Product Description
Slc35D1 Antibody | 4649 | ProSci
Host: Rabbit
Reactivity: Human, Mouse, Rat
Homology: Predicted species reactivity based on immunogen sequence: Bovine: (88%) , Pig: (81%)
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.
Research Area: Homeostasis
Tested Application: E, WB
Application: Slc35D1 antibody can be used for detection of Slc35D1 by Western blot at 1 - 2 μg/mL.
Antibody validated: Western Blot in mouse samples. All other applications and species not yet tested.
Specificiy: This antibody is predicted to not cross-react with the highly homologous Slc35D2.
Positive Control 1: Cat. No. 1288 - A20 Cell Lysate
Positive Control 2: N/A
Positive Control 3: N/A
Positive Control 4: N/A
Positive Control 5: N/A
Positive Control 6: N/A
Molecular Weight: N/A
Validation: N/A
Isoform: N/A
Purification: Slc35D1 Antibody is affinity chromatography purified via peptide column.
Clonality: Polyclonal
Clone: N/A
Isotype: IgG
Conjugate: Unconjugated
Physical State: Liquid
Buffer: Slc35D1 Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration: 1 mg/mL
Storage Condition: Slc35D1 antibody can be stored at 4˚C for three months and -20˚C, 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.
Alternate Name: Slc35D1 Antibody: UGTREL7, KIAA0260, UGTREL7, Solute carrier family 35 member D1, UGTrel7
User Note: Optimal dilutions for each application to be determined by the researcher.
BACKGROUND: 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.