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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 Kits (49) and CSF3R Proteins (26) and many more products for this protein.
Showing 10 out of 193 products:
Human Polyclonal CSF3R Primary Antibody for IF (p), IHC (p) - ABIN742275
Tajima, Waki, Tsuchiya, Hoshi et al.: Granulocyte colony-stimulating factor-producing undifferentiated carcinoma of the colon mimicking a pulmonary giant cell carcinoma: a case showing overexpression of CD44 along with highly ... in International journal of clinical and experimental pathology 2014
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Human Monoclonal CSF3R Primary Antibody for FACS - ABIN2478112
Curtis, Patel: Pharmacy-based analytical toxicology service. in American journal of hospital pharmacy 1975
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Human Monoclonal CSF3R Primary Antibody for CyTOF, FACS - ABIN4899922
Shao, Xu, Jing, Tweardy: Unique structural determinants for Stat3 recruitment and activation by the granulocyte colony-stimulating factor receptor at phosphotyrosine ligands 704 and 744. in Journal of immunology (Baltimore, Md. : 1950) 2006
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Human Monoclonal CSF3R Primary Antibody for FACS - ABIN4896903
Dror, Durie, Ginzberg, Herman, Banerjee, Champagne, Shannon, Malkin, Freedman: Clonal evolution in marrows of patients with Shwachman-Diamond syndrome: a prospective 5-year follow-up study. in Experimental hematology 2002
Human Monoclonal CSF3R Primary Antibody for CyTOF, ELISA (Capture) - ABIN4899923
deBruin, Lincoln, Hartley, Shehabeldin, Van, Szilvassy: Most purported antibodies to the human granulocyte colony-stimulating factor receptor are not specific. in Experimental hematology 2010
we report here for the first time changes in the allele frequencies of CSF3R-T618I and SETBP1 (show SETBP1 Antibodies)-G870S with response to ruxolitnib as well as insights into the clonal evolution of CNL under selective pressure from ruxolitinib.
CSF3R genetic polymorphism occurred more frequently in the individuals with Septic Arthroplasty failure - Periprosthetic Joint Infection.
G-CSF-R is C-mannosylated at W318 and that this C-mannosylation has role(s) for myeloid cell differentiation through regulating downstream signaling.
CSF3R mutations co-occur with CEBPA (show CEBPA Antibodies) mutations in pediatric acute myeloid leukemia (show BCL11A Antibodies).
we have expanded the region of the CSF3R cytoplasmic domain in which truncation or missense mutations exhibit leukemogenic capacity, which will be useful for evaluating the relevance of CSF3R mutations in patients and helpful in defining targeted therapy strategies.
our data demonstrates that E6AP (show ube3a Antibodies) facilitates ubiquitination and subsequent degradation of G-CSFR leading to attenuation of its downstream signaling and inhibition of granulocytic differentiation.
study aimed to identity and characterize novel CSF3R extracellular missense mutations from exome sequencing of leukemia patients; results show the structural and functional importance of conserved extracellular cysteine pairs in CSF3R
a central role of enhanced Mapk (show MAPK1 Antibodies) signaling in CSF3R-induced leukemia.
CSF3R T618I mutation is associated with Chronic neutrophilic leukemia.
biallelic CSF3R mutations were identified In the group of congenital neutropenia patients; CSF3R mutant clones are highly dynamic and may disappear and reappear during continuous granulocyte colony-stimulating factor (G-CSF (show CSF3 Antibodies)) therapy. The time between the first detection of CSF3R mutations and overt leukemia is highly variable
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.
this study shows that dorsal root ganglion neurons cultured in G-CSF (show CSF3 Antibodies) failed to respond to G-CSF (show CSF3 Antibodies) in vitro, and Csf3r gene expression could not be detected in dorsal root ganglion neurons by single-cell RT-PCR
Thr (show TRH Antibodies)-615 and Thr (show TRH Antibodies)-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 Antibodies) 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 Antibodies) in a G-CSF (show CSF3 Antibodies)-dependent fashion and it is associated with a distinct AML (show RUNX1 Antibodies) 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 Antibodies)-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 Antibodies) 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 Antibodies) pathology.
GCSF (show CSF3 Antibodies)/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.
, G-CSF receptor
, granulocyte colony-stimulating factor receptor
, colony stimulating factor 3 receptor (granulocyte)
, granulocyte stimulating factor receptor
, granulocyte colony-stimulating factor receptor-like