anti-BCL2-Like 2 (BCL2L2) Anticorps

Human BCL2-Like 2 (BCL2L2) interaction partners

1. HOTAIR up-regulates Bcl-w to enhance cell proliferation through sequestering miR-206 in breast cancer

2. Data found that Bcl-w promotes epithelial-mesenchymal transition by increasing respiratory complex-I activity and reactive oxygen species (ROS) levels.

3. 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.

4. 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.

5. Our comprehensive analysis indicates B-cell lymphomas commonly select for BCLW overexpression in combination with or instead of other antiapoptotic BCL2 family members.

6. BCL-W contributes to the threshold of anti-apoptotic activity during mitosis

7. 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.

8. 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.

9. 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.

10. overexpression of miR-15a in the FaDu cells was associated with significantly decreased BCL2L2 and BCL2 expression and a significant increase in the apoptosis rate. The opposite results were observed in HPV-positive HSCC, where downregulation of miR-15a suppressed apoptosis

11. 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

12. Genetic and pharmacological inhibition of BCL-W and BCL-XL causes directed elimination of senescent cells.

13. Data show that BCL2-like 2 protein (BCL2L2) is a direct target of micrRNA miR-29b.

14. 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.

15. 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.

16. The crystal structures of BCL-W and BCL-XL, along with cellular, studies reveal critical features of the BH3 domains of pro-survival proteins that distinguish them functionally from their pro-apoptotic counterparts.

17. 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

18. A structural basis for a conserved binding mechanism between p53DBD and the anti-apoptotic Bcl-2 family proteins.

19. Bcl-w-induced Sp1 activation is a potential marker for aggressiveness of glioblastoma multiforme.

20. HDMF inhibits Bcl-w-induced neurosphere formation and the expression of glioma stem cell markers, such as Musashi, Sox-2 and c-myc.

Mouse (Murine) BCL2-Like 2 (BCL2L2) interaction partners

1. MYC regulates BCL-W expression through its transcriptional regulation of specific miR.

2. Genetic and pharmacological inhibition of BCL-W and BCL-XL causes directed elimination of senescent cells.

3. NF-kappaB p65/p52 signaling mediated the effects of GDNF on Bcl-2 and Bcl-w expressions

4. Target-derived neurotrophins coordinate transcription of the antiapoptotic gene bclw with transport of bclw mRNA to the axon, and thereby prevent axonal degeneration in rat and mouse sensory neurons.

5. 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.

6. Bcl-2, Bcl-x(L) and Bcl-w have only minor roles in thymic lymphoma development elicited by defects in p53, and this may indicate that Mcl-1 and/or A1 may feature more prominently in this process.

7. Induction of autocrine Bcl-w signaling through pericytes promoting endothelial cell survival is associated with melanoma development.

8. Bcl-w(-/-) sensory neurons exhibit mitochondrial abnormalities, including alterations in axonal mitochondrial size, axonal mitochondrial membrane potential, and cellular ATP levels.

9. Bcl-x(L) and Bcl-w target protein phosphatase 1alpha to Bad

10. Bcl-2, Bcl-w, and Bax act in a redundant manner in regulating granulocyte survival and death

11. amino acid and base sequences of c98 gene (bcl-2 homolog) expressed in newborn epidermal keratinocytes treated with IGF-1

12. The crypt expression of Bax and Bcl-w is influenced by epidermal growth factor receptor signaling and is key for the regulation of apoptosis.

13. These data identify Bcl-w as an endogenous neuroprotectant that may have seizure-suppressive functions.

14. Bcl-w and Grid2 act in distinct pathways to regulate mitochondrial morphogenesis and control Purkinje cell dendrite development and synapse formation.

Cow (Bovine) BCL2-Like 2 (BCL2L2) interaction partners

1. Chromosome mapping of BCL2L2 gene in cows.