Activation of the adenosine A1 receptor inhibits HIV-1 tat-induced apoptosis by reducing nuclear factor-kappaB activation and inducible nitric-oxide synthase

Human immunodeficiency virus dementia (HIV-D) is a nonfocal central nervous system manifestation characterized by cognitive, behavioral, and motor abnormalities. The pathophysiology of neuronal damage in HIV-D includes a direct toxic effect of viral proteins on neuronal cells and an indirect effect...

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Veröffentlicht in:	Molecular pharmacology 2007-10, Vol.72 (4), p.856
Hauptverfasser:	Pingle, Sandeep C, Jajoo, Sarvesh, Mukherjea, Debashree, Sniderhan, Lynn F, Jhaveri, Krishna A, Marcuzzi, Adriana, Rybak, Leonard P, Maggirwar, Sanjay B, Ramkumar, Vickram
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenosine A1 Receptor Agonists Animals Apoptosis - physiology Blotting, Western Electrophoresis, Polyacrylamide Gel Enzyme Activation Gene Products, tat - physiology HIV-1 - physiology Immunohistochemistry Neurons - cytology NF-kappa B - metabolism Nitric Oxide Synthase Type II - metabolism PC12 Cells Rats Reverse Transcriptase Polymerase Chain Reaction
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