|Application ||WB, E|
|Other Accession||NP_055954, 14028875|
|Reactivity||Human, Mouse, Rat|
|Calculated MW||39240 Da|
|Application Notes||Slc35D1 antibody can be used for detection of Slc35D1 by Western blot at 1 - 2 µg/mL.|
|Target/Specificity||SLC35D1; This antibody is predicted to not cross-react with the highly homologous Slc35D2.|
|Reconstitution & Storage||Slc35D1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||Slc35D1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Transports both UDP-glucuronic acid (UDP-GlcA) and UDP- N-acetylgalactosamine (UDP-GalNAc) from the cytoplasm to into the endoplasmic reticulum lumen. May participate in glucuronidation and/or chondroitin sulfate biosynthesis.|
|Cellular Location||Endoplasmic reticulum membrane; Multi-pass membrane protein|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
firstname.lastname@example.org, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
Slc35D1 Antibody: 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.
Ishida N and Kawakita M. Molecular physiology and pathology of the nucleotide sugar transporter family (SLC35). Pflugers Arch.2004; 447:768-75.
Muraoka M, Kawakita M, and Ishita N. Molecular characterization of human UDP-glucuronic acid/UDP-N-acetylgalactosamine transporter, a novel nucleotide sugar transporter with dual substrate specificity. FEBS Lett.2001; 495:87-93.
Hiraoka S, Furuichi T, Nishimura G, et al. Nucleotide-sugar transporter Slc35D1 is critical to chondroitin sulfate synthesis in cartilage and skeletal development in mouse and human. Nat. Med.2007; 13:1363-7.
If you have used an Abgent product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at email@example.com.