A synthetic peptide corresponding to the N-terminus of the Human BCL2/Bcl-2
This antibody was obtained from a rabbit immunized with a synthetic peptide corresponding to the N-terminus of the Human BCL2/Bcl-2, and conjugated with PE under optimum conditions, the unreacted PE was removed.
Monoclonal Rabbit IgG Clone #204
Aqueous solution containing 0.5% BSA and 0.09% sodium azide
10 μl/Test, 0.1 mg/ml
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. Protected from prolonged exposure to light. Do not freeze ! Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.
Flow cytometric analysis of Human BCL2 expression on Jurkat cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), stained with PE-conjugated anti-Human BCL2. The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
Anti-Bcl-2 Antibody (PE): 別名
Anti-Bcl-2 Antibody; Anti-PPP1R50 Antibody
BCL2 (B-cell leukemia/lymphoma 2, N-Histidine-tagged), also known as Bcl-2, belongs to the Bcl-2 family. Bcl-2 family proteins regulate and contribute to programmed cell death or apoptosis. It is a large protein family and all members contain at least one of four BH (bcl-2 homology) domains. Certain members such as Bcl-2, Bcl-xl and Mcl1 are anti-apoptotic, whilst others are pro-apoptotic. Most Bcl-2 family members contain a C-terminal transmembrane domain that functions to target these proteins to the outer mitochondrial and other intracellular membranes. It is expressed in a variety of tissues. BCL2 blocks the apoptotic death of some cells such as lymphocytes. It also regulates cell death by controlling the mitochondrial membrane permeability and inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor. 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. Two transcript variants, produced by alternate splicing, differ in their C-terminal ends.