Very low density lipoprotein receptor; VLDL R; VLDLR; VLDL-R; VLDLRCH.
研究领域
肿瘤 心血管 免疫学 神经生物学 信号转导
抗体来源
Rabbit
克隆类型
Polyclonal
交叉反应
Human, (predicted: Mouse, Rat, Dog, Pig, Horse, Rabbit, )
产品应用
WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 ICC=1:100-500 IF=1:100-500 (石蜡切片需做抗原修复) not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user.
分 子 量
93kDa
细胞定位
细胞膜
性 状
Liquid
浓 度
1mg/ml
免 疫 原
KLH conjugated synthetic peptide derived from human VLDL Receptor :501-600/873 <Extracellular>
亚 型
IgG
纯化方法
affinity purified by Protein A
储 存 液
0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件
Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
VLDL (very low density lipoprotein) cholesterol is one of the three major types of cholesterol found in blood. VLDL receptor plays an essential role in triglyceride metabolism. It binds VLDL and transports it into cells by endocytosis. In order to be internalized, the receptor-ligand complexes must first cluster into clathrin coated pits. Binding to Reelin induces tyrosine phosphorylation of Dab1 and modulation of Tau phosphorylation.
Function: Binds VLDL and transports it into cells by endocytosis. In order to be internalized, the receptor-ligand complexes must first cluster into clathrin-coated pits. Binding to Reelin induces tyrosine phosphorylation of Dab1 and modulation of Tau phosphorylation (By similarity).
Subunit: Binds to the extracellular matrix protein Reelin. Interacts with VLDLR. Interacts with SNX17. Interacts with DAB1. Receptor for the minor-group human rhinoviruses (HRVs); binds protein VP1 through the second and third LDL-receptor class A domains.
Subcellular Location: Membrane; Single-pass type I membrane protein. Membrane, clathrin-coated pit; Single-pass type I membrane protein.
Tissue Specificity: Abundant in heart and skeletal muscle; also ovary and kidney; not in liver.
Post-translational modifications: Ubiquitinated at Lys-839 by MYLIP leading to degradation.
DISEASE: Defects in VLDLR are the cause of cerebellar ataxia mental retardation and dysequilibrium syndrome type 1 (CMARQ1) [MIM:224050]; also known as dysequilibrium syndrome (DES) or non-progressive cerebellar disorder with mental retardation. CMARQ1 is a congenital, non-progressive cerebellar ataxia associated with disturbed equilibrium, delayed ambulation, mental retardation and cerebellar hypoplasia. Additional features include short stature, strabismus, pes planus and, rarely, seizures.
Similarity: Contains 3 EGF-like domains. Contains 8 LDL-receptor class A domains. Contains 6 LDL-receptor class B repeats.