Title : Bcl-xL blocks activation of related adhesion focal tyrosine kinase/proline-rich tyrosine kinase 2 and stress-activated protein kinase/c-Jun N-terminal protein kinase in the cellular response to methylmethane sulfonate.

Pub. Date : 1999 Mar 26

PMID : 10085098






5 Functional Relationships(s)
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1 Here we demonstrate that methylmethane sulfonate (MMS)-induced activation of JNK is inhibited by overexpression of the anti-apoptotic protein Bcl-xL, but not by caspase inhibitors CrmA and p35. Methyl Methanesulfonate mitogen-activated protein kinase 8 Homo sapiens
2 Here we demonstrate that methylmethane sulfonate (MMS)-induced activation of JNK is inhibited by overexpression of the anti-apoptotic protein Bcl-xL, but not by caspase inhibitors CrmA and p35. Methyl Methanesulfonate mitogen-activated protein kinase 8 Homo sapiens
3 Hence, treatment of Bcl-xL cells with sodium vanadate, a tyrosine phosphatase inhibitor, restores MMS-induced activation of RAFTK and JNK. Vanadates mitogen-activated protein kinase 8 Homo sapiens
4 Hence, treatment of Bcl-xL cells with sodium vanadate, a tyrosine phosphatase inhibitor, restores MMS-induced activation of RAFTK and JNK. Methyl Methanesulfonate mitogen-activated protein kinase 8 Homo sapiens
5 These findings indicate that RAFTK-dependent induction of JNK in response to MMS is sensitive to Bcl-xL, but not to CrmA and p35, by a mechanism that inhibits tyrosine phosphorylation and thereby activation of RAFTK. Tyrosine mitogen-activated protein kinase 8 Homo sapiens