Solute Carrier Family 26, Member 4 (SLC26A4) (C-Term)
Clone
polyclonal
Host Species
Rabbit
Reactive Species
human
Isotype
n/a
Format
serum
Size
100 μL
Concentration
n/a
Applications
Immunohistochemistry (IHC),Western Blotting (WB)
Reviews / Ratings
If you have used this antibody, please help fellow researchers by submitting reviews to pAbmAbs and antYbuddY.
Description
Function: Sodium-independent transporter of chloride and iodide. Defects in SLC26A4 are a cause of Pendred syndrome (PDS). PDS is an autosomal recessive disorder characterized by congenital sensorineural hearing loss combined with thyroid goiter. The disorder may account for up to 10% of the cases of hereditary deafness. The deafness is most often associated with a Mondini cochlear defect. Defects in SLC26A4 are the cause of deafness autosomal recessive type 4 (DFNB4), also known as vestibular aqueduct syndrome (EVA). DFNB4 is a form of sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. DFNB4 is associated with an enlarged vestibular aqueduct.Tissue specificity: High expression in adult thyroid, lower expression in adult and fetal kidney and fetal brain. Not expressed in other tissues.Subcellular location: Membrane, Multi-pass membrane protein Also known as: Sodium-independent chloride/iodide transporter, Solute carrier family 26 member 4, SLC26A4, PDS.
Immunogen
A synthetic peptide from c-terminal region of human Pendrin (SLC26A4) conjugated to an immunogenic carrier protein was used as the antigen.