p21 is a transcriptional target of HOXA10 in differentiating myelomonocytic cells Journal Article


Authors: Bromleigh, V. C.; Freedman, L. P.
Article Title: p21 is a transcriptional target of HOXA10 in differentiating myelomonocytic cells
Abstract: The myeolomonocytic cell line U937 differentiates into macrophages in response to a variety of agents. Several genes including the cyclin-dependent kinase inhibitor p21(waf1/cip1) and the homeobox gene transcription factor HOXA10 are induced at the onset of differentiation. Ectopic expression of either gene results in U937 differentiation. In this paper, we describe a mechanism by which p21 and HOXA10 may act in concert, where HOXA10 can bind directly to the p21 promoter and, together with its trimeric partners PBX1 and MEIS1, activate p21 transcription, resulting in cell cycle arrest and differentiation. These experiments for the first time identify p21 as a selective target for a HOX protein and link the differentiative properties of a transcription factor and a cell cycle inhibitor.
Keywords: controlled study; human cell; promoter region; dna-binding proteins; proto-oncogene proteins; cell cycle; gene expression; protein targeting; neoplasm proteins; cell line; cell differentiation; homeodomain proteins; transcription, genetic; transcription regulation; genetic transfection; transactivation; transcription; cell cycle arrest; homeodomain protein; monocyte; macrophage; cyclins; cyclin dependent kinase inhibitor; protein p21; g1 phase; cell strain u937; myeloid cells; homeobox; promoter regions (genetics); trans-activation (genetics); myeloid differentiation; human; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; homeobox proteins
Journal Title: Genes and Development
Volume: 14
Issue: 20
ISSN: 0890-9369
Publisher: Cold Spring Harbor Laboratory Press  
Date Published: 2000-10-15
Start Page: 2581
End Page: 2586
Language: English
DOI: 10.1101/gad.817100
PUBMED: 11040212
PROVIDER: scopus
PMCID: PMC317001
DOI/URL:
Notes: Export Date: 18 November 2015 -- Source: Scopus
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