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The protein encoded by CSF3R is the receptor for colony stimulating factor 3, a cytokine that controls the production, differentiation, and function of granulocytes. Additionally we are shipping CSF3R Antibodies (163) and CSF3R Proteins (21) and many more products for this protein.
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CSF3R expression is significantly upregulated in human masticatory mucosa during wound healing
Results indicate that granulocyte-colony stimulating factor receptor, tissue factor, and vascular endothelial growth factor receptor bound vascular endothelial growth factor expression as well as their co-expression might influence breast cancer biology.
The Colony-Stimulating Factor (show CSF2 ELISA Kits) 3 Receptor T640N Mutation Is Oncogenic, Sensitive to JAK (show JAK3 ELISA Kits) Inhibition, and Mimics T618I
CSF3R mutations, mechanisms of mutations, and their contributions to the myeloid malignancies (Review)
In conclusion, rhCSF3 can promote melanocyte proliferation through CSF3R without affecting tyrosinase (show TYR ELISA Kits) activity
CSF3R mutations are associated with congenital neutropenia.
The leukemogenic potential of G-CSFRIV is associated with the Stat5 (show STAT5A ELISA Kits)-dependent dysregulation of miR (show MLXIP ELISA Kits)-155 and the target genes of this miRNA.
No CSF3R mutations were found in cases of MDS (show PAFAH1B1 ELISA Kits), JMML or ET. The only mutation found in the CALR (show CALR ELISA Kits) gene was a frameshift (p.L367 fs) in one ET patient.
The SETBP1 (show SETBP1 ELISA Kits) and ASXL1 (show ASXL1 ELISA Kits) mutations have pathogenetic roles in CSF3R-mutated chronic neutrophilic leukemia.
CSF3R polymorphisms are associated with chronic neutrophilic leukemia.
Thr (show TRH ELISA Kits)-615 and Thr (show TRH ELISA Kits)-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.
Fbw7 (show FBXW7 ELISA Kits) together with GSK3beta negatively regulates G-CSFR expression and its downstream signaling.
G-CSFR signaling interacts with retinoic acid receptors in the regulation of myeloid differentiation
Expression of truncated G-CSFR significantly shortens the latency of AML (show RUNX1 ELISA Kits) in a G-CSF (show CSF3 ELISA Kits)-dependent fashion and it is associated with a distinct AML (show RUNX1 ELISA Kits) presentation characterized by higher blast counts and more severe myelosuppression.
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.
Signaling mechanisms coupled to tyrosines in the granulocyte colony-stimulating factor receptor orchestrate G-CSF (show CSF3 ELISA Kits)-induced expansion of myeloid progenitor cells.
murine granulocyte colony-stimulating factor receptor binds to a low molecular weight ligand
Mice with truncated G-CSF (show CSF3 ELISA Kits) 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 (show SRI ELISA Kits) pathology.
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.
activation of both the Flt-3 (show FLT3 ELISA Kits) and G-CSF (show CSF3 ELISA Kits) receptors provides a high degree of radioprotection to the hematopoietic progenitor cell and stem cell compartment.
GCSF (show CSF3 ELISA Kits)/GCSFR is a conserved signaling system for facilitating the production of multiple myeloid cell lineages, as well as for early myeloid cell migration.
The protein encoded by this gene is the receptor for colony stimulating factor 3, a cytokine that controls the production, differentiation, and function of granulocytes. The encoded protein, which is a member of the family of cytokine receptors, may also function in some cell surface adhesion or recognition processes. Alternatively spliced transcript variants have been described. Mutations in this gene are a cause of Kostmann syndrome, also known as severe congenital neutropenia.
granulocyte colony-stimulating factor receptor
, colony stimulating factor 3 receptor (granulocyte)
, granulocyte colony-stimulating factor receptor-like
, CD114 antigen
, G-CSF receptor
, granulocyte stimulating factor receptor