Cet anticorps anti-SLC16A2/MCT8 Polyclonal Lapin (ABIN7224388) détecte spécifiquement SLC16A2/MCT8 dans WB et ELISA.
L’anticorps est réactif avec des échantillons de Humain, Souris et Rat.
SLC16A2
Reactivité: Humain, Souris, Rat, Lapin
WB, IF
Hôte: Lapin
Polyclonal
unconjugated
Indications d'application
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-1:2000,ELISA 1:40000,Not yet tested in other applications.
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
Liquid in PBS containing 50 % glycerol, 0.5 % BSA and 0.02 % sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
-20 °C
Stockage commentaire
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Date de péremption
12 months
Antigène
SLC16A2/MCT8 (SLC16A2)
(Solute Carrier Family 16 Member 2 (SLC16A2))
Autre désignation
MCT8
Sujet
SLC16A2, MCT8, XPCT, Monocarboxylate transporter 8, MCT 8, Monocarboxylate transporter 7, MCT 7, Solute carrier family 16 member 2, X-linked PEST-containing transporterSLC16A2 (solute carrier family 16 member 2) 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). SLC16A2 is expressed in many tissues and likely plays an important role in the development of the central nervous system. Loss of function mutations in SLC16A2 are associated with psychomotor retardation in males while females exhibit no neurological defects and more moderate thyroid-deficient phenotypes. SLC16A2 is subject to X-chromosome inactivation. Mutations in SLC16A2 are the cause of Allan-Herndon-Dudley syndrome.