◀ Back to STAT1

KIT — STAT1

Pathways - manually collected, often from reviews:

• Reactome Reaction: KIT → STAT1 (reaction) Brizzi et al., J Biol Chem 1999, Ning et al., Oncogene 2001, Deberry et al., Biochem J 1997
• Reactome Reaction: KIT → STAT1 (indirect_complex) Brizzi et al., J Biol Chem 1999, Ning et al., Oncogene 2001, Deberry et al., Biochem J 1997

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

Studies that report less than 10 interactions are marked with *

• IRef Bind Interaction: KIT — STAT1 Deberry et al., Biochem J 1997
• IRef Bind_translation Interaction: KIT — STAT1 (affinity chromatography technology) Deberry et al., Biochem J 1997
• IRef Bind_translation Interaction: KIT — STAT1 (coimmunoprecipitation) Deberry et al., Biochem J 1997
• IRef Bind_translation Interaction: KIT — STAT1 (experimental interaction detection) Deberry et al., Biochem J 1997
• IRef Biogrid Interaction: STAT1 — KIT (physical association, affinity chromatography technology) Deberry et al., Biochem J 1997
• IRef Biogrid Interaction: STAT1 — KIT (direct interaction, pull down) Deberry et al., Biochem J 1997
• IRef Biogrid Interaction: STAT1 — KIT (direct interaction, enzymatic study) Deberry et al., Biochem J 1997
• IRef Hprd Interaction: STAT1 — KIT (in vivo) Deberry et al., Biochem J 1997
• IRef Ophid Interaction: KIT — STAT1 (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Duensing et al., Oncogene 2004 (Gastrointestinal Neoplasms) : Using GIST in vitro models, we showed that activation of MAPK p42/44, AKT, and S6K was KIT dependent, whereas STAT1 and STAT3 phosphorylation was only partially dependent on KIT activation
Zhu et al., Oncogene 2007 (Gastrointestinal Stromal Tumors) : Activated signaling intermediates were identified by immunoaffinity purification of tyrosine phosphorylated proteins in GIST cells before and after treatment with KIT inhibitors, and these analyses show that GRB2, SHC, CBL and MAPK activation are largely KIT dependent in GISTs, whereas PI3-K, STAT1 and STAT3 activation are partially KIT dependent