◀ Back to JAK2
JAK2 — PRLR
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
PRLR
→
JAK2
(increases, PRLR Activity)
Evidence: The sentence (Jubilant) Prolactin activates prolactin receptor associated tyrosine kinase Jak2 after the activation Jak2 phosphorylates prolactin receptor. is translated to Activation of Jak2 (Rattus norvegicus) Protein by Prl (Rattus norvegicus) Protein The following edits have been made already none Links Doc Sourcerer for 7508935 JAK2 PRL (Homo sapiens) Protein
-
KEGG Jak-STAT signaling pathway:
CNTFR/CRLF2/CSF2RA/CSF2RB/CSF3R/EPOR/GHR/IFNAR1/IFNAR2/IFNGR1/IFNGR2/IFNLR1/IL10RA/IL10RB/IL11RA/IL12RB1/IL12RB2/IL13RA1/IL13RA2/IL15RA/IL20RA/IL20RB/IL21R/IL22RA1/IL22RA2/IL23R/IL2RA/IL2RB/IL2RG/IL3RA/IL4R/IL5RA/IL6R/IL6ST/IL7R/IL9R/LEPR/LIFR/MPL/OSMR/PRLR
→
JAK1/JAK2/JAK3/TYK2
(protein-protein, phosphorylation)
-
NCI Pathway Database ErbB4 signaling events:
STAT5A (STAT5A)
→
ErbB4/ErbB4/HBEGF/HBEGF/Prolactin receptor/Prolactin receptor/Prolactin/JAK2 complex (ERBB4-HBEGF-PRLR-PRL-JAK2)
(modification, collaborate)
Muraoka-Cook et al., Mol Endocrinol 2008
Evidence: mutant phenotype, other species
-
NCI Pathway Database ErbB4 signaling events:
ErbB4/ErbB4/HBEGF/HBEGF/Prolactin receptor/Prolactin receptor/Prolactin/JAK2 complex (ERBB4-HBEGF-PRLR-PRL-JAK2)
→
STAT5A (dimer) complex (STAT5A)
(modification, activates)
Muraoka-Cook et al., Mol Endocrinol 2008
Evidence: mutant phenotype, other species
-
NCI Pathway Database Signaling events mediated by PTP1B:
Prolactin Receptor/Prolactin complex (PRLR-PRL)
→
JAK2 (JAK2)
(modification, activates)
Aoki et al., Mol Endocrinol 2002*
Evidence: assay, other species
-
NCI Pathway Database ErbB4 signaling events:
ErbB4/ErbB4/HBEGF/HBEGF complex (ERBB4-HBEGF)
→
ErbB4/ErbB4/HBEGF/HBEGF/Prolactin receptor/Prolactin receptor/Prolactin/JAK2 complex (ERBB4-HBEGF-PRLR-PRL-JAK2)
(modification, collaborate)
Muraoka-Cook et al., Mol Endocrinol 2008
Evidence: assay, physical interaction, other species
-
NCI Pathway Database ErbB4 signaling events:
Prolactin receptor/Prolactin receptor/Prolactin complex (PRLR-PRL)
→
JAK2 (JAK2)
(modification, collaborate)
Muraoka-Cook et al., Mol Endocrinol 2008
Evidence: assay, physical interaction, other species
-
NCI Pathway Database ErbB4 signaling events:
Prolactin receptor/Prolactin receptor/Prolactin complex (PRLR-PRL)
→
ErbB4/ErbB4/HBEGF/HBEGF/Prolactin receptor/Prolactin receptor/Prolactin/JAK2 complex (ERBB4-HBEGF-PRLR-PRL-JAK2)
(modification, collaborate)
Muraoka-Cook et al., Mol Endocrinol 2008
Evidence: assay, physical interaction, other species
-
NCI Pathway Database ErbB4 signaling events:
JAK2 (JAK2)
→
ErbB4/ErbB4/HBEGF/HBEGF/Prolactin receptor/Prolactin receptor/Prolactin/JAK2 complex (ERBB4-HBEGF-PRLR-PRL-JAK2)
(modification, collaborate)
Muraoka-Cook et al., Mol Endocrinol 2008
Evidence: assay, physical interaction, other species
-
Reactome Reaction:
JAK2
→
PRLR
(direct_complex)
-
Reactome Reaction:
JAK2
→
PRLR
(reaction)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Tomic et al., Mol Cell Endocrinol 1999
:
Overexpression of SOCS-1 led to a significant reduction in
PRLR mediated tyrosyl phosphorylation of
Jak2 , PRLR, Stat5 and the cytoplasmic protein tyrosine phosphatase SHP2 ... Overexpression of SOCS-3 however, led to selective inhibition in
PRLR mediated tyrosyl phosphorylation of
Jak2 , the PRLR as well as SHP2
Cwikel et al., Exp Hematol 2001
:
We and others recently showed that CIS-3 and JAB abolish
PRLR mediated
JAK2 activation and STAT-5 activity, whereas CIS-1, CIS-2, and CIS-4 had a negligible effect
Kline et al., Mol Endocrinol 2002
(Breast Neoplasms) :
The deltaS1
PRLr was also shown to
activate the proximal signaling molecule
Jak2 upon addition of ligand to transfected cells, and, unlike the long PRLr, high concentrations of ligand did not function as a self-antagonist to signaling during intervals of PRL serum elevation, i.e. stress and pregnancy
Petridou et al., Transgenic Res 2003
:
The cytokine-inducible suppressor of cytokine signalling SOCS1, or JAB, has been shown to be implicated in vitro in the negative regulation of the
prolactin-receptor induced
activation of
JAK2 and STAT5
Neilson et al., Mol Endocrinol 2007
(Breast Neoplasms) :
Relative
Jak2 deficiency did not
cause PRLR activation of Jak1, because overexpression of Jak2 did not interfere with PRL activation of Jak1
Swaminathan et al., J Endocrinol 2008
:
Here, we investigated the
role of
Jak2 activity in ligand triggered increase of
PRLr phosphorylation on Ser349, PRLr ubiquitination, endocytosis, and degradation
García-Martínez et al., Cell Signal 2010
:
Previous studies indicated that
PRLR induced
Jak2 activation does not require SFK catalytic activity in favor of separate signaling operating on this cellular response ... Accordingly,
PRLR induced
Jak2/Stat5 signaling is inhibited in MCF7 breast cancer cells by Src depletion, expression of SrcK295M/Y527F or active Src harboring an inactive SH2 ( SrcR175L ) or SH3 domain ( SrcW118A ) ... We thus conclude that, in addition to Akt and p70S6K, SFK regulate
PRLR induced
Jak2 signaling through a kinase independent mechanism
Varghese et al., Mol Endocrinol 2010
(Breast Neoplasms) :
Treatment of cells with PRL inhibited pyruvate kinase activity and increased the lactate content in human cells in a manner that was dependent on the abundance of
PRLr ,
activation of
Janus kinase 2 , and tyrosine phosphorylation of the intracellular domain of PRLr