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Regulation of transcription with glucocorticoid receptor and other transcription factors

Research Project

Project/Area Number 11671102
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Endocrinology
Research InstitutionFujita Health University

Principal Investigator

OSHIMA Hisaji  Fujita Health University School of Medicine, Internal Medicine, Assistant Professor, 医学部, 助教授 (90138008)

Co-Investigator(Kenkyū-buntansha) KATAYAMA Masao  Fujita Health University School of Medicine, Intrenal Medicine, Associate Professor, 医学部, 講師 (00278285)
澤田 誠  藤田保健衛生大学, 総合医科学研究所, 教授 (10187297)
Project Period (FY) 1999 – 2000
Project Status Completed (Fiscal Year 2000)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1999: ¥1,700,000 (Direct Cost: ¥1,700,000)
Keywordsglucocorticoids / receptors / steroids / transcription
Research Abstract

Glucocorticoid receptor was a ligand-inducible transcription factor, and activates or inhibit transcription of target genes. We, in this project, have identified and clarified glucocorticoid modulatory elements binding proteins (GMEB) which works as a gene specific and tissue specific modulator of regulation of gene transcription by glucocorticoids. GMEBs are now identified as a heteroologomeric complex (GMEB-1 and GMEB-2) present in cytoplasma and nucleus in cells. GMEB-1 and GMEB-2 are 68KDa and 88KDa proteins respectively. Cloning of GMEB-1 and GMEB-2 cDAA shows that these proteins have unique primary protein sequences. We find also that GMEB functions as a transcription factor where they bind to DNA as a sequence specific manner. In vitro, GMEB binds to a palindromic sequence which is most preferentialy GCGA/CNNNG/TCGC.Biological activities of GMEB can vary in different tissues and also by a change in the growth conditions of cells. In addition, a splice variant of GMEB-1 was identified and sequenced. These findings can be a most hopeful evidence to undrestand a gene and tissue specific modulation of the glucocorticoid hormone actions and to develop more specific and powerful glucocorticoid therapies where less adverse effects are expected.

Report

(3 results)
  • 2000 Annual Research Report   Final Research Report Summary
  • 1999 Annual Research Report
  • Research Products

    (2 results)

All Other

All Publications (2 results)

  • [Publications] Fukaya S. et al.: "KL-b as a novel marker for activities of interstitial pneumonia in connective tissue diseases."Rheumatology International. 19. 223-225 (2000)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2000 Final Research Report Summary
  • [Publications] Fukaya S, Oshima H, Kato K, Komatsu, Y, Matsumura H, Ishii K, Miyama H, Nagai T Tanaka I, Mizutani A, Katayama M, Yoshida S, Torikai K: "KL-6 as a novel marker for activities of interstitial pneumonia in connective tissue diseases."Rheumatol.Int.. 19 (6). 223-225 (2000)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2000 Final Research Report Summary

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Published: 1999-04-01   Modified: 2016-04-21  

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