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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.
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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 ELISA Kits) mutations in pediatric acute myeloid leukemia (show BCL11A ELISA Kits).
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 ELISA Kits) 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 ELISA Kits) 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 ELISA Kits)) therapy. The time between the first detection of CSF3R mutations and overt leukemia is highly variable
Co-occurrence of mutations in CSF3R and CEBPA (show CEBPA ELISA Kits) in a well-defined AML (show RUNX1 ELISA Kits) subset, which uniformly responds to JAK (show JAK3 ELISA Kits) 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 (show AIF1 ELISA Kits), Cd11b (show ITGAM ELISA Kits) and CD68 (show CD68 ELISA Kits)), together with increased expression of IL6 (show IL6 ELISA Kits), IL10RA (show IL10RA ELISA Kits), colony stimulating factor (show CSF2 ELISA Kits) 3 receptor and toll-like receptor 7 (show TLR7 ELISA Kits) in the thalamus in FFI, which explains the seemingly contradictory results of the previous studies.
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 ELISA Kits) failed to respond to G-CSF (show CSF3 ELISA Kits) in vitro, and Csf3r gene expression could not be detected in dorsal root ganglion neurons by single-cell RT-PCR
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.
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.
, G-CSF receptor
, granulocyte colony-stimulating factor receptor
, colony stimulating factor 3 receptor (granulocyte)
, granulocyte stimulating factor receptor
, granulocyte colony-stimulating factor receptor-like