Transcriptional activation of the human p21(WAF1/CIP1) gene by retinoic acid receptor - Correlation with retinoid induction of U937 cell differentiation Journal Article


Authors: Liu, M.; Iavarone, A.; Freedman, L. P.
Article Title: Transcriptional activation of the human p21(WAF1/CIP1) gene by retinoic acid receptor - Correlation with retinoid induction of U937 cell differentiation
Abstract: We reported previously that the induced differentiation of the myelomonocytic cell line U937 by vitamin D-3 is facilitated by the transcriptional induction of the p21(WAF1/CIP1) gene by the vitamin D-3 receptor (Liu, M., Lee, M.-H., Cohen, M., and Freedman, L. P. (1996) Genes Dev. 10, 143-158), Retinoic acid (RA), a physiological metabolite of vitamin A, is also a potent inducer of differentiation of several cell types, including myeloid leukemic cells, Like vitamin D-3, RA acts through a subfamily of nuclear hormone receptors, RARs and RXRs (retinoid X receptors), which regulate the expression of target genes by binding to specific DNA elements and modulating transcription initiation. In this report we demonstrate that the gene encoding p21 is also a RA-responsive target gene, and we describe a functional RA response element in this gene's promoter which is required to confer RA induction through RAR . RXR heterodimers. These results correlate the RA induction of monocytic differentiation of U937 cells with the transcriptional activation of the p21 gene and suggest a role for this cyclin/cyclin-dependent kinase complex inhibitor in facilitating this differentiation pathway.
Keywords: inhibitor; cyclin-dependent kinases; p21; acute promyelocytic leukemia; expression; translocation; tgf-beta; arrest; heterodimers; rar-alpha
Journal Title: Journal of Biological Chemistry
Volume: 271
Issue: 49
ISSN: 0021-9258
Publisher: American Society for Biochemistry and Molecular Biology  
Date Published: 1996-12-06
Start Page: 31723
End Page: 31728
Language: English
ACCESSION: WOS:A1996VW68600107
DOI: 10.1074/jbc.271.49.31723
PROVIDER: wos
PUBMED: 8940196
Notes: Article -- Source: Wos
Altmetric
Citation Impact
BMJ Impact Analytics
MSK Authors