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Literature summary for 1.6.3.1 extracted from

  • Turchan-Cholewo, J.; Dimayuga, V.M.; Gupta, S.; Gorospe, R.M.; Keller, J.; Bruce-Keller, A.J.
    NADPH oxidase drives cytokine and neurotoxin release from microglia and macrophages in response to HIV-Tat (2008), Antioxid. Redox Signal., 11, 193-204.
    View publication on PubMedView publication on EuropePMC

Activating Compound

Activating Compound Comment Organism Structure
HIV regulatory protein Tat NADPH oxidase mediates Tat-induced superoxide release in microglia and macrophages Mus musculus

Application

Application Comment Organism
medicine application of HIV regulatory protein Tat to microglia or macrophages causes dose- and time-dependent increases in superoxide formation that are prevented by both pharmacologic NADPH oxidase inhibitors and by specific decoy peptides gp91ds. Inhibition of NADPH oxidase attenuates Tat-induced release of IL-6 and TNFalpha, and MCP-1, and decreases microglial-mediated neurotoxicity. Macrophages derived from NADPH oxidase deficient mice display reduced superoxide production, released lower levels of cytokines/chemokines, and induce less neurotoxicity in response to Tat compared to wild-type macrophages Mus musculus

Protein Variants

Protein Variants Comment Organism
additional information macrophages derived from NADPH oxidase deficient mice display reduced superoxide production, released lower levels of cytokines/chemokines, and induce less neurotoxicity in response to HIV regulatory protein Tat compared to wild-type macrophages Mus musculus

Inhibitors

Inhibitors Comment Organism Structure
gp91ds fusion peptide that inhibits assembly of NADPH oxidase by mimicking the gp91phox docking site for the cytoplasmic p47phox subunit. gp91ds prevents NADPH oxidase activity, cytokine release, and neurotoxicity induced by HIV regulatory protein Tat in primary microglia Mus musculus

Organism

Organism UniProt Comment Textmining
Mus musculus
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Source Tissue

Source Tissue Comment Organism Textmining
N9 cell microglial cell Mus musculus
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