Product Name: Bcl-G Antibody
Species Reactivity: Human, Mouse, Rat
Tested Applications: ELISA, IF, IHC-P, WB
Applications: Bcl-G antibody can be used for detection of Bcl-G by Western blot at 2.5 to 5 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: Bcl-G antibody was raised against a peptide corresponding to 15 amino acids near the N-terminus of human Bcl-G.The immunogen is located within the first 50 amino acids of Bcl-G.
Host Species: Rabbit
Purification: Bcl-G Antibody is Ion exchange chromatography purified.
Physical State: Liquid
CAS NO.: 464-49-3
Product: (+)-Camphor
Buffer: Bcl-G Antibody is supplied in PBS containing 0.02% sodium azide.
Concentration: 1 mg/mL
Storage Conditions: Bcl-G 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: Bcl-G Antibody: BCLG, BCLG, Apoptosis facilitator Bcl-2-like protein 14, Apoptosis regulator Bcl-G, Bcl2-L-14
Accession NO.: NM_030766
Protein Ino: 13540528
Official Symbol: BCL2L14
Geneid: 79370
Background: Bcl-G 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 is a potent death domain. BH3 domain containing pro-apoptotic proteins, including Bad, Bax, Bid, Bik, and Hrk, form a growing subclass of the Bcl-2 family. A novel BH3 domain containing protein was recently identified and designated Bcl-G. The mRNA of Bcl-G encodes 2 isoforms, Bcl-GL, which is widely expressed in multiple tissues, and Bcl-GS, which is only found in testis. The Bcl-GS protein is predominantly localized to cytoplasmic organelles whereas Bcl-GL was distributed throughout the cytosol. Overexpression of either protein induced apoptosis, although Bcl-GS was far more potent than Bcl-GS. Apoptosis induction was dependent on the BH3 domain and could be suppressed by co-expression with the anti-apoptotic Bcl-XL protein.
PubMed ID:http://aac.asm.org/content/53/11/4809.abstract
