Fem1a is a mitochondrial protein up-regulated upon ischemia-reperfusion injury.
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.
Cambier
Linda
L
CNRS UMR5237, Centre de Recherche en Biochimie Macromoléculaire, Montpellier, France.
Lacampagne
Alain
A
Auffray
Charles
C
Pomiès
Pascal
P
D000818:Animals; D018797:Cell Cycle Proteins / Q000235:genetics* / Q000378:metabolism; D006367:HeLa Cells; D006801:Humans; D051379:Mice; D024101:Mitochondrial Proteins / Q000235:genetics* / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000235:genetics* / Q000378:metabolism; D015854:Up-Regulation
D018797:Cell Cycle Proteins; C444344:FEM1A protein, human; D024101:Mitochondrial Proteins