Irina G Luzina

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Induced JunD in intestinal epithelial cells represses CDK4 transcription through its proximal promoter region following polyamine depletion.

Lan Xiao; Jaladanki N Rao; Tongtong Zou; Lan Liu; Bernard S Marasa; Jie Chen; Douglas J Turner; Antonino Passaniti; Jian-Ying Wang (Profiled Authors: Lan Liu; Antonino Passaniti; Douglas J Turner; Jian-Ying Wang; Tongtong Zou; Rao Jaladanki; Lan Xiao)

Cell Biology Group, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
The Biochemical journal 2007;403(3):573-81.

Maintenance of intestinal epithelial integrity requires cellular polyamines that regulate expression of various genes involved in cell proliferation, growth arrest and apoptosis. In prior studies, depletion of cellular polyamines has been shown to stabilize JunD, a member of the AP-1 (activator protein-1) family of transcription factors, leading to inhibition of intestinal epithelial cell proliferation, but the exact downstream targets of induced JunD remain elusive. CDK4 (cyclin-dependent kinase 4) is essential for the G1- to S-phase transition during the cell cycle and its expression is primarily controlled at the transcriptional level. In the present study, we show that induced JunD in IECs (intestinal epithelial cells) is a transcriptional repressor of the CDK4 gene following polyamine depletion. Increased JunD in polyamine-deficient cells was associated with a significant inhibition of CDK4 transcription, as indicated by repression of CDK4-promoter activity and decreased levels of CDK4 mRNA and protein, all of which were prevented by using specific antisense JunD oligomers. Ectopic expression of the wild-type junD also repressed CDK4-promoter activity and decreased levels of CDK4 mRNA and protein without any effect on CDK2 expression. Gel shift and chromatin immunoprecipitation assays revealed that JunD bound to the proximal region of the CDK4-promoter in vitro as well as in vivo, while experiments using different CDK4-promoter mutants showed that transcriptional repression of CDK4 by JunD was mediated through an AP-1 binding site within this proximal sequence of the CDK4-promoter. These results indicate that induced JunD in IECs represses CDK4 transcription through its proximal promoter region following polyamine depletion.

3 Originating Grant

• 1.

  WANG, JIAN-YING

  Surgical Studies of Gut Permeability

  25 August 2004 - 31 July 2014

  NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES

• 2.

  WANG, JIAN-YING

  Mucosal Repair in Gut Surgical Disorders

  1 July 2002 - 28 February 2013

  NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES

• 3.

  WANG, JIAN-YING

  Intestinal Mucosal Growth in Health &Surgical Diseases

  1 June 2000 - 30 June 2016

  NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES

Scientific Context

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