Rabbit Anti-MOT8/FITC Conjugated antibody

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SLC16A2; AHDS; DXS 128; DXS 128E; DXS128; DXS128 E; DXS128E; MCT 7; MCT 8; MCT7; MCT8; Monocarboxylate transporter 7; Monocarboxylate transporter 8; MOT 8; MOT8_HUMAN; MRX 22; MRX22; SLC16 A2; SLC16A 2; SLC16A2; Solute carrier family 16 (monocarboxylic ac

Cat:

SL11434R-FITC

Species Reactivity：

Rat,(predicted: Human,Mouse,Rabbit,)

Immunogen：

KLH conjugated synthetic peptide derived from human MOT8/SLC16A2 (101-200aa)

Format：

Lyophilized or Liquid

Storage instructions：

Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of ant

Buffer：

0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.

Concentration：

1mg/ml

Clonality：

Polyclonal

Isotype：

IgG

Applications：

Flow-Cyt=1:50-200ICC=1:50-200IF=1:50-200not yet tested in other applications.optimal dilutions/concentrations should be determined by the end user.

Host：

Rabbit

Calculated MW：

59kDa

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Unit:

Price: $596.00

Product PDFs

Datasheet: Down Datasheet

Other Information
Citations
Protein Attributes
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background:
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.

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.

Subunit:
Homodimer.

Subcellular Location:
Cell membrane; Multi-pass membrane protein

Tissue Specificity:
Highly expressed in liver and heart.

DISEASE:
Defects in SLC16A2 are the cause of monocarboxylate transporter 8 deficiency (MCT8 deficiency) [MIM:300523]; also known as Allan-Herndon-Dudley syndrome (AHDS). 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.

Similarity:
Belongs to the major facilitator superfamily. Monocarboxylate porter (TC 2.A.1.13) family.

Database links:

Entrez Gene: 6567 Human

Omim: 300095 Human

SwissProt: P7221 Human

Unigene: 75317 Human

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

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