Recombinant Anti-DHCR7 Vesicular Antibody, EV Displayed (VS-0425-YC45)

CAT#: VS-0425-YC45

The Recombinant Anti-DHCR7 Vesicular Antibody, EV Displayed (VS-0425-YC45) 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 DHCR7-expressed cells or tissues. The DHCR7 is an enzyme involved in cholesterol synthesis, with mutations causing Smith-Lemli-Opitz syndrome characterized by various malformations.

Gene Expression
Figure 1 IF staining of human cell line CACO-2 Figure 2 Cerebral cortex Figure 3 Colon Figure 4 Pancreas Figure 5 Kidney Figure 6 Testis Figure 7 Lymph node Figure 8 RNA cell line category: Low cell line specificity

Recombinant Antibody

  • Application
  • ELISA, FC, Cell-uptake
  • Product Type
  • Ab-Fc-EVs
  • Antibody Quantification (Ab/EV)
  • ~100 Ab/EV
  • Target
  • DHCR7
  • Host Animal
  • Mouse
  • Antibody Isotype
  • IgG
  • Species Reactivity
  • Human
  • 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
  • 7-dehydrocholesterol reductase
  • Biological Process
  • Cholesterol biosynthesis, Cholesterol metabolism, Lipid biosynthesis, Lipid metabolism, Steroid biosynthesis, Steroid metabolism, Sterol biosynthesis, Sterol metabolism
  • Molecular Function
  • Oxidoreductase
  • Cellular Localization
  • Endoplasmic reticulum
  • Introduction
  • This gene encodes an enzyme that removes the C(7-8) double bond in the B ring of sterols and catalyzes the conversion of 7-dehydrocholesterol to cholesterol. This gene is ubiquitously expressed and its transmembrane protein localizes to the endoplasmic reticulum membrane and nuclear outer membrane. Mutations in this gene cause Smith-Lemli-Opitz syndrome (SLOS); a syndrome that is metabolically characterized by reduced serum cholesterol levels and elevated serum 7-dehydrocholesterol levels and phenotypically characterized by cognitive disability, facial dysmorphism, syndactyly of second and third toes, and holoprosencephaly in severe cases to minimal physical abnormalities and near-normal intelligence in mild cases. Alternative splicing results in multiple transcript variants that encode the same protein.[provided by RefSeq, Aug 2009]
  • Alternative Names
  • SLOS
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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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