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Fem1a is a mitochondrial protein up-regulated upon ischemia-reperfusion injury.

Abstract
Various expression studies have shown a preferential muscle expression of the mouse Fem1a gene, but no data is available on the subcellular localization of the corresponding protein. Here, using a specific antibody, we show that Fem1a is expressed preferentially in cardiac muscle, brain and liver. Moreover, using immunofluorescence and electron microscopy, as well as biochemical assays, we demonstrate that Fem1a is localized within mitochondria of C2C12 myoblasts and cardiac muscle cells. Finally, we show that the expression of Fem1a, which is a cellular partner of the EP4 receptor for prostaglandin E(2), is increased in mouse hearts after myocardial infarction.
AuthorsLinda Cambier, Alain Lacampagne, Charles Auffray, Pascal Pomiès
JournalFEBS letters (FEBS Lett) Vol. 583 Issue 10 Pg. 1625-30 (May 19 2009) ISSN: 1873-3468 [Electronic] England
PMID19406122 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Cell Cycle Proteins
  • FEM1A protein, human
  • Mitochondrial Proteins
Topics
  • Animals
  • Cell Cycle Proteins (genetics, metabolism)
  • HeLa Cells
  • Humans
  • Mice
  • Mitochondrial Proteins (genetics, metabolism)
  • Myocardial Reperfusion Injury (genetics, metabolism)
  • Up-Regulation

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