LDL Receptor Antibody [G7A23] | Primary Antibodies

Application: Reactivity: Mouse, Human

Usage Information

Dilution
WB1:500 - 1:1000 IHC1:500

Application
WB, IHC

Reactivity
Mouse, Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
95 kDa 100,130,160,27,48 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Positive Control	Human liver tissue; Human hepatocellular carcinoma tissue; Human plasma total protein tissue; Mouse liver tissue; Mouse lung tissue; Raw264.7 cells (GW3965, 5uM, 8 h); PC-3 cells; Huh7 cells; HepG2 cells; HEK-293 cells
Negative Control	Mouse colon tissue; LNCaP cells

Datasheet & SDS

Biological Description

Specificity
LDL Receptor Antibody [G7A23] detects endogenous levels of total LDL Receptor protein.

Clone
G7A23

Synonym(s)
Low-density lipoprotein receptor; LDL receptor; LDLR

Background
The LDL Receptor (LDLR) is a member of the low-density lipoprotein receptor family, mediating the endocytic uptake of cholesterol-rich lipoproteins via clathrin-coated pits. LDLR consists of 860 amino acids, with an extracellular domain containing seven ligand-binding repeats (LA1–7; residues 27–292) rich in cysteine and acidic residues that coordinate calcium ions, six EGF-like domains (EGF-A–F; residues 293–692) including a β-propeller YWTD module (residues 475–599), a single transmembrane helix (residues 788–810), and a cytoplasmic tail (NPVY motif; residues 811–860) that binds adaptor proteins. Ligands such as LDL (via apoB-100) and β-VLDL (via apoE) bind to the LA4–5 repeats at neutral pH through electrostatic interactions. The receptor-ligand complexes cluster in coated pits through NPVY-mediated interactions with ARH/Disabled-2 and clathrin/AP-2, initiating endocytosis. Delivery to early endosomes exposes the complex to acidic pH, which protonates histidines in the EGF domains, causing the β-propeller to unfold and the LDLR to release its ligand, then fold into a closed conformation for recycling. LDLR rapidly recycles back to the plasma membrane (within 10 minutes), allowing 50–100 cycles per receptor daily in hepatocytes. Lysosomal degradation of endocytosed LDL releases free cholesterol, which suppresses SREBP-2, downregulates HMG-CoA reductase, activates ACAT for cholesterol esterification, and increases PCSK9 expression. The liver’s LDLR clears 60–70% of plasma LDL, keeping cholesterol levels below 100 mg/dL; statins upregulate LDLR by inhibiting cholesterol synthesis. Familial hypercholesterolemia results from over 300 LDLR mutations affecting synthesis, transport, binding, internalization, or recycling, leading to high LDL and atherosclerosis.

Background

The LDL Receptor (LDLR) is a member of the low-density lipoprotein receptor family, mediating the endocytic uptake of cholesterol-rich lipoproteins via clathrin-coated pits. LDLR consists of 860 amino acids, with an extracellular domain containing seven ligand-binding repeats (LA1–7; residues 27–292) rich in cysteine and acidic residues that coordinate calcium ions, six EGF-like domains (EGF-A–F; residues 293–692) including a β-propeller YWTD module (residues 475–599), a single transmembrane helix (residues 788–810), and a cytoplasmic tail (NPVY motif; residues 811–860) that binds adaptor proteins. Ligands such as LDL (via apoB-100) and β-VLDL (via apoE) bind to the LA4–5 repeats at neutral pH through electrostatic interactions. The receptor-ligand complexes cluster in coated pits through NPVY-mediated interactions with ARH/Disabled-2 and clathrin/AP-2, initiating endocytosis. Delivery to early endosomes exposes the complex to acidic pH, which protonates histidines in the EGF domains, causing the β-propeller to unfold and the LDLR to release its ligand, then fold into a closed conformation for recycling. LDLR rapidly recycles back to the plasma membrane (within 10 minutes), allowing 50–100 cycles per receptor daily in hepatocytes. Lysosomal degradation of endocytosed LDL releases free cholesterol, which suppresses SREBP-2, downregulates HMG-CoA reductase, activates ACAT for cholesterol esterification, and increases PCSK9 expression. The liver’s LDLR clears 60–70% of plasma LDL, keeping cholesterol levels below 100 mg/dL; statins upregulate LDLR by inhibiting cholesterol synthesis. Familial hypercholesterolemia results from over 300 LDLR mutations affecting synthesis, transport, binding, internalization, or recycling, leading to high LDL and atherosclerosis.

References
https://pubmed.ncbi.nlm.nih.gov/12493900/ https://pubmed.ncbi.nlm.nih.gov/23881912/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%