Gene interactions and pathways from curated databases and text-mining

◀ Back to IL1B

IL1B — ITIH4

Text-mined interactions from Literome

Bagetta et al., Neuroscience 1999 : These data demonstrate that gp120 enhances interleukin-1beta expression in the brain and this may be involved in the mechanism underlying apoptosis induced by gp120 in the brain cortex of rat
Corasaniti et al., Br J Pharmacol 2001 (Neuroblastoma) : HIV-1 coat protein gp120 stimulates interleukin-1beta secretion from human neuroblastoma cells : evidence for a role in the mechanism of cell death ... 3. ELISA experiments have established that gp120 enhances immunoreactive IL-1beta levels in the culture medium and this is prevented by exposure to the IL-1 converting enzyme (ICE) inhibitor t-butoxycarbonyl-L-aspartic acid benzyl ester-chloromethylketone [ Boc-Asp ( OBzl ) -CMK ] used at a concentration ( 2.5 microM ) which significantly ( P < 0.001 ) reduces cell death
Harraghy et al., Clin Diagn Lab Immunol 2005 : However, IL-1beta was shown to inhibit the IL-6 induced activation of the porcine ITIH4 promoter
Wieseler-Frank et al., Brain Behav Immun 2007 (Pain) : These studies demonstrate that : ( a ) intrathecal gp120 upregulates meningeal gene expression of proinflammatory signals, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin 6 (IL-6), and inducible nitric oxide synthase (iNOS), and ( b ) intrathecal gp120 induces meningeal release of TNF-alpha, IL-1beta , and IL-6 ... In addition, stimulation of isolated meninges in vitro with gp120 induced the release of TNF-alpha and IL-1beta , indicating that the resident cells of the meninges are able to respond without immune cell recruitment
Cheung et al., J Immunol 2008 (AIDS Dementia Complex) : In this study we showed that gp120 induces IL-1beta release from macrophages in a time- and concentration dependent manner through binding to the chemokine receptor CCR5 and coupling to G ( i ) alpha protein ... Using pharmacological inhibitors and small interfering RNA gene knockdown, we demonstrated that concomitant activation of Lyn, Pyk2, and class IA PI3K are required for gp120 induced IL-1beta production
Loram et al., Brain Behav Immun 2010 (Pain) : A second alpha7nAchR agonist, GTS-21, also significantly reversed gp120 induced mechanical allodynia and lumbar spinal cord levels of pro-inflammatory cytokine mRNAs and IL-1beta protein
Molina et al., J Virol 1990 : Our studies indicate that, in the absence of endotoxin, HIV-1, HIV-2, and HIV gp120 do not induce production of IL-1 beta , IL-6, or TNF-alpha by peripheral blood mononuclear cells
Kong et al., Cell Immunol 1996 (Inflammation) : Since nitric oxide ( NO ) and proinflammatory cytokines ( TNF-alpha, IL-1, IL-6 ) produced by glial cells have been involved in the neuropathogenesis of various diseases, this study examined the effects of gp120 obtained from two strains, HIV-1IIIB and HIV-1SF2, of the HIV-1 virus on the production of NO, TNF-alpha, IL-1 alpha, IL-1 beta , and IL-6 in murine primary mixed glial cell cultures
Ilyin et al., Biochem Biophys Res Commun 1997 : Gp120 increased IL-1 beta , IL-1Ra, TNF-alpha, and TGF-beta 1 mRNAs
Catania et al., Peptides 1998 (HIV Infections) : In separate experiments on normal peripheral blood mononuclear cells ( PBMC ), alpha-MSH ( 1-13 ) inhibited production of IL-1 beta and TNF alpha induced by HIV envelope glycoprotein gp 120