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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to STAT3

CASP3 — STAT3

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: CASP3 → STAT3 (decreases, STAT3 Activity, CASP3 Activity)
    Evidence: Several studies have further suggested that the upregulation of STAT3 directly confers a drug-resistance phenotype. For example, overexpression of this transcription factor protects epidermal keratinocytes or cervical carcinoma cells from ultraviolet radiation (UV)-induced apoptosis [74,75]. In addition, STAT3 deficiency sensitizes keratinocytes to UV-induced apoptosis. Interestingly, a simple application of a naked STAT3 plasmid on the skin is sufficient to prevent the effect of irradiation. Th...

Text-mined interactions from Literome

Adamus et al., J Autoimmun 2003 (Autoimmune Diseases...) : The present study shows that an AAV mediated delivery of CNTF may protect photoreceptors from antibody induced cell death through the activation of STAT3 and the suppression of caspase 3 activity, a key caspase leading to apoptosis
Frias et al., Cardiovasc Res 2008 : Depleting Stat3 expression by 50-60 % in isolated ventricular cardiomyocytes markedly reduced the protective effect of PGE ( 2 ) on DOX induced caspase3 activation and DNA fragmentation
Rafei et al., J Immunol 2009 (Encephalomyelitis, Autoimmune, Experimental) : Treatment of CD4 T cells derived from experimental autoimmune encephalomyelitis mice with GMME1 leads to p38 hyperphosphorylation, inhibition of p44/42, AKT and STAT3 phosphorylation, and caspase-3 activation
Jabbour et al., Transplantation 2011 (Myocardial Reperfusion Injury) : Functional improvements were accompanied by increased phosphorylation of Akt, ERK1/2, STAT3 , and GSK-3ß and reduced cleaved caspase-3 ( P < 0.01 )
Kannaiyan et al., Br J Pharmacol 2011 (Multiple Myeloma) : Celastrol also inhibited both the constitutive and IL6 induced activation of STAT3 , which induced apoptosis as indicated by an increase in the accumulation of cells in the sub-G1 phase, an increase in the expression of pro-apoptotic proteins and activation of caspase-3
Khan et al., BioMed research international 2013 (Liver Neoplasms) : This alantolactone induced apoptosis was found to be associated with GSH depletion, inhibition of STAT3 activation, ROS generation, mitochondrial transmembrane potential dissipation, and increased Bax/Bcl-2 ratio and caspase-3 activation