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BCL2 antibody - N-terminal region

Rabbit Polyclonal Antibody

     
  • IHC - BCL2 antibody - N-terminal region AI16168
    Human kidney
    detail
  • WB - BCL2 antibody - N-terminal region AI16168

    WB Suggested Anti-BCL2 Antibody Titration: 0.2-1 μg/ml
    Positive Control: Human Placenta
    detail
  • SPECIFICATION
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  • BACKGROUND
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Product Information
Application
  • Applications Legend:
  • WB=Western Blot
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin-embedded Sections)
  • IHC-F=Immunohistochemistry (Frozen Sections)
  • IF=Immunofluorescence
  • FC=Flow Cytopmetry
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • E=ELISA
  • IP=Immunoprecipitation
  • DB=Dot Blot
  • CHIP=Chromatin Immunoprecipitation
  • FA=Fluorescence Assay
  • IEM=Immuno electron microscopy
  • EIA=Enzyme Immunoassay
WB, IHC
Primary Accession P10415
Other Accession NM_000633, NP_000624
Reactivity Human
Predicted Human
Host Rabbit
Clonality Polyclonal
Calculated MW 26kDa
Additional Information
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.
PrecautionsBCL2 antibody - N-terminal region is for research use only and not for use in diagnostic or therapeutic procedures.
Protein Information
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.
Research Areas
Citations (0)
citation

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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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$ 389.00
Cat# AI16168
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