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Validated All-in-One™ qPCR Primer for CSF1R(NM_005211.3) Search again
Product ID:
HQP003158
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BANDDOS, C-FMS, CD115, CSF-1R, CSFR, FIM2, FMS, GPSC, HDLS, HDLS1, M-CSF-R
Gene Description:
colony stimulating factor 1 receptor
Target Gene Accession:
NM_005211.3(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.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene is the receptor for colony stimulating factor 1, a cytokine which controls the production, differentiation, and function of macrophages. This receptor mediates most if not all of the biological effects of this cytokine. Ligand binding activates the receptor kinase through a process of oligomerization and transphosphorylation. The encoded protein is a tyrosine kinase transmembrane receptor and member of the CSF1/PDGF receptor family of tyrosine-protein kinases.
Gene References into function
- AP-1 proteins, GR and associated co-factors regulate transcription from the c-fms first promoter in breast carcinoma cells.
- upregulated significantly in acute myeloid leukemia patients with a white blood cell count higher than 30 x 10(9)/L cells
- DNA binding to and transactivation of the M-CSF receptor promoter were deficient in acute myeloid leukemia PU.1 mutants that affected the DNA-binding domain, contibuting to the block in differentiation in AML.
- CSF-1 and its receptor are regulated by 1,25(OH)(2)D(3) and its analogue tacalcitol in human monocytes which parallels the inhibition of differentiation into dendritic cells without altering survival
- These observations correlate CSF-1R expression with changes in the growth and development of the normal and neoplastic prostate
- C-fms expression correlates with monocytic differentiation in PML-RAR alpha+ acute promyelocytic leukemias
- In t(8;21) leukaemic cells expressing the aberrant fusion protein AML1-ETO, we demonstrate that this protein is part of a transcription factor complex binding to extended sequences of the c-FMS intronic regulatory region rather than the promoter.
- findings of co-expression of KIT and/or FMS with their respective ligands implies these receptors might contribute to leukemogenesis in some patients with AML through autocrine, paracrine, or intracrine interactive stimulation.
- Lower expression of CSF1R is associated with acute myeloid leukemia-M2 and higher expression of CSF1R is associated with acute myeloid leukemia-M5
- data suggest that colony-stimulating factor receptor-1R (CSF-1R) disrupts cell adhesion by uncoupling adherens junction complexes from the cytoskeleton and promoting cadherin internalization through a Src-dependent mechanism
- CSF-1-mediated wild-type (WT)-CSF-1R phosphorylation was not markedly affected by Src-family kinases (SFK) inhibition, indicating that lack of SFK binding is not responsible for diminished Y559F phosphorylation.
- HIV-1 Nef interferes with M-CSF receptor signaling through Hck activation and thereby inhibits M-CSF functions in monocytes/macrophages.
- In c-fms transgenic mice it is determined that although the c-fms promoter is inactive in dendritic cell (DC) precursors, it is up-regulated in all DC subsets during differentiation
- the CSF1R mutation of Asp-802 to Val confers resistance to kinase inhibitor imatinib
- Inhibitory activity of lead compounds and drug candidates, such as ABT-869, against the CSF-1R protein in situ.
- No evidence that CSF1R 2033T variant was a major risk factor for Crohn's disease in New Zealand.
- Creation of a conditional allele of the Csf1r by placing LoxP sites around Exon 5 of the Csf1r gene in mice.
- 2.7 A resolution crystal structure of the cytosolic domain of c-Fms that comprises the kinase domain and the juxtamembrane domain
- method revealed the presence of an activated colony-stimulating factor 1 receptor (CSF1R) kinase in the acute megakaryoblastic leukemia (AMKL) cell line MKPL-1, essential for the growth and survival of MKPL-1 cells.
- tyrosine 559 is the major mediator of receptor activation and cell death, intracellular signaling, and cell proliferation and that the tyrosine residues at positions 697 and 807 play lesser roles in these events
- We thus conclude that Ox-LDL induces monocyte differentiation to macrophages in vivo and this phenomenon involves activation of the M-CSF-receptor.
- The results suggest that the growth factor M-CSF might have an important role in ovarian function.
- Nef perturbs the intracellular maturation and the trafficking of nascent Fms, through a unique mechanism that required both the activation of Hck and the aberrant spatial regulation of the active Hck
- c-KIT but not CSF1R mutations play a role in the leukemogenesis of childhood CBF-AML.
- analysis of the transcriptional regulation of the Colony-Stimulating Factor 1 Receptor (csf1r) gene during hematopoiesis [review]
- CSF-1 receptor RIPping can be activated by various intracellular signal transduction pathways and that RIPping is likely to play an important role during macrophage activation.
- Expression of M-CSF, CSF-1R and CD3 is a significant prognostic factor in primary prostatic cancers by predicting the development of metastases.
- VEGF expression was statistically correlated to c-fms and COX-2 expression in high-grade CIN.
- c-Fms signals are blocked by imatinib mesylate inhibition of osteoclasts, which suppresses bone metastases of breast cancer
- mutant CSF1R was constitutively phosphorylated, but rapidly dephosphorylated on exposure to imatinib, in cell line derived from a patient with an atypical myeloproliferative neoplasms, as being responsive to imatinib.
- CSF1R may be a critical factor facilitating hTERT immortalization of epithelial cells.
- Calorimetric data indicate that M-CSF cannot dimerize FMS without receptor-receptor interactions mediated by FMS domains D4 and D5