Low Density Lipoprotein From Human Plasma, Acetylated, Alexa Fluor™ 488 Conjugate (Alexa Fluor™ 488 AcLDL)
Low Density Lipoprotein From Human Plasma, Acetylated, Alexa Fluor™ 488 Conjugate (Alexa Fluor™ 488 AcLDL)
Invitrogen™

Low Density Lipoprotein From Human Plasma, Acetylated, Alexa Fluor™ 488 Conjugate (Alexa Fluor™ 488 AcLDL)

Human low-density lipoprotein (LDL) is large protein complex (∼500,000 Da) that binds to a specific receptor on the surface ofRead more
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Catalog NumberQuantity
L23380200 μL
Catalog number L23380
Price (CNY)
9,665.00
Each
Add to cart
Quantity:
200 μL
Price (CNY)
9,665.00
Each
Add to cart
Human low-density lipoprotein (LDL) is large protein complex (∼500,000 Da) that binds to a specific receptor on the surface of vertebrate cells and delivers cholesterol via receptor-mediated endocytosis—our labeled LDL complexes are useful tools for studying this phenomenon. These experiments are typically performed by adding fluorescently labeled LDL to cultured cells and analyzing them by microscopy or flow cytometry. Alternatively the fluorescently labeled LDL can be injected into test animals, and the distribution of the label can be analyzed after the specified time period. We offer an unlabeled LDL and two classes of labeled LDLs: those containing an unmodified apoprotein (used to study normal cholesterol delivery and internalization) and those with an acetylated (Ac) apoprotein (used to study cell types that express receptors specific for this acetylated version (i.e., endothelial and microglial cells)).

LDL Specifications:

Label (Ex/Em): Alexa Fluor™ 488 (495/519)
Acetylated: Yes
Amount: 200 μL (1.0 mg/mL)

Fresh LDL Produced Continually
We prepare our LDL and AcLDL products from fresh human plasma approximately every two months. The nonacetylated LDL products are shipped within two weeks of their preparation. All acetylated LDL products are available on a continuous basis.

Nonacetylated vs. Acetylated LDL
LDL containing an unmodified apoprotein is used to study normal cholesterol delivery and internalization. If the lysine residues of LDL’s apoprotein have been acetylated, the LDL complex no longer binds to the LDL receptor, but rather is taken up by endothelial and microglial cells that possess “scavenger” receptors specific for that modified form.

Key Applications for Labeled LDL
Some of the many applications for labeled LDL complexes include:
• Counting cell-surface LDL receptors, and analyzing their motion and clustering following internalization
• Quantitating LDL receptor activity in fibroblasts (replacing the radiolabeled LDL assay)
• Investigating LDL expression and identifying LDL receptor deficiencies in various cell lines

For Research Use Only. Not intended for any animal or human therapeutic or diagnostic use.
For Research Use Only. Not for use in diagnostic procedures.
Specifications
Concentration1 mg⁄ml
Detection MethodFluorescence
Dye TypeAlexa Fluor Dyes
FormLiquid
Quantity200 μL
Shipping ConditionWet Ice
Product LineAlexa Fluor
Product TypeSupplement
Unit SizeEach
Contents & Storage
Store in refrigerator (2–8°C) and protect from light.

Frequently asked questions (FAQs)

If the Low Density Lipoprotein (LDL) from Human Plasma was accidentally frozen, can I still use it?

We recommend storing Low Density Lipoprotein (LDL) from Human Plasma at 2-8 degrees C. We do not recommend using frozen product.

Find additional tips, troubleshooting help, and resources within our Cell Analysis Support Center.

Can I use Low Density Lipoprotein (LDL) from Human Plasma on other species?

We have not tested this.

Find additional tips, troubleshooting help, and resources within our Cell Analysis Support Center.

Citations & References (19)

Citations & References
Abstract
Somatic cell plasticity and Niemann-Pick type C2 protein: fibroblast activation.
Authors:Csepeggi C, Jiang M, Kojima F, Crofford LJ, Frolov A,
Journal:J Biol Chem
PubMed ID:21084287
A growing body of evidence points toward activated fibroblasts, also known as myofibroblasts, as one of the leading mediators in several major human pathologies including proliferative fibrotic disorders, invasive tumor growth, rheumatoid arthritis, and atherosclerosis. Niemann-Pick Type C2 (NPC2) protein has been recently identified as a product of the second ... More
Silence of TRIB3 suppresses atherosclerosis and stabilizes plaques in diabetic ApoE-/-/LDL receptor-/- mice.
Authors:Wang ZH, Shang YY, Zhang S, Zhong M, Wang XP, Deng JT, Pan J, Zhang Y, Zhang W,
Journal:Diabetes
PubMed ID:22275087
'Insulin resistance triggers the developments of diabetes mellitus and atherosclerosis. Tribbles homolog 3 (TRIB3) is involved in insulin resistance. We aimed to investigate whether TRIB3 is implicated in diabetic atherosclerosis. Sixty 3-week-old apolipoprotein E (ApoE-/-)/LDR receptor (LDLR-/-) mice were randomly divided into chow and diabetes groups. Diabetes was induced by ... More
Deficient p27 phosphorylation at serine 10 increases macrophage foam cell formation and aggravates atherosclerosis through a proliferation-independent mechanism.
Authors:Fuster JJ, González-Navarro H, Vinué A, Molina-Sànchez P, Andrés-Manzano MJ, Nakayama KI, Nakayama K, Díez-Juan A, Bernad A, Rodríguez C, Martínez-González J, Andrés V,
Journal:Arterioscler Thromb Vasc Biol
PubMed ID:21885849
Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide ... More
cGMP increases antioxidant function and attenuates oxidant cell death in mouse lung microvascular endothelial cells by a protein kinase G-dependent mechanism.
Authors:Stephens RS, Rentsendorj O, Servinsky LE, Moldobaeva A, Damico R, Pearse DB,
Journal:Am J Physiol Lung Cell Mol Physiol
PubMed ID:20453163
Increasing evidence suggests that endothelial cytotoxicity from reactive oxygen species (ROS) contributes to the pathogenesis of acute lung injury. Treatments designed to increase intracellular cGMP attenuate ROS-mediated apoptosis and necrosis in several cell types, but the mechanisms are not understood, and the effect of cGMP on pulmonary endothelial cell death ... More
ILK mediates LPS-induced vascular adhesion receptor expression and subsequent leucocyte trans-endothelial migration.
Authors:Hortelano S, López-Fontal R, Través PG, Villa N, Grashoff C, Boscá L, Luque A,
Journal:Cardiovasc Res
PubMed ID:20164118
The inflammatory response to injurious agents is tightly regulated to avoid adverse consequences of inappropriate leucocyte accumulation or failed resolution. Lipopolysaccharide (LPS)-activated endothelium recruits leucocytes to the inflamed tissue through controlled expression of membrane-associated adhesion molecules. LPS responses in macrophages are known to be regulated by integrin-linked kinase (ILK); in ... More