Mice Lacking Pin1 Develop Normally, but Are Defective in Entering Cell Cycle From G(0) Arrest

Biochem Biophys Res Commun. 1999 Nov 30;265(3):658-63. doi: 10.1006/bbrc.1999.1736.

Abstract

The peptidyl prolil cis/trans isomerase Ess1/Pin1 is essential for mitosis progression in yeast cells and is hypothesized to perform the same role in mammalian cells. To investigate the function of Pin1 in mammalian cells, we created mice lacking Pin1. These mice underwent normal development. Although the embryonic Pin1-/- fibroblasts grew normally, they proved significantly deficient in their ability to restart proliferation in response to serum stimulation after G(0) arrest. These results suggest that Pin1 is required for cell cycle progression from G(0) arrest as well as mitosis progression in normal mammalian cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Cell Cycle / genetics
  • Cell Cycle / physiology*
  • Cell Division / genetics
  • Cell Division / physiology
  • Cloning, Molecular
  • DNA Primers / genetics
  • DNA, Complementary / genetics
  • Exons
  • Female
  • Introns
  • Male
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Peptidylprolyl Isomerase / deficiency*
  • Peptidylprolyl Isomerase / genetics
  • Peptidylprolyl Isomerase / physiology
  • Phenotype
  • Pregnancy
  • Resting Phase, Cell Cycle / genetics
  • Resting Phase, Cell Cycle / physiology

Substances

  • DNA Primers
  • DNA, Complementary
  • NIMA-Interacting Peptidylprolyl Isomerase
  • Peptidylprolyl Isomerase
  • Pin1 protein, mouse

Associated data

  • GENBANK/AB009691
  • GENBANK/AB009692