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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. Zusätzlich bieten wir Ihnen CSF3R Antikörper (212) und CSF3R Kits (42) und viele weitere Produktgruppen zu diesem Protein an.
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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. in Blood 2006
Show all 5 Pubmed References
Human CSF3R Protein expressed in HEK-293 Cells - ABIN2181144
Ko, Chandra, Ouyang, Kwon, Karande, Han: Nanofluidic device for continuous multiparameter quality assurance of biologics. in Nature nanotechnology 2017
CSF3R mutations co-occur with CEBPA (zeige CEBPA Proteine) mutations in pediatric acute myeloid leukemia (zeige BCL11A Proteine).
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 (zeige ube3a Proteine) 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 (zeige MAPK1 Proteine) 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 (zeige CSF3 Proteine)) therapy. The time between the first detection of CSF3R mutations and overt leukemia is highly variable
Co-occurrence of mutations in CSF3R and CEBPA (zeige CEBPA Proteine) in a well-defined AML (zeige RUNX1 Proteine) subset, which uniformly responds to JAK (zeige JAK3 Proteine) inhibitors; this paves the way to personalized clinical trials for this disease.
The quantitative methods used in this study have shown non-altered expression levels of different microglial markers (Iba-1 (zeige AIF1 Proteine), Cd11b (zeige ITGAM Proteine) and CD68 (zeige CD68 Proteine)), together with increased expression of IL6 (zeige IL6 Proteine), IL10RA (zeige IL10RA Proteine), colony stimulating factor (zeige CSF2 Proteine) 3 receptor and toll-like receptor 7 (zeige TLR7 Proteine) in the thalamus in FFI, which explains the seemingly contradictory results of the previous studies.
This study proposes that acquisition of CSF3R mutations may represent a mechanism by which myeloid precursor cells carrying the ELANE (zeige ELANE Proteine) mutations evade the proapoptotic activity of the Neutrophil Elastase (zeige ELANE Proteine) mutants in SCN (zeige SRI Proteine) patients.
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 (zeige CSF3 Proteine) failed to respond to G-CSF (zeige CSF3 Proteine) in vitro, and Csf3r gene expression could not be detected in dorsal root ganglion neurons by single-cell RT-PCR
Thr (zeige TRH Proteine)-615 and Thr (zeige TRH Proteine)-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 (zeige FBXW7 Proteine) 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 (zeige RUNX1 Proteine) in a G-CSF (zeige CSF3 Proteine)-dependent fashion and it is associated with a distinct AML (zeige RUNX1 Proteine) 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 (zeige CSF3 Proteine)-induced expansion of myeloid progenitor cells.
murine granulocyte colony-stimulating factor receptor binds to a low molecular weight ligand
Mice with truncated G-CSF (zeige CSF3 Proteine) 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 (zeige SRI Proteine) pathology.
GCSF (zeige CSF3 Proteine)/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