Recombinant Human Granulocyte Colony-Stimulating Factor Receptor (CSF3R) Protein (His)

Beta LifeScience SKU/CAT #: BLC-07544P
Greater than 85% as determined by SDS-PAGE.
Greater than 85% as determined by SDS-PAGE.

Recombinant Human Granulocyte Colony-Stimulating Factor Receptor (CSF3R) Protein (His)

Beta LifeScience SKU/CAT #: BLC-07544P
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Product Overview

Description Recombinant Human Granulocyte Colony-Stimulating Factor Receptor (CSF3R) Protein (His) is produced by our E.coli expression system. This is a protein fragment.
Purity Greater than 85% as determined by SDS-PAGE.
Uniprotkb Q99062
Target Symbol CSF3R
Synonyms (G-CSF receptor)(G-CSF-R)(CD antigen CD114)
Species Homo sapiens (Human)
Expression System E.coli
Tag N-6His
Target Protein Sequence LRAGYPPAIPHNLSCLMNLTTSSLICQWEPGPETHLPTSFTLKSFKSRGNCQTQGDSILDCVPKDGQSHCCIPRKHLLLYQNMGIWVQAENALGTSMSPQLCLDPMDVVKLEPPMLRTMDPSPEAAPPQAGCLQLCWEPWQPGLHINQKCELRHKPQRGEASWALVGPLPLEALQYELCGLLPATAYTLQIRCIRWPLPGHWSDWSPSLELRTTERAPTVR
Expression Range 117-337aa
Protein Length Partial
Mol. Weight 28.8 kDa
Research Area Cancer
Form Liquid or Lyophilized powder
Buffer Liquid form: default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol. Lyophilized powder form: the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution Briefly centrifuged the vial prior to opening to bring the contents to the bottom. Reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL. It is recommended to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. The default final concentration of glycerol is 50%.
Storage 1. Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. 2. Avoid repeated freeze-thaw cycles. 3. Store working aliquots at 4°C for up to one week. 4. In general, protein in liquid form is stable for up to 6 months at -20°C/-80°C. Protein in lyophilized powder form is stable for up to 12 months at -20°C/-80°C.
Notes Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.

Target Details

Target Function 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.
Subcellular Location [Isoform 2]: Secreted.; Cell membrane; Single-pass type I membrane protein.
Protein Families Type I cytokine receptor family, Type 2 subfamily
Database References
Associated Diseases Hereditary neutrophilia (NEUTROPHILIA); Neutropenia, severe congenital 7, autosomal recessive (SCN7)
Tissue Specificity 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

Gene Functions References

  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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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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