◀ Back to CSF3
CSF3 — CSF3R
Pathways - manually collected, often from reviews:
-
OpenBEL Selventa BEL large corpus:
Complex of CSF3R-IL6ST
→
CSF3
(increases)
Kim et al., Mol Cell Biol 1999
Evidence: HepG2 cells were transfected with expression vector for G-gp130 (WT) and Myc SHP-2CS or SHP-2-Myc and then were treated for 15 minutes with G-CSF, showed that gp130-recruited SHP-2 serves as a major mediator to the ERK pathway and that this function requires the carboxy-terminal half but not the phosphatase activity of the SHP-2 protein.
-
KEGG Cytokine-cytokine receptor interaction:
CSF3
→
CSF3R
(protein-protein, activation)
-
WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway:
CSF3/EPO/IFNA7/CSH1/IFNA7/IFNA7/IFNA7/IFNA7/IFNA7/IFNA7/IFNA7/IFNA7/IFNB1/IL2/OSM/PRL/IFNA7/IFNA7
→
IL3RA/IL2RB/IFNAR1/OSMR/PRLR/IL7R/IL6R/CSF3R/IL2RA/EPOR/IL4R/IL2RG/IFNAR2/GHR
(activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Inukai et al., Leukemia 2000
(Blast Crisis...) :
Unexpectedly, ` myeloid ' cell lines showed lower
G-CSFR expression and lower
G-CSF response compared with ` biphenotypic ' cell lines
Hörtner et al., J Immunol 2002
:
G-CSF regulates granulopoiesis and acts on its target cells by inducing homodimerization of the
G-CSFR , thereby activating intracellular signaling cascades
Schuster et al., Blood 2003
:
In 32Dcl3 cells transfected with the bcr-abl gene ( 32D ( Bcr-Abl ) ),
G-CSF did not
trigger either granulocytic differentiation or the up-regulation of C/EBPalpha, C/EBPepsilon, and the
G-CSFR
Harada et al., Nat Med 2005
(Myocardial Infarction...) :
G-CSF receptor was expressed on cardiomyocytes and
G-CSF activated the Jak/Stat pathway in cardiomyocytes
Schneider et al., J Clin Invest 2005
(Brain Ischemia...) :
Surprisingly, the
G-CSF receptor was also expressed by adult neural stem cells, and
G-CSF induced neuronal differentiation in vitro
McCracken et al., J Endocrinol 1996
:
These data suggested that expression of
G-CSFR in the human placenta is regulated both temporally and spatially, and that placental
G-CSF is
involved in paracrine regulation, and indicate a role for G-CSF and G-CSFR in trophoblast growth or function during placentation
Asano et al., Cancer Res 1997
(Blast Crisis...) :
First, we found that this chimeric soluble
G-CSF receptor could
inhibit the biological activity of
G-CSF on normal bone marrow colony formation