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Molecular cloning and characterization of cellular factors which associate with HIV-1 activation

Research Project

Project/Area Number 08672595
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Human genetics
Research InstitutionTokyo Medical and Dental University

Principal Investigator

ABE Kenji  Tokyo Medical and Dental University Medical Research Institute Research associate, 難治疾患研究所, 助手 (60211702)

Co-Investigator(Kenkyū-buntansha) YAMAMOTO Kohtaro  Tokyo Medical and Dental University Medical Research Institute Professor, 難治疾患研究所, 教授 (40000971)
Project Period (FY) 1996 – 1997
Project Status Completed (Fiscal Year 1997)
Budget Amount *help
¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
KeywordsHIV-1 / cellular factors / TAR RNA
Research Abstract

To identify cellular factors which associate with HIV-1 activation, we have isolated 7 clones with their TAR RNA binding properties. Data base search revealed that 5 clones were identified as a nuclear factor 90 (NF90), one of poly A binding proteins, a human homologue of yeast 35.1kDa protein, a human homologoue of chicken inner centromere protein, and a human homologue of mouse phosphoprotein p150, respectively. The remaining 2 clones have not been identified. NF90, which is indispensable for activated T-cells to produce interleukin-2, has two domains, which contains a double-stranded RNA binding motif common to such as TAR RNA-binding protein (TRBP). TRBP is the first identified gene encoding a TAR RNA-binding protein. Thus, our screening conditions are seemed to be suitable for screening of TAR RNA-binding proteins from cDNA libraries constructed by the lambdagt11 vector. As for clone 27 (JTR27 ; a human homologue of yeast 35.1kDa protein), its full-length cDNA was sequenced and its characters were investigated. JTR27 antisense oligonucleotide repressed HIV-1 LTR-directed gene expression either in the presence or absence of Tat. Overexpression of JTR27 significantly augmented not only the HIV-1 LTR basal transcription but also Tat-activation. Taken together these results, it was suggested that JTR27 associates with HIV-1LTR gene expression.

Report

(3 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report

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Published: 1997-04-01   Modified: 2016-04-21  

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