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JAK2 — PTK2
Pathways - manually collected, often from reviews:
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NCI Pathway Database CXCR4-mediated signaling events:
SDF1/CXCR4/JAK2 complex (CXCL12-CXCR4-JAK2)
→
FAK (PTK2)
(modification, activates)
Wang et al., Blood 2000, Zhang et al., Blood 2001, Okabe et al., J Hematother Stem Cell Res 2002, Le et al., J Immunol 2005
Evidence: mutant phenotype, assay, physical interaction
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
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IRef Biogrid Interaction:
JAK2
—
PTK2
(physical association, affinity chromatography technology)
Zhu et al., J Biol Chem 1998*
-
IRef Biogrid Interaction:
JAK2
—
PTK2
(physical association, affinity chromatography technology)
Ryu et al., J Immunol 2000*
-
IRef Hprd Interaction:
PTK2
—
JAK2
(in vivo)
Ryu et al., J Immunol 2000*, Zhu et al., J Biol Chem 1998*
-
IRef Ophid Interaction:
PTK2
—
JAK2
(aggregation, confirmational text mining)
Ryu et al., J Immunol 2000*
-
IRef Ophid Interaction:
PTK2
—
JAK2
(aggregation, interologs mapping)
Brown et al., Bioinformatics 2005
Text-mined interactions from Literome
Yu et al., J Biol Chem 2003
:
IL-6 increased phosphorylation of STAT3 ( at Tyr ( 705 ) ) and ERK1/2 ( at Tyr ( 204 ) ) within 5 min that peaked at 15-30 min and returned to basal levels at 2 h. Phosphorylation of STAT3 was blocked by genistein, a
protein tyrosine kinase inhibitor, and AG490, a
JAK2 inhibitor , but not PD98059, an ERK1/2 kinase inhibitor
Xenaki et al., Cell Signal 2004
:
Activation of Bcr-Abl
PTK does not phosphorylate or
activate either ERK-1/2 or
JAK-2/STAT-5b , suggesting that these signal transduction pathways are not involved in Abl PTK mediated suppression of apoptosis in FDCP-Mix cells