추천 제품
생물학적 소스
mouse
결합
unconjugated
항체 형태
ascites fluid
항체 생산 유형
primary antibodies
클론
FLT-11, monoclonal
분자량
antigen 160-200 kDa
포함
15 mM sodium azide
종 반응성
human
기술
immunocytochemistry: suitable
immunohistochemistry (frozen sections): suitable
immunoprecipitation (IP): suitable
indirect ELISA: suitable
western blot: 1:500 using VEGF Receptor-1 (Flt-1)/Fc Chimera human recombinant
동형
IgG1
UniProt 수납 번호
배송 상태
dry ice
저장 온도
−20°C
타겟 번역 후 변형
unmodified
유전자 정보
human ... FLT1(2321)
일반 설명
Vascular Endothelial Growth Factor Receptor-2 (VEGF R2) is a 160-200kD protein that belongs to protein kinase superfamily and is expressed mainly on the surface of various endothelial cells. It plays a pivotal role in the regulation of angiogenesis, cell migration, cell survival and cancer cell invasion. ASV derived from VEGF receptor type 1 serve as a potential therapeutics for rheumatoid arthritis. Monoclonal Anti-Vascular Endothelial Growth Factor Receptor-1antibody can be used in western blotting (diluted 1:500) using VEGF Receptor-1 (Flt-1)/Fc Chimera human recombinant. It can also be used in indirect ELISA. Mouse anti-Vascular Endothelial Growth Factor Receptor-1antibody reacts specifically with an epitope within amino acids 1-251 of the extracellular domain of human VEGF Receptor-1 but not with VEGF Receptor-2 (KDR). The product has shown cross reactivity with the mouse Flt1 receptor.
Vascular endothelial growth factor (VEGF) is also called vasculotropin (VAS) and vascular permeability factor (VPF). It is a homodimeric heparin-binding glycoprotein.
특이성
Mouse monoclonal clone FLT-11 anti-VEGF R-1 antibody reacts specifically with the extracellular domain of human VEGF Receptor-1. The epitope recognized by the antibody resides within amino acid residues 1-251 of the VEGF Receptor-1 molecule. The product does not recognize VEGF Receptor-2 (KDR).
면역원
recombinant human VEGF-1 receptor.
애플리케이션
Monoclonal Anti-Vascular Endothelial Growth Factor Receptor-1 antibody can be used in several immunochemical assays like immunohistochemistry, immunocytochemistry and immunoprecipitation for the localization of VEGF-R1.
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 3
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
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.
Hypertension (Dallas, Tex. : 1979), 59(2), 256-264 (2012-01-05)
The cardinal manifestations of the pregnancy-specific disorder preeclampsia, new-onset hypertension, and proteinuria that resolve with placental delivery have been linked to an extracellular protein made by the placenta, soluble fms-like tyrosine kinase 1 (sFlt1), that injures the maternal vasculature. However
Circulation research, 97(12), 1253-1261 (2005-11-05)
Neutrophil activation and increased migration is associated with preeclampsia and is resolved after delivery. Preeclampsia is an inflammatory disorder where altered levels of vascular endothelial growth factor (VEGF) and the circulating soluble fms-like tyrosine kinase 1 (sFlt-1) have a pathogenic
Anti-VEGF therapy in ophthalmology: a qualitative analysis of transformative drug development
Drug Discovery Today, 21(6), 1019-1026 (2016)
The Journal of biological chemistry, 280(11), 9904-9912 (2005-01-08)
We previously reported that vascular endothelial growth factor (VEGF)-A(165) inflammatory effect is mediated by acute platelet-activating factor synthesis from endothelial cells upon the activation of VEGF receptor-2 (VEGFR-2) and its coreceptor, neuropilin-1 (NRP-1). In addition, VEGF-A(165) promotes the release of
The Journal of clinical endocrinology and metabolism, 99(3), 978-987 (2014-01-16)
Research examining the source of excess soluble fms-like tyrosine kinase 1 (sFLT1) in preeclampsia has focused on the placenta. The potential contribution of the releasable store of sFLT1 in the systemic vasculature is unknown. We asked whether the nonplacental releasable
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