Aiping M Zhao

Publication Detail

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Regulation of the human plasminogen activator inhibitor type 2 gene: cooperation of an upstream silencer and transactivator.

Brett Stringer; Ekemini A Udofa; Toni M Antalis (Profiled Author: Toni Antalis)

Center for Vascular and Inflammatory Diseases and Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
The Journal of biological chemistry 2012;287(13):10579-89.

Transcriptional up-regulation of the plasminogen activator inhibitor type-2 (PAI-2) gene is a major response to cellular stress. The expression of PAI-2 is induced by a variety of cytokines and growth factors that act in a cell type- and differentiation stage-dependent manner. We previously reported that the human SERPINB2 gene promoter is controlled by three major transcription regulatory domains: an inducible proximal promoter, an upstream silencer (PAUSE-1), and a distal transactivator region between -5100 and -3300, which appears to overcome inhibition mediated by the silencer. The distal transactivator region is inducible by the phorbol ester PMA, a potent activator of the protein kinase C (PKC) pathway that is a powerful inducer of PAI-2 gene expression in monocytes, macrophages, and myelomonocytic cells as well as in epidermal keratinocytes. Here we show that a 21-bp region (-4952/-4932), containing an AP-1 element, is both necessary and sufficient for PMA-induced transactivator activity in PAI-2-expressing U937 cells. This site specifically binds FosB in PAI-2-expressing U937 cells but not in HeLa cells that do not express PAI-2, and overexpression of FosB, c-Fos, or c-Jun in HeLa cells is sufficient to cause derepression of transcription from the SERPINB2 promoter. Although FosB is likely to be involved in transactivator-mediated derepression of PAI-2 transcription in macrophage-like cells, as exemplified by the U937 cell line, c-Jun may be functional in other cell types. These data suggest a model for the transcriptional control of the human PAI-2 gene and further our understanding of the molecular basis for its tissue-specific expression.

2 Originating Grant

• 1.

  Antalis, Toni M

  New Function for the Serpin PAI-2 as a Regular of pRb

  1 August 2003 - 31 May 2009

  NATIONAL CANCER INSTITUTE

• 2.

  Antalis, Toni M

  NEW FUNCTION SERPIN PAI 2 AS A REGULAR OF RB

  1 July 2002 - 30 June 2010

  NATIONAL CANCER INSTITUTE

Scientific Context

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