Recombinant Mouse Granulocyte colony-stimulating factor receptor (Csf3r), partial

1. Anti-G-CSF receptor rapidly halted the progression of established disease in collagen Ab-induced arthritis in mice. Neutrophil accumulation in joints was inhibited, without rendering animals neutropenic, suggesting an effect of G-CSF receptor blockade on neutrophil homing to inflammatory sites. PMID:27807194
2. this study shows that dorsal root ganglion neurons cultured in G-CSF failed to respond to G-CSF in vitro, and Csf3r gene expression could not be detected in dorsal root ganglion neurons by single-cell RT-PCR PMID:28320832
3. Neutrophil activation in postischemic brain injury is regulated via upregulation of the neutrophil activator, CSFR3. PMID:26538649
4. Thr-615 and Thr-618 sites of membrane-proximal mutations are part of an O-linked glycosylation cluster. Mutation at these sites prevents O-glycosylation of CSF3R and increases receptor dimerization. PMID:24403076
5. Fbw7 together with GSK3beta negatively regulates G-CSFR expression and its downstream signaling. PMID:23820376
6. G-CSFR signaling interacts with retinoic acid receptors in the regulation of myeloid differentiation PMID:23136256
7. Expression of truncated G-CSFR significantly shortens the latency of AML in a G-CSF-dependent fashion and it is associated with a distinct AML presentation characterized by higher blast counts and more severe myelosuppression. PMID:21911095
8. G-CSFR signals in bone marrow monocytic cells inhibit the production of trophic factors required for osteoblast lineage cell maintenance, ultimately leading to hematopoietic stem and progenitor cell mobilization. PMID:21282380
9. Signaling mechanisms coupled to tyrosines in the granulocyte colony-stimulating factor receptor orchestrate G-CSF-induced expansion of myeloid progenitor cells. PMID:12468431
10. murine granulocyte colony-stimulating factor receptor binds to a low molecular weight ligand PMID:12524421
11. Mice with truncated G-CSF receptors have neutropenia, susceptibility to infection, and bone marrow maturation arrest similar to severe congenital neutropenic humans, suggesting a role of receptor truncation mutations in SCN pathology. PMID:12672695
12. COOH-terminal truncation mutants of G-CSF-R, found in severe congenital neutropenia, lack internalization motifs and are completely defective in both spontaneous and ligand-induced internalization. PMID:14512302
13. activation of both the Flt-3 and G-CSF receptors provides a high degree of radioprotection to the hematopoietic progenitor cell and stem cell compartment. PMID:14585378
14. lack of negative feedback by suppressor of cytokine signaling (SOCS) proteins contribution to the signaling abnormalities of G-CSF-R mutant PMID:15069015
15. The tyrosine (Tyr) 729, located in the carboxy terminus of the G-CSF-R, controls the duration of G-CSF-stimulated activation of Stat5, Akt, and extracellular signal-regulated kinase 1/2. PMID:16033816
16. data suggested that Snapin is a new interactive protein of the granulocyte colony-stimulating factor receptor PMID:16595180
17. inappropriate Stat5 activation plays a key role in establishing clonal dominance by stem cells expressing mutant Csf3r. PMID:18292815

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UNIGENE: Mm.271701

KEGG: mmu:12986

STRING: 10090.ENSMUSP00000030673