◀ Back to STAT3

APEX1 — STAT3

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: APEX1 → STAT3 (increases, APEX1 Activity)
  Evidence: signal transducer and activator of transcription-3 (Stat3), a key signaling molecule in pathways regulated by IL-6 and related cytokines, blocks apoptotic injury in two ways: induction of anticaspase regulators; and reduction of oxidative injury via upregulation of an antioxidant protein, Ref-1 (12).

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: APEX1 — STAT3 (physical association, affinity chromatography technology) Gray et al., Oncogene 2005
• MIPS CORUM VEGF transcriptional complex: VEGF transcriptional complex complex (APEX1-HIF1A-STAT3-CITED1-CITED2-CITED4) Gray et al., Oncogene 2005
• IRef Corum Interaction: Complex of CITED4-HIF1A-CITED1-STAT3-CITED2-APEX1 (association, coimmunoprecipitation) Gray et al., Oncogene 2005

Text-mined interactions from Literome

Guo et al., Am J Transplant 2004 (Liver Diseases...) : Interestingly, Ref-1 significantly increased DNA binding of Stat3 , but not AP-1
Cardoso et al., PloS one 2012 (Adenocarcinoma...) : Overall, this work demonstrates that the transcriptional activity of STAT3 is directly regulated by the redox function of APE1/Ref-1 , and that concurrent blockade of STAT3 and APE1/Ref-1 redox synergize effectively inhibit critical PDAC cell functions