Recombinant Mouse Fibroblast growth factor receptor 2 (Fgfr2)

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

Show More

Hide All

UNIGENE: Mm.16340

KEGG: mmu:14183

STRING: 10090.ENSMUSP00000112430