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 journalArticle

28 Citations (Scopus)

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

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Virus Integration
Calcium-Calmodulin-Dependent Protein Kinase Type 2
Oncogenic Viruses
JNK Mitogen-Activated Protein Kinases
Viruses
HIV-1
Tumors
Glycoproteins
Breast Neoplasms
Cytokines
Neurology
Virus Diseases
Up-Regulation
Central Nervous System
Proteins

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

Cite this

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title = "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",
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.",
author = "Bei Li and Yuqiang Shi and Jianhong Shu and Junling Gao and Ping Wu and Shao-Jun Tang",
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T1 - 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

AU - Li, Bei

AU - Shi, Yuqiang

AU - Shu, Jianhong

AU - Gao, Junling

AU - Wu, Ping

AU - Tang, Shao-Jun

PY - 2013/5/10

Y1 - 2013/5/10

N2 - 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.

AB - 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.

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