Stress signaling by Tec tyrosine kinase in the ischemic myocardium

Am J Physiol Heart Circ Physiol. 2010 Sep;299(3):H713-22. doi: 10.1152/ajpheart.00273.2010. Epub 2010 Jun 11.

Abstract

Nonreceptor tyrosine kinases have an increasingly appreciated role in cardiac injury and protection. To investigate novel tasks for members of the Tec family of nonreceptor tyrosine kinases in cardiac phenotype, we examined the behavior of the Tec isoform in myocardial ischemic injury. Ischemia-reperfusion, but not cardiac protective agents, induced altered intracellular localization of Tec, highlighting distinct actions of this protein compared with other isoforms, such as Bmx, in the same model. Tec is abundantly expressed in cardiac myocytes and assumes a diffuse intracellular localization under basal conditions but is recruited to striated structures upon various stimuli, including ATP. To characterize Tec signaling targets in vivo, we performed an exhaustive proteomic analysis of Tec-binding partners. These experiments expand the role of the Tec family in the heart, identifying the Tec isoform as an ischemic injury-induced isoform, and map the subproteome of its interactors in isolated cells.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Cell Line
  • Cells, Cultured
  • Humans
  • Male
  • Mice
  • Microscopy, Confocal
  • Myocardial Ischemia / metabolism*
  • Myocardium / metabolism*
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / metabolism
  • Protein-Tyrosine Kinases / metabolism*
  • Signal Transduction
  • Transfection

Substances

  • Tec protein-tyrosine kinase
  • Protein-Tyrosine Kinases