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Validated All-in-One™ qPCR Primer for CSF3(NM_172219.3) Search again
Product ID:
HQP152040
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
C17orf33, CSF3OS, GCSF
Gene Description:
colony stimulating factor 3
Target Gene Accession:
NM_172219.3(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 a cytokine that controls the production, differentiation, and function of granulocytes. The active protein is found extracellularly. Three transcript variants encoding three different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- Effect of in vivo infusion of granulocyte colony-stimulating factor on immune function.
- Induces autocrine production of epithelial cell-derived neutrophil attractant-78 in neutrophils.
- effect of recombinant human GCSF on dendritic cell populations in mouse spleen
- G-CSF can induce in vitro and in vivo differentiation of M2 AML t(8;21) cells.
- Stabilizing the native state of recombinant GCSF under physiological conditions using thermodynamic stabilizers, especially high-affinity ligands binding to the native state, inhibits aggregation occurring under structurally nonperturbing conditions.
- G-CSF increases neutrophil function in patients with severe sepsis and septic shock
- expression in airway epithelial cells by interleukin-17
- Review. The synergy of granulocyte colony-stimulating factor with stem cell factor results in important biologic responses such as the down-regulation of p27kip1 and the independent phosphorylation of STAT3 on tyrosine and serine residues.
- inhibits spontaneous cytochrome c release and mitochondria-dependent apoptosis of myelodysplastic syndrome hematopoietic progenitors.
- Enhanced PMN survival was attributed to effects of epithelial G-CSF and granulocyte-macrophage colony-stimulating factor expression, which inhibit PMN apoptosis.Both CF and normal cells responded to bacteria with increased cytokine production
- results demonstrate that G-CSF is produced in the human follicle shortly before the ovulatory phase and may play an important role in the mechanism of ovulation
- granulocyte colony-stimulating factor decreased platelet-activating factor acetylhydrolase secretion by decidual macrophages
- G-CSF-mediated antiapoptosis is mediated through protein synthesis-dependent mechanisms and involves the Janus kinase-STAT pathway.
- In the presence of ATRA, G-CSF enhanced superoxide release stimulated by the chemotactic peptide, enhanced survival during differentiation, regulated chemotactic peptide receptors CD33 and CD10 but not of CD11b and CD11c.
- Endogenous G-CSF levels in chemotherapy-induced neutropenia are significantly higher than non-chemotherapy related neutropenia and controls.
- The induction of GATA-3, the master transcription factor for a Th2 immune response, can be demonstrated in T cells upon G-CSF treatment in vivo accompanied by an increase of spontaneous IL-4 secretion. G-CSF is a strong immune regulator of T cells.
- tertiary structural perturbations in G-CSF suggest the presence of an intermediate state and possible relation to ligand binding and endocytic trafficking
- Conformation change of an epitope of the granulocyte-colony stimulating factor after binding to receptors.
- TNF, GM-CSF, and G-CSF induce actin depolymerization and morphological changes through activation of ERK and/or p38 MAPK, and cytokine-induced actin reorganization may affect inhibitory effect of these cytokines on neutrophil chemotaxis.
- G-CSF 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.
- significant associations of endogenous G-CSF levels with inflammatory mediators early in the development of severe lung injury suggest an endogenous anti-inflammatory role of G-CSF in vivo
- The significantly higher level of G-CSF in follicular fluid (FF) than in serum and the expression of G-CSF and its receptor in FF by granulosa cells suggest an important role for this growth factor in ovarian function.
- G-CSF appears to be a suppressor of antitumor immunity
- G-CSF is associated with the expression of proliferation vascularization in memingioma.
- The G-CFS may provide clinically useful information, particularly regarding prognosis and response to treatment.
- G-CSF, a promoter of tolerogenic dendritic cells, may be evaluated for the treatment of human type 1 diabetes
- one of the major roles of Stat3 in the G-CSF signaling pathway is to augment the function of C/EBPalpha, which is essential for myeloid differentiation
- osteoblast activity, as measured by histomorphometry and osteocalcin expression, is strongly down-regulated during G-CSF treatment
- Correlation between endogenous G-CSF and CD34(+) cell levels supports the administration of G-CSF as an option for regeneration of myocardial tissue after acute myocardial infarct.
- Protein kinase C plays a role in activation of granulocyte-colony stimulating factor in lung cancer.
- 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
- PAR2-driven upregulation of VCAM-1 cell surface expression and the release of IL-8 and G-CSF from bronchial fibroblasts may be important in promoting neutrophilic airways inflammation.
- monocytes mobilized into the blood by G-CSF or AMD3100 stimulate angiogenesis at sites of ischemia through a paracrine mechanism
- It appears that G-CSF mobilizes more CD34(+) cells, mature Dendritic cellswithin the same donor than does GM-CSF.
- A progression-promoting effect of G-CSF and GM-CSF in human head and neck squamous cell carcinomas.
- G-CSF has a role in the induction of E-selectin ligands on myeloid cells, thus providing mechanistic insight into the pathobiology of G-CSF complications
- The observed up-regulation of G-CSF points towards a role in the pathophysiology of human ischemic stroke.
- A comparison of the relative rates of oxidation of methionine residues in short peptides with those of corresponding methionine residues in recombinant human G-CSF yields an understanding of how protein tertiary structure affects oxidation reactions.
- G-CSF and GM-CSF might accelerate tumor progression by directly regulating COX-2 expression, independently of an autocrine mechanism.
- The G-CSF/G-CSFR autocrine/paracrine signaling loop significantly promotes survival and growth of bladder cancer cells.
- preincubation with all dilutions of rhG-CSF augmented aggregation of platelets induced by ADP and collagen
- The granulocyte colony stimulating factor (G-CSF) activates Jak/STAT and MAPK pathways in a trophoblastic cell line
- Higher concentrations of interleukin-8, G-CSF, and GM-CSF in bronchoalveolar lavage fluid are associated with the development of fibrosis in sulfur mustard victims.
- We found no significant role for MMPs during the mobilization of peripheral blood stem cells stimulated by G-CSF.
- G-csf transgenic chicks can be produced from the cross of transgenic roosters with nontransgenic hens, but most of the G(1) progeny were dead within 1 month of hatching.
- Differential constitutive and cytokine-modulated expression of Toll-like receptors in primary neutrophils, monocytes, and macrophages is reported.
- production by myelodysplastic syndrome blasts
- genetic variation in colony-stimulating factor 3 is associated with cross-sectionally measured lung function in smokers
- G-CSF stimulates bone marrow cell mobilization, which may promote venous thrombus resolution.
- Studied the formation of aggregates in recombinant human granulocyte-colony stimulating factor (rHuG-CSF), lenograstim, using size-exclusion chromatography and SDS-PAGE.
- G-CSF mobilizes CD34+ cells, increases hepatocyte growth factor, and induces hepatic progenitor cells to proliferate within 7 days of administration.
- These findings suggest that the hematopoietic system may play a novel role in regulating osteoblast differentiation and apoptosis during G-CSF treatment.
- although G-CSF induces an inflammatory reaction leading to CRP production, it has direct beneficial effects protecting ECs from the deleterious effects of CRP through activation
- At birth, the concentrations of different cytokines/chemokines increased and that of granulocyte colony-stimulating factor remained high in sepsis due to GBS infection.
- TLR2 mediates SAA-induced G-CSF expression
- Case Report: Prostate cancer-producing granulocyte colony-stimulating factor.
