Anti-BCL2 monoclonal antibody, clone 211/E6

Name: Anti-BCL2 monoclonal antibody, clone 211/E6
SKU: DCABH-9805
Rating: 5 (1 reviews)

Mouse anti-Human BCL2 monoclonal antibody for WB, IP, IHC-P, FC, ICC/IF

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COA

SDS

Datasheet

Additional Formats Available

Summary

Specifications

Antibody Isotype

IgG1

Clone

211/E6

Species Reactivity

Human

Immunogen

Synthetic peptide: Cys-GAAPAPGIFSSQPG, corresponding to amino acids 41-54 of Human Bcl2 alpha

Conjugate

Unconjugated

Applications

Application Notes

WB: 1 - 2 μg/ml; IP: 2 μg/mg of lysate; IHC-P: 2 - 4 μg/ml; Flow Cyt: 1μg/10⁶ cells

Target

Alternative Names

BCL2; B-cell CLL/lymphoma 2; apoptosis regulator Bcl-2; Bcl 2; PPP1R50; protein phosphatase 1; regulatory subunit 50; protein phosphatase 1, regulatory subunit 50; Bcl-2;

Entrez Gene ID

596

UniProt ID

A0A024R2B3

Product Background

Antigen Description

BCL2 is 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. Two transcript variants (alpha and beta) produced by alternate splicing, differ in their C-terminal ends. BCL2 suppresses apoptosis in a variety of cell systems including factor-dependent lymphohematopoietic and neural cells. It regulates cell death by controlling the mitochondrial membrane permeability. It appears to function in a feedback loop system with caspases. BCL2 inhibits caspase activity either by preventing the release of cytochrome c from the mitochondria and/or by binding to the apoptosis-activating factor (APAF1). It can form homodimers, and heterodimers with BAX, BAD, BAK and BclX(L). Heterodimerization with BAX requires intact BH1 and BH2 domains, and is necessary for anti-apoptotic activity. Also interacts with APAF1, RAF1, TP53BP2, BBC3, BCL2L1 and BNIPL.

Pathway

ATF-2 transcription factor network, organism-specific biosystem; Activation of BAD and translocation to mitochondria, organism-specific biosystem; Activation of BH3-only proteins, organism-specific biosystem; Amyotrophic lateral sclerosis (ALS), organism-specific biosystem; Amyotrophic lateral sclerosis (ALS), conserved biosystem; Apoptosis, organism-specific biosystem; Apoptosis, organism-specific biosystem;

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Documents

pdf COA

pdf SDS

pdf Datasheet

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References

Anti-CD19 mAb-conjugated human serum albumin nanoparticles effectively deliver doxorubicin to B-lymphoblastic leukemia cells

PHARMAZIE

Authors: Pan, H.; Li, S.; Li, M.; Tao, Q.; Jia, J.; Li, W.; Wang, L.; Guo, Z.; Ma, K.; Liu, Y.; Cui, C.

Abstract

B-Lymphoblastic leukemia (B-LL) is the most common childhood hematological malignancy. Although its overall prognosis is good, the outcome after relapse is poor. CD19 is highly expressed on the membrane of most malignant B-cells, and was shown to be a promising therapeutic target of B-LL. In this present work, we designed and synthesized a novel drug carrier, anti-CD19 monoclonal antibody-conjugated human serum albumin nanoparticles (HSA-CD19 NPs). Doxorubicin (DOX) was well encapsulated into the HSA-CD19 NPs to form an anticancer nanodrug DOX/HSA-CD19. DOX/HSA-CD19 was preferentially uptaken by CD19(+) B-LL cell line KOPN-8. DOX/HSA-CD19 showed strong antiproliferative effect on KOPN-8 cells with an IC50 value of 4.1 mu g/mL. Further, proapoptotic Bax and caspase-3 were significantly elevated, but antiapoptotic Bcl2 was reduced in DOX/HSA-CD19 treated KOPN-8 cells, indicating the activation of the apoptosis pathway by the nanodrug. By contrast, DOX/HSA-CD19 did not show affinity to CD19-monocytic cell line, U937, and did not affect its proliferation. Collectively, HSA-CD19 NPs are a kind of effective novel drug carrier, and DOX/HSA-CD19 is a promising antitumor nanodrug for the treatment of B-LL.

Somatic copy number gains in MYC, BCL2, and BCL6 identifies a subset of aggressive alternative-DH/TH DLBCL patients

BLOOD CANCER JOURNAL

Authors: Krull, Jordan E.; Wenzl, Kerstin; Hartert, Keenan T.; Manske, Michelle K.; Sarangi, Vivekananda; Maurer, Matthew J.; Larson, Melissa C.; Nowakowski, Grzegorz S.; Ansell, Stephen M.; McPhail, Ellen; Habermann, Thomas M.; Link, Brian K.; King, Rebecca L.; Cerhan, James R.; Novak, Anne J.

Abstract

Double/triple hit lymphoma (DH/TH), known as high-grade B-cell lymphoma (HGBL), is an aggressive diffuse large B cell lymphoma (DLBCL), defined as having concurrent MYC, BCL2, and/or BCL6 gene rearrangements. While gene rearrangements represent significant genetic events in cancer, copy number alterations (CNAs) also play an important role, and their contributions to rearrangements have yet to be fully elucidated. Using FISH and high-resolution CNA data, we defined the landscape of concurrent gene rearrangements and copy gains in MYC, BCL2, and BCL6, in a cohort of 479 newly diagnosed DLBCL. We also show that concurrent translocations and copy number alterations, in combinations similar to DH/TH, identify a unique subset of DLBCL, alternative DH/TH, that have survival outcomes similar to DH/TH DLBCL patients.