Recombinant Anti-LDLR Vesicular Antibody, EV Displayed (VS-0425-YC636) (CAT#: VS-0425-YC636)

The Recombinant Anti-LDLR Vesicular Antibody, EV Displayed (VS-0425-YC636) is an antibody-displaying extracellular vesicle (Ab-EV). The product combines the benefits of both extracellular vesicle (EV) and antibody (Ab) which can guide the decorated EVs to LDLR-expressed cells or tissues. LDLR is a low-density lipoprotein receptor impacting cholesterol synthesis, with mutations causing familial hypercholesterolemia.

Specific Inquiry
  • Gene Expression
  • Datasheet
  • MSDS
  • COA
Normal Tissue
RNA Expression

Recombinant Antibody

  • Application
  • ELISA, FC, Cell-uptake
  • Product Type
  • Ab-Fc-EVs
  • Antibody Quantification (Ab/EV)
  • ~100 Ab/EV
  • Target
  • LDLR
  • Host Animal
  • Mouse
  • Antibody Isotype
  • IgG
  • Species Reactivity
  • Human, Mouse, Rat
  • Expression Cell
  • Mammalian cell

Engineered EVs

  • EV-sorting domain
  • CD63
  • Fc-binding domain
  • Protein A
  • EV Size
  • 30~150 nm
  • Producing Cell
  • HEK293F
  • Isolation Method
  • Gradient centrifugation
  • Purification
  • qEV size exclusion chromatography
  • Concentration
  • 1 x 10¹⁰
  • Size
  • 1 mL
  • Buffer
  • PBS
  • Storage
  • Store at -80°C for 12 months

Target

  • Full Name
  • Low density lipoprotein receptor
  • Biological Process
  • Cholesterol metabolism, Endocytosis, Host-virus interaction, Lipid metabolism, Lipid transport, Steroid metabolism, Sterol metabolism, Transport
  • Molecular Function
  • Host cell receptor for virus entry, Receptor
  • Cellular Localization
  • Vesicles
  • Introduction
  • 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.
  • Alternative Names
  • LDLCQ2

Related Resources

  • Related Diseases

Downloads

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For Research Use Only. Not For Clinical Use.

For research use only. Not intended for any clinical use. No products from Creative Biolabs may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative Biolabs.

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