SLC26A2, Polyclonal Antibody

DTD; EDM4; DTDST; MST153; D5S1708; MSTP157

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit

The antibody detects endogenous level of total SLC26A2 antibody.

Antibodies were purified by affinity purification using immunogen.

Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

1.0 mg/ml (lot specific)

Store at -20 degree C

Small volumes of anti-SLC26A2 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

The diastrophic dysplasia sulfate transporter is a transmembrane glycoprotein implicated in the pathogenesis of several human chondrodysplasias. It apparently is critical in cartilage for sulfation of proteoglycans and matrix organization.

Total protein Ab

Western Blot (WB), Immunofluorescence (IF)

Western blotting: 1:500 - 1:2000
Immunofluorescence: 1:50 - 1:100

Immunofluorescence analysis of HeLa cell using SLC26A2 antibody. Blue: DAPI for nuclear staining.

81,662 Da

solute carrier family 26 (anion exchanger), member 2

sulfate transporter

Sulfate transporter

DTD; DTDST  [Similar Products]

S26A2_HUMAN

The diastrophic dysplasia sulfate transporter is a transmembrane glycoprotein implicated in the pathogenesis of several human chondrodysplasias. It apparently is critical in cartilage for sulfation of proteoglycans and matrix organization. [provided by RefSeq, Jul 2008]

SLC26A2: Sulfate transporter. May play a role in endochondral bone formation. Defects in SLC26A2 are the cause of diastrophic dysplasia (DTD). DTD is an autosomal recessive disease characterized by osteochondrodysplasia with clinical features including dwarfism, spinal deformation, and specific joint abnormalities. Defects in SLC26A2 are the cause of achondrogenesis type 1B (ACG1B). ACG1B is a recessively inherited chondrodysplasia characterized by extremely poor skeletal development and perinatal death. Defects in SLC26A2 are the cause of atelosteogenesis type 2 (AO2); also known as neonatal osseous dysplasia 1. AO2 is characterized by severely shortened limbs, small chest, scoliosis, club foot of the equinovarus type (talipes equinovarus), abducted thumbs and great toes, and cleft palate. Patients die of respiratory insufficiency shortly after birth because of the collapse of the airways and pulmonary hypoplasia due to the small rib cage. Defects in SLC26A2 are the cause of multiple epiphyseal dysplasia type 4 (EDM4). EDM is a generalized skeletal dysplasia associated with significant morbidity. Joint pain, joint deformity, waddling gait, and short stature are the main clinical signs and symptoms. EDM is broadly categorized into the more severe Fairbank and the milder Ribbing types. EDM4 is a recessively inherited form, characterized by early childhood-onset hip dysplasia and recurrent patella dislocation. Short stature in EDM4 patients is not frequent. Belongs to the SLC26A/SulP transporter (TC 2.A.53) family.

Protein type: Membrane protein, integral; Transporter; Transporter, SLC family; Membrane protein, multi-pass

Chromosomal Location of Human Ortholog: 5q31-q34

Cellular Component: membrane; integral to plasma membrane; plasma membrane

Molecular Function: sulfate transmembrane transporter activity; secondary active sulfate transmembrane transporter activity

Biological Process: ossification; glycosaminoglycan metabolic process; xenobiotic metabolic process; carbohydrate metabolic process; sulfate transport; ion transport; pathogenesis; transmembrane transport; 3'-phosphoadenosine 5'-phosphosulfate metabolic process; 3'-phosphoadenosine 5'-phosphosulfate biosynthetic process

Disease: Atelosteogenesis, Type Ii; Diastrophic Dysplasia; Achondrogenesis, Type Ib; Epiphyseal Dysplasia, Multiple, 4

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