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>   首页   >   产品   >   一抗   >   精选抗体   >   BCL2 antibody - N-terminal region   

BCL2 antibody - N-terminal region

Rabbit Polyclonal Antibody

     
  • 2 - BCL2 antibody - N-terminal region AI16168
    Human kidney
  • 1 - BCL2 antibody - N-terminal region AI16168

    WB Suggested Anti-BCL2 Antibody Titration: 0.2-1 μg/ml
    Positive Control: Human Placenta
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Product Information
Application
  • Applications Legend:
  • E=ELISA
  • WB=Western Blotting
  • IHC=Immunohistochemistry
  • IHC-P=Immunohistochemistry (Paraffin)
  • IP=Immunoprecipitation
  • IF=Immunofluorescence
  • IC=Immunochemistry
  • ICC=Immunocytochemistry
  • FC=Flow Cytometry
  • DB=Dot Blot
WB, IHC
Primary Accession P10415
Other Accession NM_000633, NP_000624
Reactivity Human
Predicted Human
Host Rabbit
Clonality Polyclonal
Calculated MW 26266 Da
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.

For Research Use Only. Not For Use In Diagnostic 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

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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