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Bid Antibody (N-term S65) Blocking peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
| Primary Accession | P55957 |
|---|---|
| Clone Names | 4100456 |
| Gene ID | 637 |
|---|---|
| Other Names | BH3-interacting domain death agonist, p22 BID, BID, BH3-interacting domain death agonist p15, p15 BID, BH3-interacting domain death agonist p13, p13 BID, BH3-interacting domain death agonist p11, p11 BID, BID |
| 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 | BID |
|---|---|
| Function | Induces caspases and apoptosis (PubMed:14583606). Counters the protective effect of BCL2 (By similarity). |
| Cellular Location | Cytoplasm. Mitochondrion membrane. Mitochondrion outer membrane. Note=When uncleaved, it is predominantly cytoplasmic. [BH3-interacting domain death agonist p13]: Mitochondrion membrane {ECO:0000250|UniProtKB:P70444}. Note=Associated with the mitochondrial membrane. {ECO:0000250|UniProtKB:P70444} [Isoform 3]: Cytoplasm |
| Tissue Location | [Isoform 2]: Expressed in spleen, pancreas and placenta (at protein level). [Isoform 4]: Expressed in lung and pancreas (at protein level). |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
Bid, a BH3 domain containing proapoptotic Bcl2 family member, is localized in the cytosolic fraction of cells as an inactive precursor. Its active form is generated upon proteolytic cleavage by caspase 8 in the Fas signaling pathway. Cleaved Bid translocates to mitochondria and releases its potent proapoptotic activity, which in turn induces cytochrome c release and mitochondrial damage. The cytochrome c releasing activity of Bid was antagonized by Bcl2. Mutation in the SH3 domain can diminish the cytochrome c releasing activity. In animal model studies, Bid deficient mice are found resistant to the lethal effects of death factor signals relayed through Fas.
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