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PTPN1 — STAT3

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: STAT3 — PTPN1 (direct interaction, enzymatic study) Lund et al., J Mol Endocrinol 2005*
• IRef Intact Interaction: STAT3 — PTPN1 (dephosphorylation reaction, phosphatase assay) Zabolotny et al., Dev Cell 2002*
• IRef Intact Interaction: STAT3 — PTPN1 (dephosphorylation reaction, phosphatase assay) Lund et al., J Mol Endocrinol 2005*

Text-mined interactions from Literome

Kaszubska et al., Mol Cell Endocrinol 2002 : Over-expression of PTP1B in GT1-7 cells resulted in a dose dependent decrease in endogenous JAK2 and STAT3 tyrosine phosphorylation compared with cells transfected with lepR alone
Akasaki et al., J Biol Chem 2006 (Glioma) : Knockdown of STAT3 by STAT3-small interfering RNA negated the inhibitory effect of PTP inhibitor on troglitazone, indicating that troglitazone uses a STAT3 inactivation mechanism that makes caspase-8/9 activities susceptible to cytotoxic agents in glioma cells and that PTP1B plays a critical role in the down-regulation of activated STAT3 , as well as FLIP and Bcl-2
Yuan et al., J Biol Chem 2010 (Breast Neoplasms...) : Furthermore, PTPN9 WT expression specifically impairs EGF induced STAT3 and STAT5 activation, and inhibits the cell growth in soft agar
Handy et al., Biochem J 2011 (Liver Cirrhosis) : These results suggest two novel mechanisms whereby adiponectin inhibits hepatic fibrosis : ( i ) by promoting binding of SOCS-3 to Ob-Rb, and ( ii ) by stimulating PTP1B expression and activity, thus inhibiting JAK2/STAT3 signalling at multiple points