The protein tyrosine kinase Fyn activates transcription from the HIV promoter via activation of NFkB-like DNA-binding proteins

Naohiro Hohashi, Takuma Hayashi, Noemi Fusaki, Masakazu Takeuchi, Makoto Higurashi, Takashi Okamoto, Kentaro Semba, Tadashi Yamamoto*

*この研究の対応する著者

研究成果: Article査読

14 被引用数 (Scopus)

抄録

Protein tyrosine kinase p59fyn (Fyn) associates with the TCR-CD3 complex, which suggests that Fyn plays a significant role in the signal transduction involving TCR complex. In addition to cellular genes, viral promoters such as the HIV long terminal repeat (LTR) are also activated upon T cell activation. To elucidate the functional significance of Fyn in the expression of viral promoters, we transfected a Fyn-expression vector together with a reporter plasmid containing the chloramphenicol acetyltransferase gene driven by HIV LTR into a human T cell line, Jurkat. In this assay, Fyn stimulated the promoter in HIV LTR when the transfected cells were treated with both concanavalin A and PMA as an antigen-mimic stimulation. This activation required the intact SH2 domain of Fyn. Mutational analysis of HIV LTR showed that the NFKB binding sites were responsible for this effect. Electrophoretic mobility shift assays and UV cross-linking experiments showed that activation of T cells by anti-CD3 antibody induced four KB-binding proteins (50, 60, 65 and 100 kDa) in Fyn-overexpressing cells more efficiently than in the parental cells. Our results suggested that Fyn was able to regulate expression of a subset of genes via KB-binding proteins upon T cell activation.

本文言語English
ページ(範囲)1851-1859
ページ数9
ジャーナルInternational Immunology
7
11
DOI
出版ステータスPublished - 1995 11月
外部発表はい

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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