BD-PT2686

MCT8 Rabbit Polyclonal Antibody

SLC16A2; MCT8; XPCT; Monocarboxylate transporter 8; MCT 8; Monocarboxylate transporter 7; MCT 7; Solute carrier family 16 member 2; X-linked PEST-containing transporter

常规抗体

SLC16A2

Monocarboxylate transporter 8

WB

Human,Mouse,Rat

1 mg/ml

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% New type preservative N.

6567

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=6567

P36021

http://www.uniprot.org/uniprotkb/P36021/entry

20502

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=20502

O70324

http://www.uniprot.org/uniprot/O70324

259248

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=259248

Q8K1P8

http://www.uniprot.org/uniprot/Q8K1P8

The antiserum was produced against synthesized peptide derived from human SLC16A2. AA range:112-161

MCT8 Polyclonal Antibody detects endogenous levels of MCT8 protein.

WB 1:500 - 1:2000. ELISA: 1:40000. Not yet tested in other applications.

60kD

-20°C/1 year

Polyclonal, Rabbit,IgG

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. [provided by RefSeq, Mar 2012],

Highly expressed in liver and heart.

Cell membrane ; Multi-pass membrane protein .

disease:Defects in SLC16A2 are the cause of monocarboxylate transporter 8 deficiency (MCT8 deficiency) [MIM:300523]. MCT8 deficiency consists of a severe form of X-linked psychomotor retardation combined with abnormal thyroid hormone (TH) levels. Thyroid hormone deficiency can be caused by defects of hormone synthesis and action, but it has also been linked to a defect in cellular hormone transport. Affected patients are males with abnormal relative concentrations of three circulating iodothyronines, as well as severe neurological abnormalities, including global developmental delay, central hypotonia, spastic quadriplegia, dystonic movements, rotary nystagmus, and impaired gaze and hearing. Heterozygous females had a milder thyroid phenotype and no neurological defects.,function:Very active and specific thyroid hormone transporter. Stimulates cellular uptake of thyroxine (T4), triiodothyronine (T3), reverse triiodothyronine (rT3) and diidothyronine. Does not transport Leu, Phe, Trp or Tyr.,similarity:Belongs to the major facilitator superfamily. Monocarboxylate porter (TC 2.A.1.13) family.,tissue specificity:Highly expressed in liver and heart.,

现货

The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.