추천 제품
생물학적 소스
rabbit
결합
unconjugated
항체 형태
affinity isolated antibody
항체 생산 유형
primary antibodies
클론
polyclonal
형태
buffered aqueous solution
분자량
antigen 110-120 kDa (doublet)
종 반응성
human
기술
immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:250 using Trypsin-digested, human and animal tissue sections
western blot: 1:1,000 using whole cell extract of transfected 293T cells expressing recombinant human FGFR-3
UniProt 수납 번호
배송 상태
dry ice
저장 온도
−20°C
타겟 번역 후 변형
unmodified
유전자 정보
human ... FGFR3(2261)
일반 설명
Fibroblast Growth Factor Receptor-3 (FGFR 3) is a protein that belongs to Tyr protein kinase family and is expressed in various fetal and adult human and animal tissues. It plays a vital role in inducing apoptosis in chondrogenic ATDC5 cells. It also facilitates cell proliferation and differentiation.
특이성
The antibody reacts specifically with FGFR-3 in lysates of transfected cells. No reaction with FGFR-1 and FGFR-2 is detected.
면역원
synthetic peptide corresponding to amino acids 792-806 of the cytoplasmic region of human FGFR-3 with N-terminal added lysine.
애플리케이션
Anti-Fibroblast Growth Factor Receptor-3, cytoplasmic antibody can be used in immunohistochemistry (diluted 1:250) using Trypsin-digested, human and animal tissue sections for identification of FGFR-3. It can also be used in immunoprecipitation.
Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Immunohistochemistry (1 paper)
Western Blotting (1 paper)
Immunohistochemistry (1 paper)
Western Blotting (1 paper)
생화학적/생리학적 작용
Fibroblast Growth Factor Receptor-3 (FGFR-3) plays a vital role in inducing apoptosis in chondrogenic ATDC5 cells. It also facilitates cell proliferation and differentiation. Mutations in the FGFR-3 gene leads to Wolf-Hirshhorn syndrome (growth failure, mental retardation, cardiac and bone malformations) and achondroplasia.
물리적 형태
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% bovine serum albumin and 15 mM sodium azide.
면책조항
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 2
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
개인 보호 장비
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
시험 성적서(COA)
제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.
Multiple congenital malformations of Wolf-Hirschhorn syndrome are recapitulated in Fgfrl1 null mice
Catela C, et al.
Disease models & mechanisms, 2(5-6), 283-294 (2009)
Wolfgang Jäger et al.
Oncotarget, 6(25), 21522-21532 (2015-06-05)
Optimal animal models of muscle invasive bladder cancer (MIBC) are necessary to overcome the current lack of novel targeted therapies for this malignancy. Here we report on the establishment and characterization of patient-derived primary xenografts (PDX). Patient tumors were grafted
Davide Komla-Ebri et al.
The Journal of clinical investigation, 126(5), 1871-1884 (2016-04-12)
Achondroplasia (ACH) is the most frequent form of dwarfism and is caused by gain-of-function mutations in the fibroblast growth factor receptor 3-encoding (FGFR3-encoding) gene. Although potential therapeutic strategies for ACH, which aim to reduce excessive FGFR3 activation, have emerged over
Yongjun Yin et al.
Disease models & mechanisms, 9(5), 563-571 (2016-04-09)
Activating mutations in fibroblast growth factor receptor 3 (FGFR3) have been identified in multiple types of human cancer and in congenital birth defects. In human lung cancer, fibroblast growth factor 9 (FGF9), a high-affinity ligand for FGFR3, is overexpressed in
Daisuke Harada et al.
Bone, 41(2), 273-281 (2007-06-15)
The most frequent type of rhizomelic dwarfism, achondroplasia (ACH), is caused by mutations in the fibroblast growth factor receptor 3 (FGFR3) gene. Mutations in FGFR3 result in skeletal dysplasias of variable severity, including mild phenotypic effects in hypochondroplasia (HCH), severe
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