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Bcl-2 Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P |
|---|---|
| Primary Accession | P10415 |
| Reactivity | Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 26266 Da |
| Gene ID | 596 |
|---|---|
| Other Names | B-cell CLL/lymphoma 2 |
| Dilution | WB~~WB 1:500-2000, ELISA 1:10000-20000 IHC 1:50-300 IHC-P~~N/A |
| Format | Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.09% (W/V) sodium azide. |
| Storage Conditions | -20℃ |
| Name | BCL2 |
|---|---|
| Function | Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells (PubMed:1508712, PubMed:8183370). Regulates cell death by controlling the mitochondrial membrane permeability (PubMed:11368354). Appears to function in a feedback loop system with caspases (PubMed:11368354). Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1) (PubMed:11368354). Also acts as an inhibitor of autophagy: interacts with BECN1 and AMBRA1 during non-starvation conditions and inhibits their autophagy function (PubMed:18570871, PubMed:20889974, PubMed:21358617). May attenuate inflammation by impairing NLRP1- inflammasome activation, hence CASP1 activation and IL1B release (PubMed:17418785). |
| Cellular Location | Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein. Cytoplasm {ECO:0000250|UniProtKB:P10417} |
| Tissue Location | Expressed in a variety of tissues. |
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
Suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. Regulates cell death by controlling the mitochondrial membrane permeability. Appears to function in a feedback loop system with caspases. Inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF-1). May attenuate inflammation by impairing NLRP1-inflammasome activation, hence CASP1 activation and IL1B release (PubMed:17418785).
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