Caspase-1 inhibitors abolish deleterious enhancement of COX-2 expression induced by HIV-1 gp120 in human neuroblastoma cells

scientific article published on April 2003

Caspase-1 inhibitors abolish deleterious enhancement of COX-2 expression induced by HIV-1 gp120 in human neuroblastoma cells is …
instance of (P31):
scholarly articleQ13442814

External links are
P356DOI10.1016/S0378-4274(02)00436-8
P698PubMed publication ID12628757

P2093author name stringDi Renzo G
Corasaniti MT
Russo R
Amantea D
Bellizzi C
Colica C
P433issue2-3
P921main subjectneuroblastomaQ938205
P304page(s)213-219
P577publication date2003-04-01
P1433published inToxicology LettersQ1796854
P1476titleCaspase-1 inhibitors abolish deleterious enhancement of COX-2 expression induced by HIV-1 gp120 in human neuroblastoma cells
P478volume139

Reverse relations

cites work (P2860)
Q40173450COX-2 Induction during Murine Gammaherpesvirus 68 Infection Leads to Enhancement of Viral Gene Expression
Q45403949Ceftriaxone protects against the neurotoxicity of human immunodeficiency virus proteins
Q40275891Cyclooxygenase-1 and -2 are required for production of infectious pseudorabies virus
Q48496328Cyclooxygenase-2 is involved in HIV-1 Tat-induced inflammatory responses in the brain
Q34795283HIV neurotoxicity: potential therapeutic interventions
Q44270579Human immunodeficiency virus type 1 clade B and C gp120 differentially induce neurotoxin arachidonic acid in human astrocytes: implications for neuroAIDS.
Q38603237Immune activation in the course of HIV-1 infection: Causes, phenotypes and persistence under therapy
Q35721334Inhibitory effect of Phyllanthus urinaria L. extract on the replication of lamivudine-resistant hepatitis B virus in vitro
Q40176664Spike protein of SARS-CoV stimulates cyclooxygenase-2 expression via both calcium-dependent and calcium-independent protein kinase C pathways
Q28388594The role of inflammasome modulation in virulence
Q35741691The tyrosine kinase inhibitor genistein blocks HIV-1 infection in primary human macrophages

Search more.