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1997 Fiscal Year Final Research Report Summary

Molecular and Functional Analysis of Heparan sulfate Proteoglycan-Ryudocan.

Research Project

Project/Area Number 08671224
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Hematology
Research InstitutionNagoya University

Principal Investigator

KOJIMA Tetsuhito  Nagoya U Sch.Med., 1st Dep.Int.Med., Assistant, 医学部, 助手 (40161913)

Co-Investigator(Kenkyū-buntansha) TUZUKI Shinobu  Nagoya U Sch.Med., 1st Dep.Int.Med., Clin.Staff, 医学部, 医員
TOWATARI Masayuki  Nagoya U Sch.Med., 1st Dep.Int.Med., Clin.Staff, 医学部, 医員
Project Period (FY) 1996 – 1997
Keywordsmouse ryudocan / heparan sulfate proteoglycan / ryudocan cDNA / ryudocan gene / promoter activity / Tissue Factor Pathway Inhibitor(TFPI)
Research Abstract

Ryudocan, a ubiquitous heparan sulfate proteoglycan, is a member of the syndecan family of cell surface proteoglycans. The full-length cDNA encoding the murine ryudocan core protein has now been cloned and sequenced. The deduced primary structure of mouse ryudocan, including the three glycosaminoglycan attachment sites in the extracellular domain as well as the transmembrane and cytoplasmic regions, is highly similar to those of the rat, human, and chicken proteins. Northern analysis detected a 2.7-kb transcript in all mouse tissues examined, with the highest concentrations apparent in liver, kidney, and lung. The mouse ryudocan gene was shown to span approximately 19.7 kb of genomic DNA and to contain five exons, with an intron-exon organization identical to that of the human gene. The promoter region of the mouse gene contains various cis-acting elements, including a TATA-like box and GC box as well as potential binding sites for the transcription factors NF-IL6, MyoD,GATA,C/EBP,AP-2, NF-kB,AP-1, and Sp1. Transient transfection experiments with a construct containing the 690 bp upstream of the transcription start site fused to a luciferase reporter gene showed functional promoter activity. Deletion analysis suggested that the proximal promoter region including the TATA-like box, GC box, and other Sp1 binding sites was required for full transcriptional activity. These findings will be useful for the study of ryudocan gene regulation and the generation of mice with targeted disruption of the gene.

  • Research Products

    (13 results)

All Other

All Publications (13 results)

  • [Publications] T.Kojima, A.Katsumi, T.Yamazaki, etal.: "Human Ryudocan from Endothelium-like Cells Binds Basic Fibroblast Growth Factor,Midkine,and Tissue Factor Pathway Inhibitor." J.Biol.Chem.271(10). 5914-5920 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] A.Katsumi, T.Senda, T.Kojima, et al.: "Protein C Nagoya,an Elongated Mutant of Protein C,Is Retained Within the Endoplasmic Reticulum and Is Associated With GRP78 and GRP94." Blood. 87(10). 4164-4175 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] T.Yamazaki, A.Katsumi, T.Kojima, et al.: "Molecular Basis of a Hereditary Type I Protein S Deficiency Caused By a Substitution of Cys for Arg474." Blood. 87(11)). 4643-4650 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Y.Okamoto, T.Yamazaki, T.Kojima, et al.: "A Novel Nonsense Mutation Associated with an Exon Skipping in a Patient with Protein S Deficiency Type I" Thromb.Haemost.75(6). 877-882 (1996)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] S.Tsuzuki, T.Kojima, A.Katsumi, et al.: "Morecular Cloning,Genomic Organization,Promoter Activity,and Tissue-Specific Expression of the Mouse Ryudocan Gene." J.Biochem.122. 17-24 (1997)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] T.Yamazaki, A.Katsumi, T.Kojima, et al.: "Two Distinct Novel Splice Site Mutations in a Compound Heterozygous Patient with Protein S Deficiency." Thromb.Haemost.77. 14-20 (1997)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] 小嶋 哲人: "今日の治療指針(分担14.血液・造血器疾患、播種性血管内凝固症候群)" 医学書院(東京), 529-530 (1997)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] T.Kojima, A.Katsumi, T.Yamazaki, et al.: "Human Ryudocan from Endothelium-like Cells Binds Basic Fibroblast Growth Factor, Midkine, and Tissue Factor Pathway Inhibitor" J.Biol.Chem.271 (10). 5914-5920 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] A.Takagi, T.Kojima, A.Katsumi, et al.: "Structural Organization and Promoter Activity of the Human Ryudocan Gene" J.Biochem., (Tokyo). 119 (5). 979-984 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] A.Katsumi, T.Senda, T.Kojima et al.: "Protein C Nagoya, an Elongated Mutant of Protein C,Is Retained Within the Endoplasmic Reticulum and Is Associated With GRP78 and GRP94" Blood. 87 (10). 4164-4175 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] T.Yamazaki, A.Katsumi, T.Kojima, et al.: "Molecular Basis of a Hereditary Type I Protein S Deficiency Caused By a Substitution of Cys for Arg474" Blood. 87 (11). 4643-4650 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] S.Tsuzuki, T.Kojima, A.Katsumi et al.: "Morecular Cloning, Genomic Organization, Promoter Activity, and Tissue-Specific Expression of the Mouse Ryudocan Gene" J.Biochem.122. 17-24 (1997)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] T.Yamazaki, A.Katsumi, T.Kojima, et al.: "Two Distinet Novel Splice Site Mutations in a Compound Heterozygous Patient with Proteins S Deficiency" Thromb.Haemost.77. 14-20 (1997)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 1999-03-16  

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