Bcl-2 Monoclonal Antibody (Bcl-2/100), eBioscience™, Invitrogen™

Description

• This bcl-2/100 monoclonal antibody reacts to human Bcl-2 (B-cell Lymphoma 2), the founding member of a family of pro-apoptotic proteins which includes Bcl-XL, Bcl-w, and Mcl-1
• Bcl-2 plays a role in protecting against apoptosis-inducing insults such as dexamethasone and staurosporine, as well as irradiation and cytokine withdrawal
• The mechanism is thought to include regulation of mitochondrial membrane permeability, resulting in sequestration of caspase proforms, or by preventing the release of apoptosis-mediating mitochondrial factors, such as cytochrome c and AIF (apoptosis-inducing factor), into the cytoplasm
• Bcl-2 is localized to the cytoplasmic side of the mitochondrial membrane, the nuclear envelope, and the endoplasmic reticulum
• Interestingly Bcl-2 does not play a role in preventing cell death of autoreactive T cells in the thymus or Fas-mediated apoptosis
• Two isoforms, termed alpha and beta of Bcl-2 have been identified and are a result of alternative splicing at the C-terminus
• This antibody recognizes both forms
• Applications Reported: This Bcl-2/100 antibody has been reported for use in immunoblotting (WB)
• Applications Tested: This Bcl-2/100 antibody has been tested by immunoblot analysis of the Jurkat cell line
• This can be used at 1-5 μg/mL for detection of reduced and denatured protein
• Purity: Greater than 90%, as determined by SDS-PAGE
• Aggregation: Less than 10%, as determined by HPLC
• Filtration: 0.2 μm post-manufacturing filtered
• BCL-2 is a key regulator of apoptosis that functions to either inhibit or promote cell death
• The BCL-2 family members are also characterized by dimerizing to further modulate apoptosis
• Bag1, for example, has been found to form a heterodimer with BCL-2 resulting in the enhancement of the anti-apoptotic effect of BCL-2
• Bax and Bak have been shown to play a critical role in cytochrome c release from mitochondria and thus initiate apoptosis
• Bax exerts a pro-apoptotic rather than an anti-apoptotic effect on cells
• 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
• In most follicular lymphomas, neoplastic germinal centers express high levels of BCL-2 alpha protein, whereas the normal or hyperplastic germinal centers are negative
• Two transcript variants of BCL-2, produced by alternate splicing, differ in their C-terminal ends
• The overexpression of BCL-2 has been linked to human cancers such as B-cell lymphoma and prostate cancer.