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PTPN1 — STAT5A

Pathways - manually collected, often from reviews:

• NCI Pathway Database Signaling events mediated by PTP1B: PTP1B (PTPN1) → STAT5A (STAT5A) (modification, activates) Aoki et al., J Biol Chem 2000*
  Evidence: assay, other species

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: STAT5A — PTPN1 (direct interaction, unspecified method) Espanel et al., Protein Sci 2002*
• IRef Hprd Interaction: STAT5A — PTPN1 (in vitro) Espanel et al., Protein Sci 2002*
• IRef Intact Interaction: STAT5A — PTPN1 (dephosphorylation reaction, phosphatase assay) Espanel et al., Protein Sci 2002*
• IRef Intact Interaction: STAT5A — PTPN1 (direct interaction, filter binding) Espanel et al., Protein Sci 2002*
• STRING interaction: STAT5A — PTPN1 (interaction, mapped from grid kegg_pathways intact)
• STRING interaction: PTPN1 — STAT5A (interaction, mapped from grid)

Text-mined interactions from Literome

Donato et al., Blood 2001 (Leukemia) : Expression of bcr-abl in interleukin-3 (IL-3)/granulocyte-macrophage colony stimulating factor ( GM-CSF ) -dependent Mo7e cells ( MBA ) resulted in growth factor independence, constitutive activation of Stat-5 phosphorylation, engagement of mitogen activated protein ( MAP ) kinase signals, and increased expression of PTP1B and bcl-x ( L )
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
Johnson et al., Am J Pathol 2010 (Breast Neoplasms...) : Conversely, PTP1B overexpression suppressed prolactin induced Stat5 tyrosine phosphorylation