • Nerve Tissue Proteins / genetics*
  • Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide
  • Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I
  • Receptors, Pituitary Hormone / genetics*
  • Zinc Fingers*

Substances

  • ADCYAP1R1 protein, human
  • Nerve Tissue Proteins
  • Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide
  • Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I
  • Receptors, Pituitary Hormone