Application Note
*Optimal dilutions/concentrations should be determined by the researcher.
Application |
Recommended Dilution |
1 - 2 μg/mL |
Assay dependent |
Not tested in other applications.
Calculated MW
Positive Control
A20 Cell Lysate(GTX27180)
Product Note
This antibody is predicted to not cross-react with the highly homologous Slc35D2.
Form
Liquid
Buffer
PBS
Preservative
0.02% Sodium azide
Storage
Store as concentrated solution. Centrifuge briefly prior to opening vial. For short-term storage (1-2 weeks), store at 4ºC. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles.
Concentration
1 mg/ml (Please refer to the vial label for the specific concentration.)
Antigen Species
Human
Immunogen
Slc35D1 antibody was raised against a 14 amino acid synthetic peptide near the amino terminus of the human Slc35D1.The immunogen is located within the first 50 amino acids of Slc35D1.
Purification
Purified by antigen-affinity chromatography
Conjugation
Unconjugated
Note
For laboratory research use only. Not for any clinical, therapeutic, or diagnostic use in humans or animals. Not for animal or human consumption.
Purchasers shall not, and agree not to enable third parties to, analyze, copy, reverse engineer or otherwise attempt to determine the structure or sequence of the product.
Synonyms
solute carrier family 35 member D1 , SHNKND , UGTREL7
Cellular Localization
Endoplasmic reticulum membrane
Background
The solute carrier family Slc35 consists of at least 17 proteins that act as nucleotide sugar transporters localized to the Golgi apparatus and endoplasmic reticulum. The role of the ER-resident Slc family member Slc35D1 is to transport both UDP-glucuronic acid and UDP-N-acetylgalactosamine. These molecules can serve as substrates for chondroitin sulfate biosynthesis and mice lacking the Slc35D1 gene developed a lethal form of skeletal dysplasia with severe shortening of limbs and facial structures. Examination of epiphyseal cartilage in these mice revealed a decreased proliferating zone with round chrondrocytes, scarce matrices, and reduced proteoglycan aggregates. Loss of function mutations in human Slc35D1 cause Schneckenbecken dysplasia, a severe skeletal dysplasia. This antibody is predicted to not cross-react with the highly homologous Slc35D2.
Database