Title : Protein kinase Ciota activity is necessary for Bcr-Abl-mediated resistance to drug-induced apoptosis.

Pub. Date : 1999 Feb 12

PMID : 9933579






3 Functional Relationships(s)
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1 In contrast, Bcr-Abl-negative HL60 myeloid leukemia cells, which are sensitive to taxol-induced apoptosis, do not exhibit sustained PKCiota activation in response to taxol. Paclitaxel ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
2 Treatment of K562 cells with tyrphostin AG957, a selective Bcr-Abl inhibitor, blocks taxol-induced PKCiota activation and sensitizes these cells to taxol-induced apoptosis, indicating that PKCiota is a relevant downstream target of Bcr-Abl-mediated resistance. Paclitaxel ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
3 Treatment of K562 cells with tyrphostin AG957, a selective Bcr-Abl inhibitor, blocks taxol-induced PKCiota activation and sensitizes these cells to taxol-induced apoptosis, indicating that PKCiota is a relevant downstream target of Bcr-Abl-mediated resistance. Paclitaxel ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens