BCL2 Recombinant Monoclonal Antibody (RACO0591)

The BCL2 recombinant monoclonal antibody is produced through a complex series of steps. The process begins with the harvesting of the BCL2 monoclonal antibody and sequencing of its genetic sequence. Next, a vector carrying the BCL2 monoclonal antibody gene is created and transfected into a host cell line for culturing. A synthesized peptide derived from human BCL2 is used to stimulate the BCL2 monoclonal antibody production. The BCL2 recombinant monoclonal antibody is purified using affinity chromatography to achieve high specificity and purity. Finally, the specificity of the antibody is confirmed using ELISA, WB, and IHC assays to verify its ability to detect BCL2. It reacts with human and mouse BCL2 proteins.
The BCL2 protein plays a key role in regulating apoptosis, which is a programmed cell death process that is essential for normal development and homeostasis in multicellular organisms. BCL2 is an anti-apoptotic protein that promotes cell survival by inhibiting the pro-apoptotic members of the family. BCL2 also plays a role in the regulation of mitochondrial function. BCL2 can interact with and modulate the activity of several mitochondrial proteins, including the voltage-dependent anion channel (VDAC), which regulates mitochondrial outer membrane permeability, and the adenine nucleotide translocator (ANT), which is involved in mitochondrial energy metabolism. It also has a role in the regulation of the cell cycle. Dysregulation of BCL2 expression or function is associated with cancer and resistance to chemotherapy.

1. long noncoding RNA HOTAIR suppresses TNF-alpha induced nucleus pulposus cell apoptosis by regulating miR-34a/Bcl-2 axis. PMID: 30138895
2. The mitochondrial depolarization also stems from the Bcl-2 inhibition mediated by DFMT, followed by the cytochrome c release that activates caspase signaling. With the participation of the two-pronged mechanism, a programmed apoptosis is induced in response to DFMT treatment. PMID: 28805013
3. miR-7-5p reduced energy consumption via inhibiting PARP-1 expression, and miR-7-5p increased energy generation by suppressing the expression of Bcl-2. PMID: 30219819
4. Venetoclax-based combination treatment for newly diagnosed elderly patients for whom intense chemotherapy is not an option may be the first setting in which this agent may be employed in Acute myeloid leukemia. Based on pre-clinical evidence, BCL-2 inhibition may be useful in relapsed/refractory disease in conjunction with cytotoxic therapy, but has modest single agent activity. PMID: 29264938
5. Glandular, menopause-independent DFF40, DFF45, and Bcl-2 overexpression may play an important role in the pathogenesis of endometrial polyps and benign endometrial hyperplasia PMID: 28914671
6. data strongly suggest that XIAP-mediated inhibition of final caspase-3 processing is the last and major hurdle in TRAIL-induced apoptosis in NCI-H460 cells, which can be overcome by Smac in a Bcl-2 level dependent manner. PMID: 29927992
7. could not find any relationship between Bcl-2, c-Myc and EBER-ISH positivity and the low/high IPS groups in classical Hodgkin lymphoma PMID: 29708579
8. Fluorescence in situ hybridization studies (histologic sections) confirmed translocations of MYC (8q24), BCL2 (18q21) and BCL6 (3q27) in all patients. PMID: 30043475
9. High BCL-2 expression is associated with colorectal cancer. PMID: 30015962
10. MiR-29a down-regulation is correlated with drug resistance of nasopharyngeal carcinoma cell line CNE-1 and MiR-29a up-regulation decreases Taxol resistance of nasopharyngeal carcinoma CNE-1 cells possibly via inhibiting STAT3 and Bcl-2 expression. PMID: 29914005
11. Results revealed that BCL-2 protein is highly expressed in colon cancer tissues and was identified as a direct target for mir-184. BCL-2 appeared to participate in cell cycle regulation and malignant transformation to colon cancer. PMID: 28782841
12. Results indicate that full-length B-cell leukemia 2 family protein (Bcl-2) Ile14Gly/Val15Gly displayed severely reduced structural stability and a shortened protein half-life. PMID: 29131545
13. Data show the regulation of BCL2 mainly associated with methylation across the molecular subtypes of breast cancer. Luminal A and B subtypes showed upregulated expression of BCL2 protein, mRNA, and hypomethylation. Although copy number alteration may have played a minor role, mutation status was not related to BCL2 regulation. Upregulation of BCL2 was associated with better prognosis than downregulation of BCL2. PMID: 28701032
14. c-MYC/BCL2 protein co-expression in non-germinal center B-cell subtype constituted a unique group with extremely inferior outcome regardless of ethnicity PMID: 29801406
15. Overexpression of LIN28B promotes colon cancer development by increasing BCL-2 expression. PMID: 29669301
16. High BCL2 expression is associated with Prostate Cancer. PMID: 29641255
17. The findings of the present study indicated that icariin prevented injury and apoptosis in HUVECs following oxLDL treatment, in particular via the regulation of protein and mRNA expression levels of Bcl-2 and caspase-3. PMID: 29532884
18. BCL2 expression is also a strong predictive marker for DLBCL patients treated with R-CHOP. PMID: 28154089
19. High BCL2 expression is associated with drug resistance in ovarian cancer. PMID: 29286126
20. Elevated expression of Bcl-2 was an independent prognostic factor for poorer overall survival in triple-negative breast cancer and as such a significant marker for tumor aggressiveness. PMID: 28777433
21. CD30+ diffuse large B-cell lymphoma has characteristic clinicopathological features mutually exclusive with MYC gene rearrangement and negatively associated with BCL2 protein expression. PMID: 29666157
22. Phosphorylated and activated deoxycytidine kinase inhibits ionizing radiation (IR)-induced total cell death and apoptosis, and promotes IR-induced autophagy through the mTOR pathway and by inhibiting the binding of Bcl2 protein to BECN1 in breast cancer cells. PMID: 29393406
23. It was demonstrated that hypoxia stimulates migration and invasion in the MG63 human osteosarcoma cell line, which was correlated with the downregulation of miR15a and upregulation of B-cell lymphoma 2 (Bcl2) expression PMID: 29484432
24. miR-21 may promote salivary adenoid cystic carcinoma progression via PDCD4 and PTEN down-regulation and Bcl-2 up-regulation. PMID: 29328455
25. Paper analyses results of serum cytokines and lymphocyte apoptosis study in nodular goiter against the background of autoimmune thyroiditis and thyroid adenoma based on the cell preparedness to apoptosis, the number of apoptotic lymphocytes and the content of proapoptotic tumor necrosis factor-alpha, interleukins in serum, considering the polymorphism of BCL-2, CTLA-4 and APO-1 genes. PMID: 29250672
26. Permeabilisation of the mitochondrial outer membrane (MOMP) is directly regulated by the BCL-2 (B cell lymphoma 2) family in mammals [Review]. PMID: 28396106
27. The present study demonstrated that TATfused inositol 1,4,5trisphosphate receptorderived peptide (TATIDPS), which targets the BH4 domain of Bcl2, increased cisplatininduced Ca2+ flux from the endoplasmic reticulum (ER) into the cytosol and mitochondria. PMID: 29207009
28. we highlight the emerging recognition of MYC and BCL2 coexpression as the most robust predictor of diffuse large B cell lymphoma outcome, and discuss rationally conceived experimental approaches to treat these high-risk patients. PMID: 29198442
29. Bcl-2 binding to ARTS involves the BH3 domain of Bcl-2. Lysine 17 in Bcl-2 serves as the main acceptor for ubiquitylation, and a Bcl-2 K17A mutant has increased stability and is more potent in protection against apoptosis. PMID: 29020630
30. The expression levels of miR-204-5p were downregulated in prostate cancer cells compared with normal prostate epithelial cells. BCL2 mRNA and protein expression decreased in miR-204-5p-transfected cells, which led to cytochrome C release from mitochondria. Cotransfection of a reporter vector harboring the BCL2 3'-untranslated region to compete with endogenous transcripts partially rescued miR-204-5p-induced apoptosis. PMID: 27519795
31. GATA4 was a transcription factor that activated mouse double minute 2 homolog (MDM2) and B cell lymphoma 2 (BCL2) expression in ALL cells. PMID: 28849107
32. High BCL2 expression is associated with oncogenicity and chemoresistance in hepatocellular carcinoma. PMID: 28445151
33. Gastrin and BCL2 apoptosis regulator (Bcl2) are highly expressed in gastric cancer tissues, and they are correlated with the clinicopathologic features. PMID: 29268861
34. This study utilized a lentiviral vector that overexpressed the human VEGF and Bcl-2 genes simultaneously. Co-overexpression of VEGF and Bcl-2 inhibits the oxygen glucose deprivation induced apoptosis of mesenchymal stem cells. PMID: 28627637
35. Double-hit lymphoma (DHL) is an aggressive form of DLBCL with an unmet treatment need, in which MYC rearrangement is present with either BCL2 or BCL6 rearrangement PMID: 28952038
36. The expression of Bcl-2 and E cadherin immunopositivity was associated positively with tumor grade, high T category and histopathological grades. The results of this study points to the significance of cell proliferation and invasion as a major determinant of prognosis in OSCC. PMID: 28393810
37. meta-analysis suggests a role BCL-2 promoter polymorphisms in cancer susceptibility and prognosis; rs2279115 was associated with higher risk of cancer susceptibility in Asia but not in Caucasian; rs2279115 was associated with a higher risk in digestive system cancer and endocrine system cancer but not breast cancer, respiratory cancer and hematopoietic cancer PMID: 28445963
38. In this study, we investigated whether APG-1252-12A inhibits the growth of five leukemia cell lines in a concentration- or time-dependent manner by MTS assay.APG-1252-12A is a Bcl-2 homology (BH)-3 mimetic that specifically binds to Bcl-2 and Bcl-xl, which has shown efficacy in some Bcl-2 dependent hematological cancers PMID: 28586007
39. Multiple lines of evidence suggest formation of a potential cruciform DNA structure at MBR peak III, which was also supported by in silico studies. The formation of a non-B DNA structure could be a basis for fragility at BCL2 breakpoint regions, eventually leading to chromosomal translocations. PMID: 29246583
40. The upregulation of miR-219-5p inhibited melanoma growth and metastasis and strengthened melanoma cells chemosensitivity by targeting Bcl-2. Therefore, the modulation of miR-219-5p expression may be a novel treatment strategy in melanoma. PMID: 28884131
41. The expression of the anti-apoptotic protein Bcl-2 was greater in luminal A breast cancer tissue samples compared to triple-negative breast cancer. PMID: 28801774
42. Lnc_ASNR interacted with the protein ARE/poly (U)-binding/degradation factor 1(AUF1), which is reported to promote rapid degradation of the Bcl-2 mRNA, an inhibitor of apoptosis. Lnc_ASNR binds to AUFI in nucleus, decreasing the cytoplasmic proportion of AUF1 which targets the B-cell lymphoma-2 (Bcl-2) mRNA. PMID: 27578251
43. Bcl-2 high expression was significantly correlated with favorable overall survival and better disease/recurrence free survival in colorectal cancer.[meta-analysis] PMID: 28785155
44. High expression of bcl-2 in KCOT supports the general agreement that some features of KCOT are those of a neoplasia. The bcl-2 expression in connective tissue cells suggests that these cells may also be important as epithelial cells in the biological behavior odontogenic keratocyst PMID: 28862228
45. Results identified BCL2 as a direct target of miR-139-5p in colorectal cancer cells and showed that the tumor suppressor activity of miR-139-5p is mediated by the modulation of BCL2 expression. PMID: 27244080
46. Polo-like kinase inhibition can sensitize cholangiocarcinoma cells to cisplatin-induced apoptosis with proteasomal Bcl-2 degradation as an additional pro-apoptotic effect. PMID: 28652654
47. Lipid oxidation product 4-hydroxy-2-nonenal is at the crossroads of NF-kappaB pathway and anti-apoptotic Bcl2 expression. (Review) PMID: 27840321
48. Ibrutinib-resistant TMD8 cells had higher BCL2 gene expression and increased sensitivity to ABT-199, a BCL-2 inhibitor. Consistently, clinical samples from ABC-DLBCL patients who experienced poorer response to ibrutinib had higher BCL2 gene expression. We further demonstrated synergistic growth suppression by ibrutinib and ABT-199 in multiple ABC-DLBCL, GCB-DLBCL, and follicular lymphoma cell lines. PMID: 28428442
49. MUC1-C Stabilizes MCL-1 in the Oxidative Stress Response of Triple-Negative Breast Cancer Cells to BCL-2 Inhibitors PMID: 27217294
50. The BCL2 c.-938C>A and c.21G>A single-nucleotide polymorphisms showed a significant impact on outcome with transitional cell carcinoma of the bladder PMID: 28417194

HGNC: 990

OMIM: 151430

KEGG: hsa:596

STRING: 9606.ENSP00000329623

UniGene: Hs.150749