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[Mechanism Underlying Increased Expression of a Member of the Serine/Threonine Kinase Family (Citron kinase) Induced by HIV-1 Infection].

Abstract
Human immunodeficiency virus (HIV)-1 infection changes transcriptional profiles and regulates. the factors and machinery of the host that facilitate viral replication. Our previous study suggested that the serine/threonine kinase citron kinase (citK) promotes HIV-1 egress. To ascertain if HIV-1 infection affects citK expression in primary cells, peripheral blood mononuclear cells were infected with vesicular stomatitis virus G protein (VSV-G)-pseudotyped HIV-1 vector NL4-3-luc viruses, which resulted in remarkably increased expression of citK. citK overexpression led to a more than two-fold increase in HIV-1 production, whereas a significant decrease was observed when citK was depleted in CD4+ T cells. Infection with HIV-1 pseudoviruses induced increases in the mRNA and protein levels of citK by 2. 5- and 2. 7-fold in HEK293T cells, respectively. By cloning the 5-kb promoter of citK into a luciferase reporter system and transfecting the construct into HEK293T cells, enhanced luciferase activity was observed during HIV-1 infection. Taken together, these data demonstrate that HIV-1 infection upregulates citK expression at the transcriptional level, and thereby renders the host more susceptible to invasion by HIV-1.
AuthorsJiwei Ding, Zeyun Mi, Jianyuan Zhao, Jinming Zhou, Xiaoyu Li, Shan Cen
JournalBing du xue bao = Chinese journal of virology (Bing Du Xue Bao) Vol. 31 Issue 4 Pg. 388-94 (Jul 2015) ISSN: 1000-8721 [Print] China
PMID26524911 (Publication Type: Journal Article)
Chemical References
  • Intracellular Signaling Peptides and Proteins
  • citron-kinase
  • Protein Serine-Threonine Kinases
Topics
  • CD4-Positive T-Lymphocytes (virology)
  • Cloning, Molecular
  • Gene Expression Regulation, Enzymologic
  • HEK293 Cells
  • HIV-1 (physiology)
  • Humans
  • Intracellular Signaling Peptides and Proteins (genetics)
  • Protein Serine-Threonine Kinases (genetics)
  • Up-Regulation
  • Virus Replication

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