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Upingbio
SKU:YP-Ab-18036-53UL
BCL-2 (PTR2303) Mouse mAb
BCL-2 (PTR2303) Mouse mAb
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- Reaction species: Human;Mouse;Rat
- Gene Name: BCL2
- Protein name: Apoptosis regulator Bcl-2
- Molecular weight (DA): 26kD
- Immunogen: Synthetic Peptide of human Bcl-2 AA range: 1-100
- Specificity: The antibody detects endogenous Bcl-2 proteins.
- Composition: PBS, pH 7.4, containing 0.5%BSA, 0.02% sodium azide as Preservative and 50%
- Source: Monoclonal, Mouse IgG2b, Kappa
- Dilution ratio: WB 1:1000-2000
- Purification process: The antibody was affinity-purified from mouse ascites by affinity-chromatography using specific immunogen.
- Concentration: 0.73mg/mL
- Storage: -15°C to -25°C/1 year(Do not lower than -25°C)
- Other Names: BCL2;Apoptosis regulator Bcl-2
- Background: BCL2, apoptosis regulator(BCL2) Homo sapiens This gene encodes an integral outer mitochondrial membrane protein that blocks the apoptotic death of some cells such as lymphocytes. Constitutive expression of BCL2, such as in the case of translocation of BCL2 to Ig heavy chain locus, is thought to be the cause of follicular lymphoma. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Feb 2016],
- Function: disease:A chromosomal aberration involving BCL2 may be a cause of follicular lymphoma (FL) [MIM:151430]; also known as type II chronic lymphatic leukemia. Translocation t(14;18)(q32;q21) with immunoglobulin gene regions. BCL2 mutations found in non-Hodgkin lymphomas carrying the chromosomal translocation could be attributed to the Ig somatic hypermutation mechanism resulting in nucleotide transitions.,domain:The BH4 motif is required for anti-apoptotic activity and for interaction with RAF-1.,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-activati
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