|Application ||WB, IHC-P, E|
|Calculated MW||19194 Da|
|Antigen Region||80-110 aa|
|Other Names||Peptidyl-tRNA hydrolase 2, mitochondrial, PTH 2, Bcl-2 inhibitor of transcription 1, PTRH2, BIT1, PTH2|
|Target/Specificity||This Bit1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 80-110 amino acids from the Central region of human Bit1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Bit1 Antibody (Center) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||The natural substrate for this enzyme may be peptidyl- tRNAs which drop off the ribosome during protein synthesis.|
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Provided below are standard protocols that you may find useful for product applications.
Adhesion to extracellular matrix regulates cell survival via integrin engagement and cell spreading. Anoikis is the molecular mechanism of apop-tosis induced by integrin detachment. A role for Bit1 (Bcl-2 inhibitor of transcription 1) has been identified in this process. Bit1 is a mitochondrial protein released into the cytoplasm upon onset of apoptosis where it forms a complex with AES, a small Groucho/transducin-like enhancer of split (TLE) protein and induces caspase-independent apoptosis. AES and TLE proteins are transcriptional co-repressors that play important roles in neurogenesis, segmentation, and sex determination. Bit1-AES complexes may switch off a survival-promoting gene transcription program controlled by TLE. Apoptosis of Bit1/AES transfected cells is inhibited when cells are permitted to attach to fibronectin through the alpha-beta integrin, suggesting that the contribution of the Bit1-AES pathway to anoikis is regulated by integrins.
Cell 116(5):751-762 (2004).
Biochim Biophys Acta. 1692:145-57 (2004).
Gene 2000; 249:1-16.
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