BCL2 antibody - N-terminal region
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IHC |
---|---|
Primary Accession | P10415 |
Other Accession | NM_000633, NP_000624 |
Reactivity | Human |
Predicted | Human |
Host | Rabbit |
Clonality | Polyclonal |
Calculated MW | 26kDa |
Gene ID | 596 |
---|---|
Alias Symbol | Bcl-2, PPP1R50 |
Other Names | Apoptosis regulator Bcl-2, BCL2 |
Format | Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose. |
Reconstitution & Storage | Add 50 ul of distilled water. Final anti-BCL2 antibody concentration is 1 mg/ml in PBS buffer with 2% sucrose. For longer periods of storage, store at 20°C. Avoid repeat freeze-thaw cycles. |
Precautions | BCL2 antibody - N-terminal region is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | BCL2 |
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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).
References
Tsujimoto Y.,et al.Proc. Natl. Acad. Sci. U.S.A. 83:5214-5218(1986).
Eguchi Y.,et al.Nucleic Acids Res. 20:4187-4192(1992).
Cleary M.L.,et al.Cell 47:19-28(1986).
Seto M.,et al.EMBO J. 7:123-131(1988).
Hua C.,et al.Oncogene Res. 2:263-275(1988).
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