Human FGFR2 / CD332 Protein (His Tag)

BBDS,BEK,BFR-1,CD332,CEK3,CFD1,ECT1,JWS,K-SAM,KGFR,TK14,TK25

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Catalog Number	P10824-H08H
Organism Species	Human
Host	Human Cells
Synonyms	BBDS,BEK,BFR-1,CD332,CEK3,CFD1,ECT1,JWS,K-SAM,KGFR,TK14,TK25
Molecular Weight	The recombinant human FGFR2 consists of 367 amino acids after removal of the signal peptide and has a calculated molecular mass of 41 kDa. In SDS-PAGE under reducing conditions, the apparent molecular mass of rhFGFR2 is approximately 65-75 kDa due to glycosylation.
predicted N	Arg 22
SDS-PAGE
Purity	> 97 % as determined by SDS-PAGE
Protein Construction	A DNA sequence encoding the human FGFR2 (NP_000132.3) extracellular domain (Met 1-Glu 377) was expressed, fused with a polyhistidine tag at the C-terminus.
Bio-activity	Measured by its ability to inhibit FGF acidic dependent proliferation of Balb/c3T3 mouse embryonic fibroblasts. The ED₅₀ for this effect is typically 200-400 ng/mL .
Research Area	Signaling \|Signal Transduction \|Protein Kinase \|Receptor Tyrosine Kinase (RTK)
Formulation	Lyophilized from sterile PBS, pH 7.4 1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
Background	FGFR2, also known as CD332, belongs to the fibroblast growth factor receptor subfamily where amino acid sequence is highly conserved between members and throughout evolution. FGFR2 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. It is required for normal embryonic patterning, trophoblast function, limb bud development, lung morphogenesis, osteogenesis and skin development. FGFR2 plays an essential role in the regulation of osteoblast differentiation, proliferation and apoptosis, and is required for normal skeleton development. It also promotes cell proliferation in keratinocytes and imature osteoblasts, but promotes apoptosis in differentiated osteoblasts. FGFR2 signaling is down-regulated by ubiquitination, internalization and degradation. Mutations that lead to constitutive kinase activation or impair normal CD332 maturation, internalization and degradation lead to aberrant signaling. Over-expressed FGFR2 promotes activation of STAT1. Defects in CD3322 are the cause of Crouzon syndrome, Jackson-Weiss syndrome, Apert syndrome, Pfeiffer syndrome, Beare-Stevenson cutis gyrata syndrome, familial scaphocephaly syndrome, lacrimo-auriculo-dento-digital syndrome and Antley-Bixler syndrome without genital anomalies or disordered steroidogenesis.
Reference	Marie PJ, et al. (2003) Regulation of human cranial osteoblast phenotype by FGF-2, FGFR-2 and BMP-2 signaling. Histol. 17(3):877-85. Park WJ, et al. (1996) Novel FGFR2 mutations in Crouzon and Jackson-Weiss syndromes show allelic heterogeneity and phenotypic variability. Hum Mol Genet. 4(7):1229-33. Orr-Urtreger A, et al. (1993) Developmental localization of the splicing alternatives of fibroblast growth factor receptor-2 (FGFR2). Dev Biol. 158(2):475-86.