BCL2L2 Antibody

1. the present study demonstrates that miR-422a may serve as a tumor suppressor in osteosarcoma via inhibiting BCL2L2 and KRAS translation both in vitro and in vivo Therefore, miR-422a could be developed as a novel therapeutic target in osteosarcoma. PMID: 29358307
2. BCL2L2 knockdown was attenuated the effects of SNHG1 overexpression on cell viability, cell apoptosis and protein levels of cleaved caspase-3, cleaved caspase-9 and Bax in H2O2-treated human cardiomyocytes. PMID: 30355909
3. Our comprehensive analysis indicates B-cell lymphomas commonly select for BCLW overexpression in combination with or instead of other antiapoptotic BCL2 family members. PMID: 28855351
4. BCL-W contributes to the threshold of anti-apoptotic activity during mitosis PMID: 27231850
5. we demonstrated that miR-126-5p plays an inhibitory role in human cervical cancer progression, regulating the apoptosis of cancer cells via directly targeting Bcl2l2. PMID: 28438233
6. High expression of Bcl-w was associated with mesenchymal changes and invading populations in the glioblastoma multiforme; Bcl-w functions as a positive regulator of invasion by enhancing mesenchymal traits of glioblastoma multiforme, consequently contributing to malignancy. PMID: 23826359
7. BCL2L2 was the virtual target of miR-133b, and we found a negative regulatory relationship between miR-133b and BCL2L2. MiR-133b and BCL2L2 interfered with the viability and apoptosis of cells. PMID: 27802259
8. we conclude that BER treatment reduces cisplatin resistance of gastric cancer cells by modulating the miR-203/Bcl-w apoptotic axis. BER may be a novel agent to enhance chemotherapeutic responses in cisplatin-resistant gastric cancer patients PMID: 27142767
9. Data show that BCL2-like 2 protein (BCL2L2) is a direct target of micrRNA miR-29b. PMID: 26155940
10. these results indicate that miR-335 acts as a novel tumor suppressor to regulate ccRCC cell proliferation and invasion through downregulation of BCL-W expression. PMID: 25846734
11. miR-15a acts as a tumor suppressor in NSCLC by directly targeting BCL2L2 and may serve as a potential diagnostic biomarker and therapeutic target for NSCLC. PMID: 25874488
12. over-expression of miR-195 sensitized resistant cells to DOX and enhanced cell apoptosis activity, all of which can be partly rescued by BCL2L2 siRNA and cDNA expression PMID: 23526568
13. Bcl-w-induced Sp1 activation is a potential marker for aggressiveness of glioblastoma multiforme. PMID: 24552705
14. HDMF inhibits Bcl-w-induced neurosphere formation and the expression of glioma stem cell markers, such as Musashi, Sox-2 and c-myc. PMID: 24946210
15. Crystal structure of human BCL-W in complex with different DARPins is virtually identical to the ligand-free conformation of its closest relative BCL-XL. PMID: 24747052
16. MiR-335 lacks of expression brings about the abnormal accumulation of Bcl-w. PMID: 23708561
17. Expression of miR-214 reduces cell survival, induces apoptosis and enhances sensitivity to cisplatin through directly inhibiting Bcl2l2 expression. PMID: 23337879
18. Bcl-w protein plays a significant role in the carcinogenesis of human small intestinal adenocarcinoma. Down-regulation of Bcl-w protein in HuTu-80 cells makes them susceptible to 5-Fu. PMID: 22780970
19. These findings indicate that miR-29c-mediated BCL2L2 suppression is involved in influenza virus-induced cell death in A549 cells. PMID: 22850539
20. By using human cancer cells and mouse embryonic fibroblasts, the study shows that BCL-W functions in the mitochondria to increase the levels of reactive oxygen species (ROS), which subsequently stimulates the invasion-promoting signaling pathway. PMID: 22570867
21. our results provide evidence that miR-335 might function as a metastasis suppressor in gastric cancer by targeting SP1 directly and indirectly through the Bcl-w-induced phosphoinositide 3-kinase-Akt-Sp1 pathway PMID: 21822301
22. Data show that ABT-737, a small molecule inhibitor of Bcl-2, Bcl-X(L), and Bcl-w, significantly induced apoptosis in HTLV-1 infected T-cell lines as well as in fresh adult T-cell leukemia/lymphoma (ATLL) cells. PMID: 22138435
23. miR-195 could improve the drug sensitivity at least in part by targeting Bcl-w to increase cell apoptosis in hepatocellular carcinoma cells. PMID: 21947305
24. The alpha4-alpha5 hinge region is required for dimerization of BCL-W, and functioning of both pro- and antiapoptotic BCL-2 proteins. PMID: 22000515
25. although the cytosolic domain of BCL-w exhibits an overall structure similar to that of BCL-xL and BCL-2, the unique organization of its C-terminal helix may modulate BCL-w interactions with pro-apoptotic binding partners PMID: 12651847
26. structure of reveals a role for the C-terminal residues in modulating biological activity PMID: 12660157
27. Bcl-w may play an important protective role in neurons in the Alzheimer disease brain and this aspect could be therapeutically harnessed to afford neuroprotection PMID: 15147516
28. Peptide = to BH3 region of proapoptotic protein BID, bound in cleft of antiapoptotic protein BCL-w.Binding induced major conformational rearrangements in both peptide & protein components & led to displacement & unfolding of BCL-w C-terminal alpha-helix. PMID: 16475813
29. overexpressed BCL2L2, through amplification or other mechanisms, promotes the growth of a non-smalll cell lung caner cell line. PMID: 17459056
30. Bcl-w is a direct target of miR-122 that functions as an endogenous apoptosis regulator in these human hepatocellular carcinoma -derived cell lines. PMID: 18692484
31. both uPA and MMP-2 contribute to Bcl-w-induced invasion via the stimulation of the FAK-dependent migratory pathway. PMID: 19097687
32. Bcl-w is a new member of the Akt pathway PMID: 19114998
33. BCL-W may function as a downstream effector of inappropriate WNT/beta-catenin signalling. PMID: 19124064
34. Results show that the folate-induced DNA methylation limits proliferation and increases the sensitivity to temozolomide-induced apoptosis in glioma cells through methylation of PDGF-B, MGMT, survivin, and bcl-w genes. PMID: 19451595
35. over-expression of miR-133B increased apoptosis in response to gemcitabine and reduced MCL-1 and BCL2L2 expression. PMID: 19654003

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HGNC: 995

OMIM: 601931

KEGG: hsa:599

STRING: 9606.ENSP00000250405

UniGene: Hs.410026