期刊论文详细信息
FEBS Letters
Negative regulation of the anti‐human immunodeficiency virus and chemotactic activity of human stromal cell‐derived factor 1α by CD26/dipeptidyl peptidase IV
Morimoto, Chikao1  Souta, Akiko1  Munakata, Yasuhiko2  Shioda, Tatsuo3  Hosono, Osamu1  Ohtsuki, Takashi1  Kobayashi, Hiroshi1 
[1] Department of Clinical Immunology and AIDS Research Center, Institute of Medical Science, University of Tokyo, 4-6-1 Shiroganedai, Minato-ku, Tokyo 108-0071, Japan;Division of Tumor Immunology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, MA 02115, USA;Department of Infectious Disease, Institute of Medical Science, University of Tokyo, 4-6-1 Shiroganedai, Minato-ku, Tokyo 108-0071, Japan
关键词: Anti-human immunodeficiency virus and chemotactic activity;    CD26/dipeptidyl peptidase IV;    Human immunodeficiency virus infection;    N-terminal cleavage;    Stromal cell-derived factor 1α;    A 595;    optical absorbance at 595 nm;    aa;    amino acid(s);    ADA;    adenosine deaminase;    CHO;    Chinese hamster ovary;    DPPIV;    dipeptidyl peptidase IV;    HIV;    human immunodeficiency virus;    mCD26;    recombinant CD26 which lacks the majority of DPPIV activity;    PBS;    phosphate-buffered saline;    RANTES;    regulated upon activation;    normal T cell expressed and secreted;    sCD26;    recombinant soluble CD26 having DPPIV activity;    SDF-1α;    stromal cell-derived factor 1α;   
DOI  :  10.1016/S0014-5793(98)00763-7
学科分类:生物化学/生物物理
来源: John Wiley & Sons Ltd.
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【 摘 要 】

Stromal cell-derived factor 1α (SDF-1α) is a chemokine that has been shown to prevent infection of T-tropic HIV strains and is a possible substrate of CD26/dipeptidyl peptidase IV (DPPIV). In this study, we show that SDF-1α was cleaved at the N-terminal region by CD26/DPPIV and as a result the inhibitory activity of SDF-1α against HIV infection disappeared. Moreover, the chemotactic activity of SDF-1α also disappeared specifically by DPPIV activity of recombinant soluble CD26. These results suggested that dissemination of T-tropic HIV strains in vivo may be facilitated by CD26/DPPIV via inactivation of functional SDF-1α.

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