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Validated All-in-One™ qPCR Primer for CSF3R(NM_156039.3) Search again
Product ID:
HQP093425
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD114, GCSFR, SCN7
Gene Description:
colony stimulating factor 3 receptor
Target Gene Accession:
NM_156039.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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. Four transcript variants encoding four different isoforms have been found for this gene, with three of the isoforms being membrane-bound and the other being secreted and soluble. Mutations in this gene are a cause of Kostmann syndrome, also known as severe congenital neutropenia. [provided by RefSeq].
Gene References into function
- the dimerization interface of the complete receptor complex is different from that in the x-ray structure of a partial complex. A model of the tetrameric G-CSF.G-CSF-R complex was prepared
- The C-terminus of the G-CSF receptor, truncated in patients with severe congenital neutropenia/acute myeloid leukemia, is required for SH2-containing phosphatase-1 suppression of G-CSF-stimulated Stat activation.
- Lack of STAT3beta function in a differentiation-competent murine cell line expressing human G-CSFR argues against its having a role in Kip1 expression or neutrophil differentiation.
- Novel variant involved in induction of cell proliferation; myelodysplastic syndrome; a deletion of three nucleotides (2128-2130) in the juxtamembrane domain of the G-CSFR resulted in a conversion of Asn(630)Arg(631) to Lys(630).
- abnormalities of primitive myeloid progenitor cells expressing G-CSFR may play an important role in the impairment of granulopoiesis in patients with severe congenital neutropenia
- the carboxy-terminal region of hGCSFR plays a role in the phagocytosis and Syk and Hck kinase tyrosine phosphorylation is involved.
- selective inhibition of G-CSF receptor expression by C/EBPalphap30-ER is due in part to its variable affinity for C/EBP sites
- G-CSFR expression in some bladder cancers appears to be an early event during malignant transformation that increases beta1-integrin expression and adhesion and thereby may promote tissue invasion.
- Thermodynamic data for the interaction of GCSF-GCSFR induced by GCSF binding suggest that the activated structure of GCSFR is a 2:2 complex structure.
- reviewed the knowledge of the expression of G-CSFR and its role in the disorders of granulopoiesis, including myelodysplastic syndrome, and neutropenia in myelodysplastic patients
- lifelong altered G-CSF response by the G-CSF-R_785Lys may render individuals susceptible to development of high-risk M
- The Tyr 729 of the G-CSF-R is required for SOCS3-mediated negative regulation of G-CSF-R signaling and that the duration and intensity of G-CSF-induced Stat5 activation are regulated by two distinct mechanisms.
- crystal structure of the signaling complex between human granulocyte colony-stimulating factor (GCSF) and a ligand binding region of GCSF receptor (GCSF-R), has been determined to 2.8 A resolution
- Deleterious G-CSFR-mediated signaling events, such as aberrant Stat3 activation demonstrated in a subset of acute myeloid leukemia (AML) patients with poor prognosis, could be exploited for the treatment of AML patients.
- CSF3R nonsense mutations (10 new) in SCN at 17 sites lead to a loss Tyr residues in the intracellular domain of the receptor. CSF3R mutation is an early event in leukemogenesis that has to be accompanied by as yet undefined cooperating molecular events
- single-nucleotide polymorphism (Glu785Lys) is associated with myelodysplastic syndromes and acute myeloid leukemia with multlineage dysplasia
- The observed up-regulation of G-CSF receptors towards a role in the pathophysiology of human ischemic stroke.
- that mutations of CSF3R may provide the "activated tyrosine kinase signal" that is thought to be important for leukemogenesis.
- The G-CSF/G-CSFR autocrine/paracrine signaling loop significantly promotes survival and growth of bladder cancer cells.
- REVIEW: Congenital neutropenia patients with acquired CSF3R mutations define a group with high risk for development of leukemia; discussion of possible pathomechanism
- results indicate ubiquitination required for regulation of G-CSFR-mediated proliferation & cell survival; mutation disrupting G-CSFR ubiquitination induce aberrant signaling & proliferative response to G-CSF; this may contribute to leukemic transformatio