This antibody is predicted to not cross-react with the highly homologous Slc35D2.
纯化方法
Slc35D1 Antibody is affinity chromatography purified via peptide column.
免疫原
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.
Slc35D1 antibody can be used for detection of Slc35D1 by Western blot at 1 - 2 μ,g/mL.
Antibody validated: Western Blot in mouse samples. All other applications and species not yet tested.
限制
仅限研究用
状态
Liquid
浓度
1 mg/mL
缓冲液
Slc35D1 Antibody is supplied in PBS containing 0.02 % sodium azide.
储存液
Sodium azide
注意事项
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
储存条件
-20 °C,4 °C
储存方法
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.
抗原
SLC35D1
(Solute Carrier Family 35 (UDP-Glucuronic Acid/UDP-N-Acetylgalactosamine Dual Transporter), Member D1 (SLC35D1))
UGTREL7 antibody, AI834976 antibody, C330011J09 antibody, mKIAA0260 antibody, UDP-glucuronic acid/UDP-N-acetylgalactosamine transporter antibody, solute carrier family 35 member D1 antibody, solute carrier family 35 (UDP-glucuronic acid/UDP-N-acetylgalactosamine dual transporter), member D1 antibody, Tc00.1047053510611.20 antibody, Tc00.1047053506793.40 antibody, SLC35D1 antibody, Slc35d1 antibody
背景
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.