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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. De plus, nous expédions CSF3R Anticorps (193) et CSF3R Kits (49) et beaucoup plus de produits pour cette protéine.
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Human CSF3R Protein expressed in HEK-293 Cells - ABIN2181144
Ko, Chandra, Ouyang, Kwon, Karande, Han: Nanofluidic device for continuous multiparameter quality assurance of biologics. dans Nature nanotechnology 2017
Human CSF3R Protein expressed in Human Cells - ABIN2002378
Germeshausen, Ballmaier, Welte: Incidence of CSF3R mutations in severe congenital neutropenia and relevance for leukemogenesis: Results of a long-term survey. dans Blood 2006
Show all 5 Pubmed References
Expression and role of granulocyte macrophage colony-stimulating factor receptor (Montrer CSF2RA Protéines) (GM-CSFR (Montrer CSF2RA Protéines)) and granulocyte colony-stimulating factor receptor (G-CSFR) on Ph-positive acute B lymphoblastic leukemia.
we report here for the first time changes in the allele frequencies of CSF3R-T618I and SETBP1 (Montrer SETBP1 Protéines)-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 (Montrer CEBPA Protéines) mutations in pediatric acute myeloid leukemia (Montrer BCL11A Protéines).
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 (Montrer ube3a Protéines) 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 (Montrer MAPK1 Protéines) signaling in CSF3R-induced leukemia.
CSF3R T618I mutation is associated with Chronic neutrophilic leukemia.
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 (Montrer CSF3 Protéines) failed to respond to G-CSF (Montrer CSF3 Protéines) in vitro, and Csf3r gene expression could not be detected in dorsal root ganglion neurons by single-cell RT-PCR
Thr (Montrer TRH Protéines)-615 and Thr (Montrer TRH Protéines)-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 (Montrer FBXW7 Protéines) 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 (Montrer RUNX1 Protéines) in a G-CSF (Montrer CSF3 Protéines)-dependent fashion and it is associated with a distinct AML (Montrer RUNX1 Protéines) 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 (Montrer CSF3 Protéines)-induced expansion of myeloid progenitor cells.
murine granulocyte colony-stimulating factor receptor binds to a low molecular weight ligand
Mice with truncated G-CSF (Montrer CSF3 Protéines) 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 (Montrer SRI Protéines) pathology.
GCSF (Montrer CSF3 Protéines)/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