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Bcl-2 Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF |
|---|---|
| Primary Accession | P10415 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Calculated MW | 26266 Da |
| Gene ID | 596 |
|---|---|
| Other Names | BCL2; Apoptosis regulator Bcl-2 |
| Dilution | WB~~Western Blot: 1/500 - 1/2000. Immunohistochemistry: 1/100 - 1/300. Immunofluorescence: 1/200 - 1/1000. ELISA: 1/10000. Not yet tested in other applications. |
| 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. |
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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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