Title : ZAK is required for doxorubicin, a novel ribotoxic stressor, to induce SAPK activation and apoptosis in HaCaT cells.

Pub. Date : 2010 Aug 1

PMID : 20559024






4 Functional Relationships(s)
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1 By employing siRNA mediated knockdown of ZAK or administration of sorafenib and nilotinib, kinase inhibitors that have a high affinity for ZAK, we provide evidence that ZAK is required for doxorubicin-induced proinflammatory and apoptotic responses in HaCaT cells, a pseudo-normal keratinocyte cell line, but not in HeLa cells, a cancerous cell line. Sorafenib mitogen-activated protein kinase kinase kinase 20 Homo sapiens
2 By employing siRNA mediated knockdown of ZAK or administration of sorafenib and nilotinib, kinase inhibitors that have a high affinity for ZAK, we provide evidence that ZAK is required for doxorubicin-induced proinflammatory and apoptotic responses in HaCaT cells, a pseudo-normal keratinocyte cell line, but not in HeLa cells, a cancerous cell line. Sorafenib mitogen-activated protein kinase kinase kinase 20 Homo sapiens
3 Abrogation of these changes after exposure of cells to sorafenib and nilotinib suggests that these alterations occur following stimulation of ZAK. Sorafenib mitogen-activated protein kinase kinase kinase 20 Homo sapiens
4 We suggest that ZAK inhibitors such as sorafenib or nilotinib may be effective when combined with doxorubicin to treat cancer patients. Sorafenib mitogen-activated protein kinase kinase kinase 20 Homo sapiens