Title : Glucocorticoids stimulate p21 gene expression by targeting multiple transcriptional elements within a steroid responsive region of the p21waf1/cip1 promoter in rat hepatoma cells.

Pub. Date : 1998 Jan 23

PMID : 9442036






4 Functional Relationships(s)
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1 In these cells, dexamethasone, a synthetic glucocorticoid, stimulated a rapid and selective increase in expression of the p21 cyclin-dependent kinase (CDK) inhibitor mRNA and protein and virtually abolished CDK2 phosphorylation of the retinoblastoma protein. Dexamethasone KRAS proto-oncogene, GTPase Rattus norvegicus
2 Dexamethasone stimulated p21 promoter activity in a p53-independent manner that required functional glucocorticoid receptors. Dexamethasone KRAS proto-oncogene, GTPase Rattus norvegicus
3 Analysis of 5" deletions of the p21 promoter uncovered a glucocorticoid responsive region between nucleotides -1481 and -1184, which does not contain a canonical glucocorticoid response element but which can confer dexamethasone responsiveness to a heterologous promoter. Dexamethasone KRAS proto-oncogene, GTPase Rattus norvegicus
4 Finally, ectopic expression of p21 had no effect on hepatoma cell growth in the absence of glucocorticoids but facilitated the ability of dexamethasone to inhibit cell proliferation. Dexamethasone KRAS proto-oncogene, GTPase Rattus norvegicus