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CSF3R Antibody, FITC conjugated

  • 中文名稱:
    CSF3R兔多克隆抗體, FITC偶聯
  • 貨號:
    CSB-PA860321LC01HU
  • 規格:
    ¥880
  • 其他:

產品詳情

  • 產品名稱:
    Rabbit anti-Homo sapiens (Human) CSF3R Polyclonal antibody
  • Uniprot No.:
  • 基因名:
  • 別名:
    CD 114 antibody; CD114 antibody; CD114 antigen antibody; Colony stimulating factor 3 receptor (granulocyte) antibody; Colony stimulating factor 3 receptor antibody; CSF 3R antibody; CSF3R antibody; CSF3R_HUMAN antibody; Csfgr antibody; G CSF R antibody; G-CSF receptor antibody; G-CSF-R antibody; GCSFR antibody; Granulocyte colony stimulating factor receptor antibody; Granulocyte colony-stimulating factor receptor antibody; OTTHUMP00000009703 antibody; OTTHUMP00000009704 antibody; OTTHUMP00000009705 antibody
  • 宿主:
    Rabbit
  • 反應種屬:
    Human
  • 免疫原:
    Recombinant Human Granulocyte colony-stimulating factor receptor protein (117-337AA)
  • 免疫原種屬:
    Homo sapiens (Human)
  • 標記方式:
    FITC
  • 克隆類型:
    Polyclonal
  • 抗體亞型:
    IgG
  • 純化方式:
    >95%, Protein G purified
  • 濃度:
    It differs from different batches. Please contact us to confirm it.
  • 保存緩沖液:
    Preservative: 0.03% Proclin 300
    Constituents: 50% Glycerol, 0.01M PBS, pH 7.4
  • 產品提供形式:
    Liquid
  • 儲存條件:
    Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
  • 貨期:
    Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
  • 用途:
    For Research Use Only. Not for use in diagnostic or therapeutic procedures.

產品評價

靶點詳情

  • 功能:
    Receptor for granulocyte colony-stimulating factor (CSF3), essential for granulocytic maturation. Plays a crucial role in the proliferation, differientation and survival of cells along the neutrophilic lineage. In addition it may function in some adhesion or recognition events at the cell surface.
  • 基因功能參考文獻:
    1. Expression and role of granulocyte macrophage colony-stimulating factor receptor (GM-CSFR) and granulocyte colony-stimulating factor receptor (G-CSFR) on Ph-positive acute B lymphoblastic leukemia. PMID: 29338593
    2. we report here for the first time changes in the allele frequencies of CSF3R-T618I and SETBP1-G870S with response to ruxolitnib as well as insights into the clonal evolution of CNL under selective pressure from ruxolitinib. PMID: 28209656
    3. CSF3R genetic polymorphism occurred more frequently in the individuals with Septic Arthroplasty failure - Periprosthetic Joint Infection. PMID: 29305046
    4. G-CSF-R is C-mannosylated at W318 and that this C-mannosylation has role(s) for myeloid cell differentiation through regulating downstream signaling. PMID: 29501745
    5. CSF3R mutations co-occur with CEBPA mutations in pediatric acute myeloid leukemia. PMID: 27143256
    6. 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. PMID: 28439110
    7. our data demonstrates that E6AP facilitates ubiquitination and subsequent degradation of G-CSFR leading to attenuation of its downstream signaling and inhibition of granulocytic differentiation. PMID: 28578910
    8. 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 PMID: 28652245
    9. a central role of enhanced Mapk signaling in CSF3R-induced leukemia. PMID: 28031554
    10. CSF3R T618I mutation is associated with Chronic neutrophilic leukemia. PMID: 28209919
    11. 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) therapy. The time between the first detection of CSF3R mutations and overt leukemia is highly variable PMID: 27270496
    12. Co-occurrence of mutations in CSF3R and CEBPA in a well-defined AML subset, which uniformly responds to JAK inhibitors; this paves the way to personalized clinical trials for this disease. PMID: 27034432
    13. The quantitative methods used in this study have shown non-altered expression levels of different microglial markers (Iba-1, Cd11b and CD68), together with increased expression of IL6, IL10RA, colony stimulating factor 3 receptor and toll-like receptor 7 in the thalamus in FFI, which explains the seemingly contradictory results of the previous studies. PMID: 27056979
    14. This study proposes that acquisition of CSF3R mutations may represent a mechanism by which myeloid precursor cells carrying the ELANE mutations evade the proapoptotic activity of the Neutrophil Elastase mutants in SCN patients. PMID: 28073911
    15. CSF3R expression is significantly upregulated in human masticatory mucosa during wound healing PMID: 28005267
    16. Results indicate that granulocyte-colony stimulating factor receptor, tissue factor, and vascular endothelial growth factor receptor bound vascular endothelial growth factor expression as well as their co-expression might influence breast cancer biology. PMID: 27629739
    17. The Colony-Stimulating Factor 3 Receptor T640N Mutation Is Oncogenic, Sensitive to JAK Inhibition, and Mimics T618I PMID: 26475333
    18. CSF3R mutations, mechanisms of mutations, and their contributions to the myeloid malignancies (Review) PMID: 26956865
    19. In conclusion, rhCSF3 can promote melanocyte proliferation through CSF3R without affecting tyrosinase activity PMID: 25666388
    20. CSF3R mutations are associated with congenital neutropenia. PMID: 26324699
    21. The leukemogenic potential of G-CSFRIV is associated with the Stat5-dependent dysregulation of miR-155 and the target genes of this miRNA. PMID: 25730818
    22. No CSF3R mutations were found in cases of MDS, JMML or ET. The only mutation found in the CALR gene was a frameshift (p.L367 fs) in one ET patient. PMID: 25858548
    23. The SETBP1 and ASXL1 mutations have pathogenetic roles in CSF3R-mutated chronic neutrophilic leukemia. PMID: 25850813
    24. CSF3R polymorphisms are associated with chronic neutrophilic leukemia. PMID: 25708716
    25. CSF3R T618I mutation as a disease-specific marker of atypical CML post allo-SCT in two patients. PMID: 24614839
    26. the incorporation of CSF3R mutation testing can be a useful point-of-care diagnostic to evaluate the presence of a clonal myeloid disorder, as well as providing the potential for genetically informed therapy. PMID: 25533830
    27. study to see if the CSF3R p.T618I mutation was present in acute myelogenous leukemia (AML) and solid tumors of Korean patients; data revealed that CSF3R p.T618I mutation occurred in an AML with myelodysplasia-related changes and a refractory anemia with excess blasts in transformation PMID: 25404019
    28. A de novo CSF3R mutation was associated with the transformation of myeloproliferative neoplasm to atypical chronic myeloproliferative leukemia. PMID: 25865944
    29. mutation analysis of CSF3R, SETBP1 and CALR should be included in the diagnostic criteria for chronic neutrophilic leukemia PMID: 25316523
    30. The expression of G-CSFR before preoperative irradiation may predict the radiosensitivity of rectal cancer. PMID: 24574781
    31. this study describes a novel genetic Severe congenital neutropenia type in 2 unrelated families associated with recessively inherited loss-of-function mutations in CSF3R, encoding the granulocyte colony-stimulating factor (G-CSF) receptor. PMID: 24753537
    32. concurrent CSF3R and SETBP1 mutations are associated with Chronic neutrophilic leukemia. PMID: 24445868
    33. frequency of CSF3R mutations is highly prevalent among acute myeloid leukemia patients secondary to severe congenital neutropenia compared to de novo AML. PMID: 24746896
    34. The detection of both RUNX1 and CSF3R mutations could be used as a marker for identifying Congenital neutropenia patients with a high risk of progressing to leukemia or myelodysplastic syndromes. PMID: 24523240
    35. Thr-615 and Thr-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. PMID: 24403076
    36. Fbw7 together with GSK3beta negatively regulates G-CSFR expression and its downstream signaling. PMID: 23820376
    37. Mice transplanted with human CSF3R T618I-expressing hematopoietic cells developed a myeloproliferative disorder characterized by overproduction of granulocytes and granulocytic infiltration of the spleen and liver, which was uniformly fatal. PMID: 24081659
    38. The stimulating factor 3 receptor mutation (CSF3R-T595I) found in acute myeloid leukemia patients was found to have ligand independent activation properties. PMID: 23508011
    39. findings show CSF3R somatic mutations can be identified in 4 percent of the patients with chronic myelomonocytic leukemia (CMML); these mutations, which affect distinct residues in CSF3R are frequently associated with mutations in ASXL1 gene and have a poor prognostic impact on overall and AML-free survival PMID: 23774674
    40. In myelodysplastic syndromes, altered CD114 distribution was more informative than density changes. In CML, CD114 density was significantly decreased on early blasts and expression was essentially limited to late blasts. PMID: 23897249
    41. A subpopulation of GCSFR positive neuroblastoma cells exhibit enhanced tumorigenicity and a stem cell phenotype. PMID: 23687340
    42. Certain missense single nucleotide polymorphisms, especially which are placed in the conserved regions of G-CSFR may possess the capacity to influence the response to G-CSF treatment. PMID: 23159284
    43. Mutations in CSF3R are common in patients with CNL or atypical CML and represent a potentially useful criterion for diagnosing these neoplasms. PMID: 23656643
    44. CSF3R gene polymorphism plays a significant role in hematopoietic stem and progenitor cells for transplantation. PMID: 22796466
    45. An acquired CSF3R mutation in an adult chronic idiopathic neutropenia patient who developed acute myeloid leukaemia. PMID: 22146088
    46. Pretreatment of PMNs with IFN-gamma or G-CSF for a long-time (22 h)induced a significant lower fungal damage against biofilms compared with planktonic cells. PMID: 21641233
    47. Gemcitabine can enhance in vitro the expression rate of bone marrow G-CSFR in chronic myeloid leukemia patients at chronic or blastic phases. PMID: 21129254
    48. Two cases of X-linked neutropenia are reported that evolved to acute myeloid leukemia or myelodysplasia, with acquisition of G-CSF receptor mutations. PMID: 19794089
    49. There was no significant difference in expression rate of G-CSFR on CD34+ cells between aplastic anemia, myelodysplastic syndrome, and controls. PMID: 19099633
    50. CD123+CD34+CD38- cells exhibited lower expression of G-CSF receptors, which might partly explain why MDS clone responds worse to G-CSF in vitro and in vivo. PMID: 20819538

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  • 相關疾病:
    Hereditary neutrophilia (NEUTROPHILIA); Neutropenia, severe congenital 7, autosomal recessive (SCN7)
  • 亞細胞定位:
    [Isoform 2]: Secreted.; Cell membrane; Single-pass type I membrane protein.
  • 蛋白家族:
    Type I cytokine receptor family, Type 2 subfamily
  • 組織特異性:
    One or several isoforms have been found in myelogenous leukemia cell line KG-1, leukemia U-937 cell line, in bone marrow cells, placenta, and peripheral blood granulocytes. Isoform GCSFR-2 is found only in leukemia U-937 cells. Isoform GCSFR-3 is highly e
  • 數據庫鏈接:

    HGNC: 2439

    OMIM: 138971

    KEGG: hsa:1441

    STRING: 9606.ENSP00000362195

    UniGene: Hs.524517



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