Sentences with phrase «activated abl»

Activated Abl kinase inhibits oncogenic transforming growth factor - β signaling and tumorigenesis in mammary tumors.

Not exact matches

The activity of tyrosine kinases is typically regulated in an auto - inhibitory fashion, but the BCR - Abl fusion gene codes for a protein that is «always on» or continuously activated leading to unregulated cell division (i.e. cancer).

[11] Since ABL activates a number of cell cycle - controlling proteins and enzymes, the result of the BCR - Abl fusion is to speed up cell divisiABL activates a number of cell cycle - controlling proteins and enzymes, the result of the BCR - Abl fusion is to speed up cell divisiAbl fusion is to speed up cell division.

Inhibition of c - Abl with STI571 attenuates stress - activated protein kinase activation and apoptosis in the cellular response to 1 - β - d - arabinofuranosylcytosine.

STAT5 is also activated by the oncogenic breakpoint cluster region (BCR)-- ABL tyrosine kinase and contributes to the transformation of leukemia cells (45).

These mutant kinases are attractive therapeutic targets, as demonstrated by the efficacy of imatinib in BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknown.

Together, our findings suggest that ABL kinases activate the TAZ and STAT5 pathways and that coactivation of their downstream targets promote the bone metastasis of breast cancer cells in mouse models.

In breast cancer cells, the ABL kinases activated the transcriptional coactivator TAZ and the transcription factor STAT5, which triggered the transcription of genes encoding factors that activate osteoclasts (cells that break down bone) and those that enhance the survival of breast cancer cells in the bone microenvironment.

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