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 >  Protein>LDL R >LDR-H5224

Human LDL R Protein, His Tag (MALS verified)

分子别名(Synonym)

LDLR,FH,FHC,LDLCQ2

表达区间及表达系统(Source)

Human LDL R, His Tag (LDR-H5224) is expressed from human 293 cells (HEK293). It contains AA Ala 22 - Arg 788 (Accession # NP_000518.1).

Predicted N-terminus: Ala 22

Request for sequence

蛋白结构(Molecular Characterization)

LDL R Structure

This protein carries a polyhistidine tag at the C-terminus.

The protein has a calculated MW of 85.9 kDa. The protein migrates as 120-140 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>90% as determined by SDS-PAGE.

>90% as determined by SEC-MALS.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

LDL R SDS-PAGE

Human LDL R, His Tag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 90% (With Star Ribbon Pre-stained Protein Marker).

SEC-MALS

LDL R SEC-MALS

The purity of Human LDL R, His Tag (Cat. No. LDR-H5224) is more than 90% and the molecular weight of this protein is around 100-140 kDa verified by SEC-MALS.

Report

 

活性(Bioactivity)-ELISA

LDL R ELISA

Immobilized Human LDL R, His Tag (Cat. No. LDR-H5224) at 2 μg/mL (100 μL/well) can bind Biotinylated Human PCSK9 (D374Y), Avitag,His Tag (Cat. No. PCY-H82E7) with a linear range of 4-63 ng/mL (QC tested).

Protocol

 

活性(Bioactivity)-BLI

LDL R BLI

Loaded Human PCSK9, Fc Tag (Cat. No. PC9-H5256) on Protein A Biosensor, can bind Human LDL R, His Tag (Cat. No. LDR-H5224) with an affinity constant of 12.7 nM as determined in BLI assay (ForteBio Octet Red96e) (Routinely tested).

Protocol

 
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背景(Background)

Low-Density Lipoprotein (LDL) Receptor is also known as LDLR, FH, FHC, LDLCQ2, and is a mosaic protein of ~840 amino acids (after removal of signal peptide) that mediates the endocytosis of cholesterol-rich LDL. It is a cell-surface receptor that recognizes the apoprotein B100 which is embedded in the phospholipid outer layer of LDL particles. The receptor also recognizes the apoE protein found in chylomicron remnants and VLDL remnants (IDL). It belongs to the Low density lipoprotein receptor gene family. LDL receptor complexes are present in clathrin-coated pits (or buds) on the cell surface, which when bound to LDL-cholesterol via adaptin, are pinched off to form clathrin-coated vesicles inside the cell. This allows LDL-cholesterol to be bound and internalized in a process known as endocytosis and prevents the LDL just diffusing around the membrane surface. This occurs in all nucleated cells (not erythrocytes), but mainly in the liver which removes ~70% of LDL from the circulation. Synthesis of receptors in the cell is regulated by the level of free intracellular cholesterol; if it is in excess for the needs of the cell then the transcription of the receptor gene will be inhibited. LDL receptors are translated by ribosomes on the endoplasmic reticulum and are modified by the Golgi apparatus before travelling in vesicles to the cell surface. LDL is directly involved in the development of atherosclerosis, due to accumulation of LDL-cholesterol in the blood. Atherosclerosis is the process responsible for the majority of cardiovascular diseases.

文献引用(Citations)

 

前沿进展

Cinnamaldehyde attenuates diabetic cardiomyopathy by ameliorating energy metabolism disturbance and activating autophagy
Hu, Wei, Wu et al
J Cardiovasc Pharmacol (2025)
Abstract: Diabetic Cardiomyopathy (DCM) is a diabetes mellitus-induced pathophysiological condition that can lead to heart failure. Cinnamaldehyde (CA), a bioactive phytochemical derived from the bark of Cinnamon, exhibits cardioprotective properties against heart injury in metabolic syndrome. This study aims to explore the role of CA on DCM and its cardioprotective mechanisms. Diabetic rats were established by injection of streptozotocin (STZ, 60∼85 mg/kg). Subsequently, CA (50 mg/kg) was administered via gavage daily for 28-day duration. Following this treatment, abnormalities levels of fasting blood glucose (FBG), triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and LDL-C to HDL-C ratio were ameliorated. Additionally, CA inhibited cardiac histopathological alterations and hypertrophy, reduced brain natriuretic peptide (BNP) level, shortened S-T and P-R intervals on electrocardiogram, decreased tissue malondialdehyde content, and enhanced myocardial energy metabolism, including Creatine (Cr), adenosine triphosphate (ATP), adenosine monophosphate (AMP) and total adenine nucleotides (TAN). Furthermore, CA improved oxidative stress, improved myocardial Ca2+-Mg2+-ATPase activity and downregulated the mRNA expression of AMP protein activation kinase α2 (AMPK-α2), receptor γ coactivator-1 alpha (PGC-1α) and peroxisome proliferator-activated receptor α (PPARα), while also ameliorating protein expressions, including ratio of phosphorylated mammalian target of rapamycin to mechanistic target of rapamycin (p-mTOR/mTOR), level of SQSTM1/p62, and ratio of microtubule-associated protein 1 light chain 3 beta to microtubule-associated protein 1 light chain 3 alpha (LC3Ⅱ/ LC3Ⅰ). In conclusion, these findings indicate that CA can alleviate DCM by modulating AMPK-α2/PPAR-α/PGC-1α signaling pathway to restore energy metabolism and activating autophagy through mTOR signaling pathway.Copyright © 2025 Wolters Kluwer Health, Inc. All rights reserved.
Changes in glucose-related parameters according to LDL-cholesterol concentration ranges in non-diabetic patients
Kron, Verner, Smetana et al
J Appl Biomed (2025) 23 (1), 26-35
Abstract: The study focused on the changes in C-peptide, glycemia, insulin concentration, and insulin resistance according to LDL-cholesterol concentration ranges. The metabolic profile of individuals in the Czech Republic (n = 1840) was classified by quartiles of LDL-cholesterol into four groups with the following ranges: 0.46-2.45 (n = 445), 2.46-3.00 (n = 474), 3.01-3.59 (n = 459), and 3.60-7.18 mmol/l (n = 462). The level of glucose, C-peptide, insulin, and area of parameters during OGTT and HOMA IR were compared with a relevant LDL-cholesterol range. The evaluation involved correlations between LDL-cholesterol and the above parameters, F-test and t-test. Generally, mean values of glucose homeostasis-related parameters were higher with increasing LDL-cholesterol levels, except for mean HOMA IR values which rapidly increased (2.7-3.4) between LDL-cholesterol ranges of 3.00-3.59 and 3.60-7.18 mmol/l. Glucose, C-peptide, insulin concentrations, and the area of parameters reached greater changes especially after glucose load during OGTT (p ≤ 0.001). Considerable changes were already observed for the above parameters between groups with LDL-cholesterol ranges of 2.46-3.00 and 3.01-3.59 mmol/l. HOMA IR increased with higher LDL-cholesterol concentrations, but the differences in mean values were not statistically significant. Most important differences appeared in glucose metabolism at LDL-cholesterol concentrations of 3.60-7.18 mmol/l in comparison to LDL-cholesterol lower ranges. In particular, the areas of C-peptide, glucose, and insulin ranges showed statistically significant differences between all groups with growing LDL-cholesterol ranges. The variances of HOMA IR statistically differed between groups created according to LDL-cholesterol concentrations ranges.
Familial hypercholesterolemia in patients with hypertension: the China H-type Hypertension Registry Study
Shen, Luo, Jiang et al
Lipids Health Dis (2025) 24 (1), 116
Abstract: Familial hypercholesterolemia (FH) significantly amplifies the risk of developing atherosclerotic cardiovascular disease (ASCVD). This study investigated the prevalence and clinical characteristics of FH in a hypertensive rural population.In the China H-type Hypertension Registry Study, a prospective observational cohort study with a 4-year follow-up, 14,234 hypertensive participants from rural areas were enrolled in 2018, with onsite exams conducted in 2022. FH was identified using the Chinese-modified Dutch Lipid Clinic Network criteria.Among the 10,900 patients with hypertension, 5,675 (52.1%) were women, the median age was 65 years, the median blood pressure was 146/89 mmHg, 629 (5.8%) had previous coronary heart disease (CHD), and 4,726 (43.4%) were smokers. Among the cohort, 78 (0.72%) met the C-DLCN criteria for probable or definite FH. The rate of lipid-lowering therapy (LLT) usage in patients with FH reached 35.9%. After a median follow-up period of 1,477 days, a total of 658 deaths, 535 strokes, and 309 cardiovascular disease (CVD) events were observed. At baseline and subsequent follow-up, all patients with FH were at high or ultra/very high risk for ASCVD. During follow-up, a greater decrease in LDL-C was shown in patients with FH (FH: - 31%, 95% CI - 44.6% to -14.6%; P < 0.001) than patients without FH (2%, 95% CI: - 12.1% to 17.4%); however, only 3.6% of them achieved the recommended LDL-C targets based on ASCVD risk assessment. The risks of stroke and CVD were not significantly different between patients with and without FH after 4 years of follow-up.This study highlights a marked gap between the high prevalence and low treatment rates of FH in rural populations with hypertension. These findings suggest the need to improve knowledge regarding FH and the need to treat this condition, especially when associated risk factors are present.© 2025. The Author(s).
Changes in polyunsaturated fatty acids are linked to metabolic syndrome in children with steroid-sensitive nephrotic syndrome-a clinical observation
Li, Fu, Liu et al
Lipids Health Dis (2025) 24 (1), 115
Abstract: Alterations in lipid metabolic pathways constitute a pivotal characteristic of Steroid-Sensitive Nephrotic Syndrome (SSNS). Despite the significance, there has been scant exploration into the influence of polyunsaturated fatty acids (PUFAs) on metabolic syndrome (MetS) in children with SSNS. This study endeavors to elucidate the association between PUFAs and MetS in this specific pediatric population.This study enrolled a total of 185 children aged 0-7 years with SSNS between May 2023 and May 2024. Based on international guidelines for MetS, patients were classified into a MetS group (n = 73) and a non-MetS group (n = 112). A healthy control group (n = 82) was also established. Surveys, anthropometric measurements, and blood samples were used to assess lipid profiles, glucose, insulin, and Hemoglobin A1C (HbA1C). The concentrations of serum PUFAs were quantitatively analyzed utilizing gas chromatography-mass spectrometry (GC-MS) techniques.The MetS group exhibited significantly elevated levels of fasting blood glucose, triglyceride (TG), low-density lipoprotein (LDL) cholesterol, HbA1C, insulin, the ratio of TG to high-density lipoprotein (HDL) cholesterol, and the ratio of total cholesterol to HDL cholesterol compared to the non-MetS group. Significant differences were observed among healthy controls, MetS group, and non-MetS group in terms of ω-3 alpha-linolenic acid (ALA), ω-3 docosahexaenoic acid (DHA), ω-6 arachidonic acid, and ω-6 to ω-3 ratio.High ω-6 arachidonic acid, ω-6/ω-3 ratio and low ω-3 ALA and ω-3 DHA were associated with elevated TG levels. An elevation in TG concentrations among pediatric patients with SSNS may have been implicated to MetS.© 2025. The Author(s).
Showing 1-4 of 10875 papers.
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LDL R靶点信息
英文全称:LDL receptor
中文全称:低密度脂蛋白受体
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:5详情
最高研发阶段:临床二期
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