Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca2+/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways

Bei Li, Yuqiang Shi, Jianhong Shu, Junling Gao, Ping Wu, Shao Jun Tang

    Research output: Contribution to journalArticlepeer-review

    51 Scopus citations

    Abstract

    Background: HIV-1 infection causes chronic neuroinflammation in the central nervous system (CNS). Results: The spinal cytokine up-regulation induced by HIV-1 gp120 protein depends on Wnt5a/CaMKII and/or Wnt5a/JNK pathways. Conclusion: gp120 stimulates cytokine expression in the spinal cord dorsal horn by activating Wnt5a signaling. Significance: The finding reveals Wnt signaling-mediated novel mechanisms by which HIV-1 may cause neuroinflammation.

    Original languageEnglish (US)
    Pages (from-to)13610-13619
    Number of pages10
    JournalJournal of Biological Chemistry
    Volume288
    Issue number19
    DOIs
    StatePublished - May 10 2013

    ASJC Scopus subject areas

    • Biochemistry
    • Molecular Biology
    • Cell Biology

    Fingerprint

    Dive into the research topics of 'Wingless-type mammary tumor virus integration site family, member 5A (Wnt5a) regulates human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein 120 (gp120)-induced expression of pro-inflammatory cytokines via the Ca2+/calmodulin-dependent protein kinase II (CaMKII) and c-Jun N-terminal kinase (JNK) signaling pathways'. Together they form a unique fingerprint.

    Cite this