We have a suspicion that you are an automated web bot software, not a real user. To keep our site fast for other users, we have slowed down this page. The slowdown will gradually disappear. If you think this is a mistake, please contact us at genome-www@soe.ucsc.edu. Also note that all data for hgGeneGraph can be obtained through our public MySQL server and all our software source code is available and can be installed locally onto your own computer. If you are unsure how to use these resources, do not hesitate to contact us.
UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to CASP4

CASP4 — ITIH4

Text-mined interactions from Literome

Singh et al., J Neurovirol 2004 (Nerve Degeneration) : Both HIV-1 Tat and gp120 significantly increased caspase-3 activation in a concentration dependent manner in striatal neurons at 4 h following continuous exposure in vitro ... Tat ( 1-72 ) and gp120 caused significant neuronal losses at 48 h and/or 72 h. Tat ( 1-72 ) increased cytochrome c release, and caspase-3 and endo G activation at 4 h, 24 h, and/or 72 h ... By contrast, gp120 increased caspase-3 activation, but failed to increase cytochrome c or endo G levels in the cytoplasm at 4 h, 24 h, and/or 72 h
Fiala et al., Cardiovasc Toxicol 2004 (Cardiomyopathies...) : HIV-1, gp120 , or Tat induced Erk 1/2 phosphorylation, activation of caspase-3 , and apoptosis of NRVMs and CAECs ; all of these were inhibited by a MAPK/ERK-kinase (MEK) inhibitor U0126
Singh et al., Neuroscience 2005 (Nerve Degeneration) : Both Tat and gp120 caused significant increases in p38 and c-jun-N-terminal kinase mitogen activated protein kinase phosphorylation, caspase-3 activity, neurite losses and cell death in striatal neurons ... Alternatively, gp120 induced increases in caspase-3 activity, neurite losses and neuronal death were prevented by p38, but not c-jun-N-terminal kinase, mitogen activated protein kinase inhibition
Tun et al., J Neurochem 2007 : As caspase-8 induced apoptosis does not typically require p53, we examined the possibility of a novel role for p53 in caspase-8 activation initiated by gp120 ... We observed that gp120 treatment of cultured cortical neurons induced caspase-8 activity and Bid cleavage independently of p53, but induction of caspase-3 enzymatic activity required p53 expression
Alirezaei et al., J Neurosci 2007 (AIDS Dementia Complex) : PKR inactivation also inhibited gp120 induced caspase-3 activation, consistent with its neuroprotective effect
Peng et al., J Neurovirol 2008 (Neuroblastoma) : Additionally, gp120 mediated activation of caspase-3 was also significantly reduced in cells pretreated with PDGF-BB
Janda et al., Br J Pharmacol 2011 : Tianeptine showed an anti-apoptotic effect and prevented caspase-3 activation by gp120