We examined the role of intracellular Ca2+ in c-Jun NH2-terminal kinase (JNK) activation and DNA fragmentation in the rat myoblast cell line H9c2 using small GTP-binding protein Rac1. A constitutively active mutant of Rac1 (V12-Rac1) increased JNK-responsive gene expression 6-fold, although this increase was attenuated by the intracellular Ca2+ chelator BAPTA-AM. V12-Rac1 also increased the number of DNA fragmentated cells. However, V12-Rac1-mediated JNK activation was not affected by BAPTA-AM as determined by direct measurement of active forms, and V12-Rac1 did not affect intracellular Ca2+ concentration. These results suggest that Rac1 can activate JNK and induces cell injury, but [Ca2+](i) is necessary for V12-Rac1 to induce DNA fragmentation downstream of JNK activation.
|Number of pages||5|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Aug 27 1999|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology