TAB2 antibody is human specific. TAB2 antibody is predicted not to cross-react with other TAB proteins.
Aufreinigung
TAB2 Antibody is affinity chromatography purified via peptide column.
Immunogen
TAB2 antibody was raised against a 14 amino acid synthetic peptide near the carboxy terminus of human TAB2. The immunogen is located within the last 50 amino acids of TAB2.
TAB2 antibody can be used for detection of TAB2 by immunohistochemistry at 5 μ,g/mL.
Antibody validated: Immunohistochemistry in human samples. All other applications and species not yet tested.
Beschränkungen
Nur für Forschungszwecke einsetzbar
Format
Liquid
Konzentration
1 mg/mL
Buffer
TAB2 Antibody is supplied in PBS containing 0.02 % sodium azide.
Konservierungsmittel
Sodium azide
Vorsichtsmaßnahmen
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Lagerung
-20 °C,4 °C
Informationen zur Lagerung
TAB2 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.
Target
TAB2
(TGF-beta Activated Kinase 1/MAP3K7 Binding Protein 2 (TAB2))
TAB2 Antibody: TAB2 is an activator of MAP3K7/TAK1, which is required for for the IL-1 induced activation NF-kappaB and MAPK8/JNK. This protein forms a kinase complex with TRAF6, MAP3K7 and TAB1, thus serves as an adaptor linking MAP3K7 and TRAF6. This protein, TAB1, and MAP3K7 also participate in the signal transduction induced by TNFSF11/RANKL through the activation of the receptor activator of NF-kappaB (TNFRSF11A/RANK), which may regulate the development and function of osteoclasts. Recent experiments have shown that TAB2 and the related protein TAB3 constitutitvely interact with the autophagy mediator Beclin-1, upon induction of autophagy, these proteins dissociate from Beclin-1 and bind TAK1. Overexpression of TAB2 and TAB3 inhibit autophagy, while their depletion triggers it, suggesting that TAB2 and TAB3 act as a control point for autophagy.