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Bit1 Antibody (Center) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | Q9Y3E5 |
|---|---|
| Clone Names | 4031703 |
| Gene ID | 51651 |
|---|---|
| Other Names | Peptidyl-tRNA hydrolase 2, mitochondrial, PTH 2, Bcl-2 inhibitor of transcription 1, PTRH2, BIT1, PTH2 |
| Target/Specificity | The synthetic peptide sequence used to generate the antibody AP1323a was selected from the Center region of human Bit1. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay. |
| Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
| Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
| Name | PTRH2 |
|---|---|
| Synonyms | BIT1, PTH2 |
| Function | Peptidyl-tRNA hydrolase which releases tRNAs from the ribosome during protein synthesis (PubMed:14660562). Promotes caspase- independent apoptosis by regulating the function of two transcriptional regulators, AES and TLE1. |
| Cellular Location | Mitochondrion outer membrane; Single-pass membrane protein |
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Provided below are standard protocols that you may find useful for product applications.
Background
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.
References
Cell 116(5):751-762 (2004).Biochim Biophys Acta. 1692:145-57 (2004).Gene 2000; 249:1-16.
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