Title : c-Abl-mediated tyrosine phosphorylation of JunB is required for Adriamycin-induced expression of p21.

Pub. Date : 2015 Oct 1

PMID : 26217035






6 Functional Relationships(s)
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1 c-Abl-mediated tyrosine phosphorylation of JunB is required for Adriamycin-induced expression of p21. Doxorubicin ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
2 Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression. Doxorubicin ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
3 Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression. Doxorubicin ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
4 Because c-Abl promotes expression of the cyclin-dependent kinase inhibitor p21 upon stimulation with the DNA-damaging agent Adriamycin (doxorubicin), we analysed the involvement of JunB in Adriamycin-induced p21 expression. Doxorubicin ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
5 Taken together, these results suggest that, although JunB represses p21 promoter activity, c-Abl phosphorylates JunB and conversely inhibits its suppressive role on p21 promoter activity upon Adriamycin stimulation. Doxorubicin ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens
6 Therefore JunB is likely to be a key target of c-Abl in expression of p21 in Adriamycin-induced DDR. Doxorubicin ABL proto-oncogene 1, non-receptor tyrosine kinase Homo sapiens