Gene interactions and pathways from curated databases and text-mining

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JAK1 — TYK2

Pathways - manually collected, often from reviews:

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Shang et al., Cancer Sci 2007 (Carcinoma, Renal Cell...) : The results suggest that the resistance of RCC to IFN-alpha is associated with the lack of Jak1, Tyk2 and Stat1 expression and defective Jak-Stat activation , but not with a lack of IFN-alpha receptor, suppressors of cytokine signaling induction or other factors examined
Simmons et al., J Virol 2009 : Furthermore, at times when STAT1 activation was efficiently inhibited, VRP infection did not limit tyrosine phosphorylation of Jak1, Tyk2 , or STAT2 after IFN-beta treatment but did inhibit Jak1 and Jak2 activation in response to IFN-gamma, suggesting that VEEV interferes with STAT1 activation by the type I and II receptor complexes through distinct mechanisms
Dedoni et al., J Neurochem 2010 (Neuroblastoma) : Janus kinase inhibition reduced IFN-ß stimulated TyK2 and STAT1 phosphorylation, STAT1 transcriptional activity, induction of double stranded RNA activated protein kinase ( PKR ) and caspase cleavage
Murata et al., J Biol Chem 1995 (Colonic Neoplasms) : The phosphorylation of JAK1 and JAK2 was induced by IL-4 stimulation ; however, Tyk2 was constitutively phosphorylated, and IL-4 treatment further augmented this phosphorylation
Eilers et al., Cell Growth Differ 1996 : TYK2 activity led to an IFN-alpha independent appearance of tyrosine phosphorylated STAT1 but not STAT2 or JAK1 proteins