LDLR Rabbit pAb
LDLR Rabbit pAb
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- 背景知识
Application
| WB |
|---|---|
| Primary Accession | P01130 |
| Reactivity | Human, Mouse |
| Predicted | Rat, Dog, Pig, Horse, Rabbit, Guinea Pig |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 95376 Da |
| Physical State | Liquid |
| Immunogen | KLH conjugated synthetic peptide derived from human LDL-R |
| Epitope Specificity | 781-860/860 |
| Isotype | IgG |
| Purity | affinity purified by Protein A |
| Buffer | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| SUBCELLULAR LOCATION | Cell membrane; Single-pass type I membrane protein. Endomembrane system; Single-pass type I membrane protein. Membrane, clathrin-coated pit; Single-pass type I membrane protein. Note=Found distributed from the plasma membrane to intracellular compartments. |
| SIMILARITY | Belongs to the LDLR family. Contains 3 EGF-like domains. Contains 7 LDL-receptor class A domains. Contains 6 LDL-receptor class B repeats. |
| SUBUNIT | Interacts with LDLRAP1. Interacts with SNX17. Interacts with HCV E1/E2 heterodimer. Interacts with HIV-1 Tat. |
| Post-translational modifications | N- and O-glycosylated. Ubiquitinated by MYLIP leading to degradation. |
| Important Note | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| Background Descriptions | The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. The encoded protein is normally bound at the cell membrane, where it binds low density lipoprotein/cholesterol and is taken into the cell. Lysosomes release the cholesterol, which is made available for repression of microsomal enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting step in cholesterol synthesis. At the same time, a reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in this gene cause the autosomal dominant disorder, familial hypercholesterolemia. Alternate splicing results in multiple transcript variants.[provided by RefSeq, May 2022] |
| Gene ID | 3949 |
|---|---|
| Other Names | Low-density lipoprotein receptor, LDL receptor, LDLR |
| Target/Specificity | Binds LDL, the major cholesterol-carrying lipoprotein of plasma, and transports it into cells by endocytosis. In order to be internalized, the receptor-ligand complexes must first cluster into clathrin-coated pits. In case of HIV-1 infection, functions as a receptor for extracellular Tat in neurons, mediating its internalization in uninfected cells. |
| Dilution | WB=1:500-2000,ICC/IF=1:100-500,Flow-Cyt=1 µg/Test |
| Storage | Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. |
| Name | LDLR |
|---|---|
| Function | Binds low density lipoprotein /LDL, the major cholesterol- carrying lipoprotein of plasma, and transports it into cells by endocytosis. In order to be internalized, the receptor-ligand complexes must first cluster into clathrin-coated pits. Forms a ternary complex with PGRMC1 and TMEM97 receptors which increases LDLR-mediated LDL internalization (PubMed:30443021). |
| Cellular Location | Cell membrane; Single-pass type I membrane protein {ECO:0000250|UniProtKB:P01131}. Membrane, clathrin-coated pit. Golgi apparatus. Early endosome. Late endosome. Lysosome Note=Rapidly endocytosed upon ligand binding. Localized at cell membrane, probably in lipid rafts, in serum-starved conditions (PubMed:30443021). |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
The low density lipoprotein receptor (LDLR) gene family consists of cell surface proteins involved in receptor-mediated endocytosis of specific ligands. The encoded protein is normally bound at the cell membrane, where it binds low density lipoprotein/cholesterol and is taken into the cell. Lysosomes release the cholesterol, which is made available for repression of microsomal enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, the rate-limiting step in cholesterol synthesis. At the same time, a reciprocal stimulation of cholesterol ester synthesis takes place. Mutations in this gene cause the autosomal dominant disorder, familial hypercholesterolemia. Alternate splicing results in multiple transcript variants.[provided by RefSeq, May 2022]
REFERENCES
Yamamoto T.,et al.Cell 39:27-38(1984).
Suedhof T.C.,et al.Science 228:815-822(1985).
Jia S.,et al.Submitted (MAY-2002) to the EMBL/GenBank/DDBJ databases.
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Kalnine N.,et al.Submitted (OCT-2004) to the EMBL/GenBank/DDBJ databases.
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