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Title: Stat3 is involved in control of MASP2 gene expression

Journal Article · · Biochemical and Biophysical Research Communications
 [1];  [2];  [3];  [4];  [1];  [5];  [6];  [5];  [7];  [4];  [1];  [7]
  1. Clinical Cooperation Group Inflammatory Lung Diseases - GSF-National Research Center for Environment and Health, Asklepios Fachkliniken, Gauting (Germany)
  2. Anthropology and Human Genetics, Department Biology II, Ludwig-Maximilians-Universitaet Munich (Germany)
  3. Genomatix Software GmbH, Munich (Germany)
  4. Anthropology and Human Genetics, Department Biology II, Ludwig-Maximilians-Universitaet Muenchen (Germany)
  5. Department of Biochemistry, Fukushima Medical University School of Medicine, Fukushima (Japan)
  6. Department of Applied Biochemistry, Tokai University, Hiratsuka (Japan)
  7. Department of Infection, Immunity and Inflammation, University of Leicester, University Road, Leicester LE1 9HN (United Kingdom)

Little is known about determinants regulating expression of Mannan-binding lectin associated serine protease-2 (MASP-2), the effector component of the lectin pathway of complement activation. Comparative bioinformatic analysis of the MASP2 promoter regions in human, mouse, and rat, revealed conservation of two putative Stat binding sites, termed StatA and StatB. Site directed mutagenesis specific for these sites was performed. Transcription activity was decreased 5-fold when StatB site was mutated in the wildtype reporter gene construct. Gel retardation and competition assays demonstrated that proteins contained in the nuclear extract prepared from HepG2 specifically bound double-stranded StatB oligonucleotides. Supershift analysis revealed Stat3 to be the major specific binding protein. We conclude that Stat3 binding is important for MASP2 promoter activity.

OSTI ID:
21033034
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 364, Issue 4; Other Information: DOI: 10.1016/j.bbrc.2007.10.114; PII: S0006-291X(07)02295-4; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English

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