Recombinant Mouse Fibroblast growth factor receptor 2 (Fgfr2), partial

Code CSB-YP008645MO1
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Source Yeast
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Code CSB-EP008645MO1
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Source E.coli
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Code CSB-EP008645MO1-B
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP008645MO1
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Source Baculovirus
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Code CSB-MP008645MO1
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Source Mammalian cell
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Product Details

>85% (SDS-PAGE)
Target Names
Uniprot No.
Alternative Names
Fgfr2; Bek; Ect1; Fibroblast growth factor receptor 2; FGFR-2; Keratinocyte growth factor receptor; KGFR; CD antigen CD332
Mus musculus (Mouse)
Protein Length
Tag Info
Tag type will be determined during the manufacturing process.
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer before Lyophilization
Tris/PBS-based buffer, 6% Trehalose, pH 8.0
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Please contact us to get it.

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Target Background

Tyrosine-protein kinase that acts as cell-surface receptor for fibroblast growth factors and plays an essential role in the regulation of cell proliferation, differentiation, migration and apoptosis, and in the regulation of embryonic development. Required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. Plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development. Promotes cell proliferation in keratinocytes and immature osteoblasts, but promotes apoptosis in differentiated osteoblasts. Phosphorylates PLCG1, FRS2 and PAK4. Ligand binding leads to the activation of several signaling cascades. Activation of PLCG1 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5-trisphosphate. Phosphorylation of FRS2 triggers recruitment of GRB2, GAB1, PIK3R1 and SOS1, and mediates activation of RAS, MAPK1/ERK2, MAPK3/ERK1 and the MAP kinase signaling pathway, as well as of the AKT1 signaling pathway. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation. Mutations that lead to constitutive kinase activation or impair normal FGFR2 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1.
Gene References into Functions
  1. During embryogenesis, SOX9-positive (+) cells inside hair follicles, which were previously known to give rise to hair follicle stem cells (HFSCs) and cells of the hair follicle lineage, can also give rise to Merkel Cells. Interestingly, while SOX9 is critical for HFSC specification, it is dispensable for Merkel cell formation. Conversely, FGFR2 is required for Merkel cell formation but is dispensable for HFSCs. PMID: 29899403
  2. Fgfr2 mediated FGF signaling in palate mesenchymal cells is functionally required for palate development at various stages including a possible role in shelf initiation out of the maxillary process on E11.5. PMID: 29526646
  3. gain-of-function mutation in FGFR2 exerts a Wnt/beta-catenin-dependent anabolic effect on trabecular bone by promoting bone formation. PMID: 28650109
  4. Testis determination involves FGFR2c-mediated repression of both the WNT4- and FOXL2-driven ovarian-determining pathways. PMID: 28938467
  5. The results of this study showed that GF22KO mice display longer duration of floating and decreased latency to float in the forced swim test, increased immobility in the tail suspension test, and decreased preference for sucrose in the sucrose preference test, which are all suggestive of a depressive-like phenotype. PMID: 27036645
  6. FGFR2 signalling correlates with maintenance of expression of a key transcription factor for basal cell self-renewal and differentiation: SOX2. PMID: 28348168
  7. Fgfr2 is seen within submucosal glandular epithelial cells. The medial nasal glands were missing in Fgfr2b mutants. PMID: 27590203
  8. Results show that Fgfr2 regulates both the formation and resolution of tetrads and rosettes in the mouse embryo, possibly in part by spatially restricting atypical protein kinase C, a negative regulator of non-muscle myosin IIB. PMID: 28538157
  9. Fgfr2 is critical for bladder mesenchyme patterning by virtue of its role in modulation of hedgehog signaling PMID: 28052872
  10. Ectopic expression of Fgfr2c was detected within the affected sutures of Bcl11b(-/-) mice. Ectopic expression of Fgfr2c in the sutural mesenchyme, without concomitant changes in the expression of FGF ligands, appears to induce the RUNX2-dependent osteogenic program and craniosynostosis in Bcl11b(-/-) mice. PMID: 26453795
  11. Calvarial osteoblasts from Fgfr2c gain-of-function mice had enhanced osteoblastic function and maturation with concomitant increase in ERK-MAPK activation. In vitro inhibition with U0126 mitigated ERK protein activation levels and reduced alkaline phosphatase activity. FGFR2c-mediated ERK-MAPK signaling is a key mediator of craniofacial growth and coronal suture development. PMID: 27034231
  12. these data suggest that tropism of influenza Virus to distal lung stem cell niches represents an important factor of pathogenicity and highlight impaired Fgfr2b signaling as underlying mechanism PMID: 27322618
  13. isolated deletion of Pten failed to stimulate ectopic fiber cell differentiation, and the combined deletion of Pten and Fgfr2 failed to restore differentiation-specific Aquaporin0 and DnaseIIbeta expression in the lens fiber cells PMID: 26764128
  14. work suggests that FGFR2IIIb and IIIc isoforms largely act redundantly to promote expansion of the adrenocortical primordium. PMID: 26141512
  15. Conditional knockout of Fgfr2 revealed stage- and tissue-specficic roles of FGF signaling in multiple processes of external genitalia development among the 3 tissue layers at each developmental stage. PMID: 25820239
  16. Study demonstrates that FGFR2 plays an essential role in controlling cell proliferation and differentiation, and maintaining Pax6 levels in corneal epithelium via ERK-independent pathways during embryonic development. PMID: 25615698
  17. Fgfr2 mutant, hobbyhorse, exhibits complete XY gonadal sex reversal. PMID: 24956260
  18. the gain-of-function mutation in FGFR2 resulted in histopathological abnormalities and development deformity of mandibular condyle cartilage in mice. PMID: 26351052
  19. The finding that ectodermal deletion of Fgfr2 results in the most severe hypospadias highlights a major role for Fgfr2 in the developing genital surface epithelium, where epithelial maturation is required for maintenance of a closed urethral tube. PMID: 26081573
  20. endogenous Fgfr2b ligands do not significantly protect against bleomycin injury, nor do they expedite the resolution of bleomycin-induced lung injury in mice. PMID: 25820524
  21. There are region-specific requirements for FGFR2 signaling in the developing caudal Wolffian duct epithelia. PMID: 25678108
  22. The study shows that PDGFRB and FGFR2 mediate endothelial cell differentiation capability of triple negative breast carcinoma. PMID: 24747080
  23. The S252W mutation in FGFR2 directly affects endochondral ossification, resulting in growth retardation of the long bone. PMID: 24489893
  24. sFGFR2IIIc(S252W) may partially prevent craniosynostosis in the Apert mouse model by affecting the CS and IFS in vivo. PMID: 24259495
  25. The influence of the FGFR2 P253R mutation on bone volume changes across the prenatal period and again after birth, while its influence on relative bone density is more stable. PMID: 24504751
  26. Loss of FGFR2 in the uterus after birth alters its development, resulting in luminal epithelial stratification and peri-implantation pregnancy loss. PMID: 24227756
  27. Data indicate that unique fibroblast growth factor receptor 2 (Fgfr2)-related cranial morphologies are exacerbated by late embryonic growth patterns. PMID: 24580805
  28. These findings show that FGFR2b-ligands signaling has critical stage-specific roles in maintaining the AER during limb development. PMID: 24167544
  29. FGFR2-associated craniosynostosis occurs in association with diminished cranial bone tissue PMID: 23358860
  30. Altogether, these results identify an intriguing ligand-dependent mechanism for the control of receptor fate and cellular outputs that may explain the pathogenic role of deregulated FGFR2b, thus offering therapeutic opportunities. PMID: 24011590
  31. Marrow stromal cells of Fgfr2(C342Y/+) mice have an autonomous defect in osteoblast differentiation and bone mineralization. PMID: 23762837
  32. Fgfr2(S252W/+) mutation may retard mandibular bone formation, decreased bone volume, and compromised skeletal architecture by regulating both osteoblastogenesis and osteoclastogenesis. PMID: 23495007
  33. Our approach thus led to the identification of new target genes directly or indirectly associated with FGFR2 which are contributing to the pathophysiology of AS. PMID: 23593218
  34. study demonstrate that Fgfr 2 isoforms IIIb and IIIc are expressed mainly in the adrenal subcapsule during embryogenesis and that deletion of the Fgfr2 IIIb isoform impairs adrenal development, causing reduced adrenal growth and impaired expression of SF1 and steroidogenic enzymes PMID: 23376610
  35. FGFR2 is essential in sustaining the breast tumor-initiating cell pool through promotion of self-renewal and maintenance of bipotent TICs PMID: 23300950
  36. Deletion of fibroblast growth factor receptor 2 from the peri-wolffian duct stroma leads to ureteric induction abnormalities and vesicoureteral reflux. PMID: 23409123
  37. Local differences in skull morphology and coronal suture patency found between Fgfr2c(C342Y/+) mice and unaffected littermates, as well as changes in brain shape but not brain size, and significant reductions in nasopharyngeal and eye volumes. PMID: 23172727
  38. The disrupted cerebellar size and laminar architecture resulting from loss of FGFR2 signaling impair motor learning and coordination in FGFR double knockout mice. PMID: 22578469
  39. Fgfr2 loss-of-function in the ectoderm caused derepression of Shh, revealing a role for FGF in Shh regulation in the hair follicle. PMID: 23123965
  40. Frs2alpha enhances fibroblast growth factor-mediated survival and differentiation in lens development. PMID: 23136392
  41. FGFR2 is not required cell-autonomously in motor neurons during the formation of initial motor projections towards limb and axial musculature PMID: 22815929
  42. The Fgfr2 W290R mouse model can be used as a model system to further investigate the cellular, molecular, and biochemical mechanisms of Crouzon syndrome. PMID: 22872266
  43. Mouse models of both of S252W and P253R these two causative mutations of Fgfr2 have been created and display many of the phenotypes typical of Apert syndrome. PMID: 22872267
  44. rendered Fgfr2IIIb(-/-) embryos haploinsufficient for the Raldh2 and examined these embryos for the incidence and severity of duodenal atresia PMID: 23021139
  45. FGFR2 induces rapid but reversible Nanog repression within ES cells. PMID: 22787153
  46. In the Fgfr2IIIb-/- genetic animal model neither disruptions in notochord development nor the presence of exogenous Shh protein are causative in intestinal atresia. PMID: 22572615
  47. Data show that fibroblast growth factor receptor 2 Fgfr2(S252W) mutation of the mesoderm alone is necessary and sufficient to cause craniosynostosis. PMID: 22664175
  48. The data revealed a regulatory paradigm for FGRF2 signaling and identified MT1-MMP as a critical negative modulator of ADAM9 activity to maintain FGFR2 signaling in calvarial osteogenesis. PMID: 22632802
  49. Fgfr2+/Y394C mice with a p38 kinase inhibitor attenuated skin abnormalities by reversing cell proliferation and differentiation to near normal levels. PMID: 22585574
  50. Our findings also suggest that altered FGFR2 signaling in osteoblasts is mostly responsible for the phenotypes seen in Apert syndrome, therefore these osteoblast cell lines are useful tools for investigating the pathogenesis of Apert syndrome PMID: 22105374

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Subcellular Location
Cell membrane; Single-pass type I membrane protein. Golgi apparatus. Cytoplasmic vesicle.
Protein Families
Protein kinase superfamily, Tyr protein kinase family, Fibroblast growth factor receptor subfamily
Database Links
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