TMEM38B Antibody is affinity chromatography purified via peptide column.
Immunogène
TMEM38B antibody was raised against a 17 amino acid synthetic peptide from near the carboxy terminus of human TMEM38B. The immunogen is located within the last 50 amino acids of TMEM38B.
TMEM38B antibody can be used for detection of TMEM38B by Western blot at 1 - 2 μ,g/mL. Antibody can also be used for immunohistochemistry starting at 5 μ,g/mL. For immunofluorescence start at 20 μ,g/mL.
Antibody validated: Western Blot in rat samples, Immunohistochemistry in mouse samples and Immunofluorescence in mouse samples. All other applications and species not yet tested.
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
TMEM38B Antibody is supplied in PBS containing 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,4 °C
Stockage commentaire
TMEM38B antibody can be stored at 4°C for three months and -20°C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
TMEM38B Antibody: TMEM38A and TMEM38B are two recently identified trimeric intracellular cation (TRIC) channel subtypes. TMEM38B is expressed in most mammalian tissues, while TMEM38A is preferentially expressed in excitable tissues such as striated muscle and brain. Mice deficient in both TMEM38A and TMEM38B suffer embryonic cardiac failure, the cardiac myocytes display severe dysfunction in SR Ca2+ handling, weakened Ca2+ release, and reduced K+ permeability indicating that the TRIC cation channels are likely to act as counter-ion channels that function in synchronization with Ca2+ release from intracellular stores. Mice that were lacking only TMEM38B however, die shortly after birth due to respiratory failure and have lungs exhibiting severe histological defect and ultrastructural abnormalities in their alveolar type II epithelial cells, indicating that TMEM38B are essential for perinatal lung maturation. Other experiments have shown that TMEM38A and TMEM38B can act with junctophilin proteins to support efficient ryanodine receptor-mediated Ca2+ release in muscle cells.