SLC16A2 Antibody | 19-114

SLC16A2 Antibody | 19-114 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat

Homology: N/A

Immunogen: Recombinant fusion protein containing a sequence corresponding to amino acids 1-100 of human SLC16A2 (NP_006508.2) .

Research Area: Cell Cycle, Growth Factors, Neuroscience, Signal Transduction

Tested Application: WB

Application: WB: 1:500 - 1:2000

Specificiy: N/A

Positive Control 1: LO2

Positive Control 2: HT-29

Positive Control 3: 293T

Positive Control 4: Mouse heart

Positive Control 5: Mouse kidney

Positive Control 6: Mouse liver

Molecular Weight: Observed: 70kDa

Validation: N/A

Isoform: N/A

Purification: Affinity purification

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.

Concentration: N/A

Storage Condition: Store at -20˚C. Avoid freeze / thaw cycles.

Alternate Name: AHDS, DXS128, DXS128E, MCT 7, MCT 8, MCT7, MCT8, MRX22, XPCT, monocarboxylate transporter 8, X-linked PEST-containing transporter, monocarboxylate transporter 7, solute carrier family 16, member 2 (thyroid hormone transporter)

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: This gene encodes an integral membrane protein that functions as a transporter of thyroid hormone. The encoded protein facilitates the cellular importation of thyroxine (T4) , triiodothyronine (T3) , reverse triiodothyronine (rT3) and diidothyronine (T2) . This gene is expressed in many tissues and likely plays an important role in the development of the central nervous system. Loss of function mutations in this gene are associated with psychomotor retardation in males while females exhibit no neurological defects and more moderate thyroid-deficient phenotypes. This gene is subject to X-chromosome inactivation. Mutations in this gene are the cause of Allan-Herndon-Dudley syndrome.