|Application ||WB, IHC-P, E|
|Reactivity||Human, Mouse, Rat|
|Description||Rabbit IgG polyclonal antibody for Bcl-2 detection. Tested with WB, IHC-P, Direct ELISA in Human;Mouse;Rat.|
|Reconstitution||Add 0.2ml of distilled water will yield a concentration of 500ug/ml.|
|Other Names||Apoptosis regulator Bcl-2, BCL2|
|Calculated MW||26266 Da|
|Application Details||Western blot, 0.1-0.5 µg/ml|
Immunohistochemistry(Paraffin-embedded Section), 0.5-1 µg/ml
Direct ELISA, 0.1-0.5 µg/ml
|Subcellular Localization||Mitochondrion outer membrane.|
|Tissue Specificity||Expressed in a variety of tissues.|
|Contents||Each vial contains 4mg Trehalose, 0.9mg NaCl, 0.2mg Na2HPO4, 0.05mg NaN3.|
|Immunogen||E. coli-derived human Bcl-2 recombinant protein (Position: Q118-E165).|
|Cross Reactivity||No cross reactivity with other proteins.|
|Storage||At -20˚C; for one year. After r˚Constitution, at 4˚C; for one month. It˚Can also be aliquotted and stored frozen at -20˚C; for a longer time. Avoid repeated freezing and thawing.|
|Function||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).|
|Cellular Location||Mitochondrion outer membrane; Single-pass membrane protein. Nucleus membrane; Single-pass membrane protein. Endoplasmic reticulum membrane; Single-pass membrane protein|
|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.
Immunoreactive BCL2 protein in the neoplastic cells of almost all follicular lymphomas whereas no BCL2 protein was detected in follicles affected by nonneoplastic processes or in normal lymphoid tissue. Every tumor with molecular-genetic evidence of t(14;18) translocation expressed detectable levels of BCL2 protein, regardless of whether the breakpoint was located in or at a distance from the BCL2 gene. Overexpression of BCL2 blocks the apoptotic death of a pro-B-lymphocyte cell line.
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