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GW20089F

Sigma-Aldrich

Anti-LDL antibody produced in chicken

affinity isolated antibody, buffered aqueous solution

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About This Item

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

chicken

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

human

manufacturer/tradename

Genway 15-288-20089F

technique(s)

indirect ELISA: suitable
western blot: suitable

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... APOB(338)

Immunogen

Human LDL native protein.

Application

Anti-LDL antibody produced in chicken is suitable for indirect ELISA and western blotting analysis at a dilution of 1:500, for tissue or cell staining at a dilution of 1:200.

Biochem/physiol Actions

The Low-Density Lipoprotein (LDL) Receptor is a mosaic protein encoded by the LDLR gene in humans and belongs to the Low density lipoprotein receptor gene family. It is located on chromosome number 19. LDL receptor is a mosaic protein constituiting of exons shared with different proteins. It is crucial for cholesterol homeostasis and deficiency in LDLR functions leads to hypercholesterolemia. LDLR is a type I transmembrane protein that needs O-glycosylation for stable expression at the cell surface. Mutation in this gene may cause familial hypercholesterolemia (FH), which is an autosomal dominant disease.

Physical form

Solution in phosphate buffered saline containing 0.02% sodium azide.

Disclaimer

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 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Núria Ros-Rocher et al.
Proceedings of the National Academy of Sciences of the United States of America, 120(18), e2216668120-e2216668120 (2023-04-24)
Regulated cellular aggregation is an essential process for development and healing in many animal tissues. In some animals and a few distantly related unicellular species, cellular aggregation is regulated by diffusible chemical cues. However, it is unclear whether regulated cellular
Manuela Sauter et al.
STAR protocols, 3(3), 101664-101664 (2022-09-14)
Different types of immune cells are involved in atherogenesis and may act atheroprotective or atheroprogressive. Here, we describe an in vitro approach to analyze CD11c+ cells and CD11c+-derived ApoE in atherosclerosis. The major steps include harvesting mouse bone marrow, plating
Isabel De Castro-Orós et al.
BMC medical genomics, 7, 17-17 (2014-04-09)
GWAS have consistently revealed that LDLR locus variability influences LDL-cholesterol in general population. Severe LDLR mutations are responsible for familial hypercholesterolemia (FH). However, most primary hypercholesterolemias are polygenic diseases. Although Cis-regulatory regions might be the cause of LDL-cholesterol variability; an
Nis Borbye Pedersen et al.
The Journal of biological chemistry, 289(25), 17312-17324 (2014-05-07)
The low density lipoprotein receptor (LDLR) is crucial for cholesterol homeostasis and deficiency in LDLR functions cause hypercholesterolemia. LDLR is a type I transmembrane protein that requires O-glycosylation for stable expression at the cell surface. It has previously been suggested
Paulo Caleb Junior Lima Santos et al.
Atherosclerosis, 233(1), 206-210 (2014-02-18)
Familial hypercholesterolemia (FH) is an autosomal dominant disease caused mainly by LDLR mutations. This study assessed the influence of the presence and type of LDLR mutation on lipid profile and the response to lipid-lowering therapy in Brazilian patients with heterozygous

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