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PTK2 — RAC1

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: PTK2 → RAC1 (increases) Chaturvedi et al., J Biol Chem 2007*
  Evidence: Src or Rac1 inhibition also prevented strain-induced FAK phosphorylation at Tyr(576) and ERK phosphorylation but not FAK phosphorylation at Tyr(397).
• NCI Pathway Database Signaling events mediated by focal adhesion kinase: RAC1/GDP complex (RAC1) → FAK/Src-Yes-Fyn/p130 CAS/CRK/DOCK1/ELMO1 complex (PTK2-YES1_SRC_FYN-BCAR1-CRK-DOCK1-ELMO1) (modification, collaborate)
  Cho et al., J Cell Biol 2002, Hsia et al., J Cell Biol 2003, Sharma et al., BMC cell biology 2008, Kiyokawa et al., Genes Dev 1998, Dolfi et al., Proc Natl Acad Sci U S A 1998
  Evidence: mutant phenotype, physical interaction
• NCI Pathway Database Netrin-mediated signaling events: RAC1/GDP complex (RAC1) → netrin 1/DCC/FAK/Fyn/p130 CAS complex (NTN1-DCC-PTK2-FYN-BCAR1) (modification, collaborate)
  Liu et al., J Neurosci 2007
  Evidence: mutant phenotype
• NCI Pathway Database Netrin-mediated signaling events: netrin 1/DCC/FAK/Fyn/p130 CAS complex (NTN1-DCC-PTK2-FYN-BCAR1) → RAC1/GTP complex (RAC1) (modification, activates) Liu et al., J Neurosci 2007
  Evidence: mutant phenotype
• Reactome Reaction: PTK2 → RAC1 (reaction) Brugnera et al., Nat Cell Biol 2002, Li et al., Nat Neurosci 2008, Briançon-Marjollet et al., Mol Cell Biol 2008
• Reactome Reaction: PTK2 → RAC1 (indirect_complex) Li et al., Nat Neurosci 2008, Briançon-Marjollet et al., Mol Cell Biol 2008

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: RAC1 — PTK2 (direct interaction, two hybrid) Bandyopadhyay et al., Nat Methods 2010
• IRef Intact Interaction: PTK2 — RAC1 (physical association, two hybrid pooling approach) Bandyopadhyay et al., Nat Methods 2010
• IRef Intact Interaction: Complex of ITGB5-ANGPTL4-ITGB5-RAC1-PTK2 (association, anti bait coimmunoprecipitation) Zhu et al., Cancer Cell 2011*

Text-mined interactions from Literome

Sundberg et al., J Biol Chem 2003 : Instead, FRNK expression markedly attenuated PDGF-BB-, angiotensin II-, and integrin stimulated Rac1 activity and attenuates downstream signaling to JNK
Xue et al., Int J Cancer 2006 (Carcinoma, Hepatocellular...) : The hypoxia stimulated activities of Rac1 and Cdc42 could be blocked by the phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and the protein tyrosine kinase ( PTK ) inhibitor genistein but were not affected by the p38MAPK inhibitor SB203580 or the MEK-1 inhibitor PD98059, suggesting that the hypoxia mediated signals were through PI3K and PTK ... Our results indicate that PI3K and PTK mediated activations of Rac1 and Cdc42 are involved in the hypoxia induced production of angiogenesis promoting factors and tumor suppressors, and suggest that the Rho family GTPases Rac1 and Cdc42 may contribute to the hypoxia mediated angiogenesis
Saito et al., Biol Pharm Bull 2008 (Wounds and Injuries) : TNIIIA2-treatment unaffected autophosphorylation of focal adhesion kinase ( FAK ), but induced its physical association with phospho-paxillin ( Tyr118 ), suggesting the FAK/paxillin dependent negative regulation of Rac activation