Product Name: BAD Antibody
Species Reactivity: Human, Mouse, Rat
Tested Applications: ELISA, IF, IHC-P, WB
Applications: Bad antibody can be used for detection of Bad by Western blot at 0.5 to 2 μg/mL. Antibody can also be used for immunohistochemistry starting at 2 μg/mL. For immunofluorescence start at 10 μg/mL.
User Note: Optimal dilutions for each application to be determined by the researcher.
Predicted Molecular Weight:
Immunogen: Bad antibody was raised against a peptide corresponding to 15 amino acids near the C-terminus of human Bad.The immunogen is located within amino acids 90 – 140 of BAD.
Host Species: Rabbit
Purification: BAD Antibody is Ion exchange chromatography purified.
Physical State: Liquid
CAS NO.: 932986-18-0
Product: Azoramide
Buffer: BAD Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration: 1 mg/mL
Storage Conditions: BAD 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.
Clonality: Polyclonal
Conjugate: Unconjugated
Alternate Names: BAD Antibody: BBC2, BCL2L8, BBC6, Bcl2 antagonist of cell death, Bcl-2-binding component 6, BAD
Accession NO.: Q92934
Protein Ino: 17371773
Official Symbol: BAD
Geneid: 572
Background: BAD Antibody: Members in the Bcl-2 family are critical regulators of apoptosis by either inhibiting or promoting cell death. Bcl-2 homology 3 (BH3) domain containing pro-apoptotic proteins, such as Bax, Bid, and Bik, form a growing subclass of the Bcl-2 family. Another such protein is the Bcl-2-antagonist of cell death (Bad). Bad regulates apoptosis by forming heterodimers with anti-apoptotic proteins Bcl-2 and Bcl-xL, thereby preventing them from binding with Bax. Bad activity is regulated by its phosphorylation; it is inactivated by kinases such as Akt and MAP kinase and thus promotes cell survival, whereas JNK-induced phosphorylation promotes the apoptotic role of Bad.
PubMed ID:http://aac.asm.org/content/53/10/4069.abstract
