Aperçu des produits pour anti-BCL2L10 (BCL2L10) Anticorps

Human BCL2-Like 10 (Apoptosis Facilitator) (BCL2L10) interaction partners

1. BCL2L10 (Nrh protein) is localized to the endoplasmic reticulum and is a poor prognostic marker linked with chemotherapy resistance in breast cancer.

2. marrow BCL2L10 positive cells may be a biomarker for azacitidine response and OS, with a potential impact in clinical practice.

3. These results suggest that by inhibiting Bcl2l10 activity and promoting contact between endoplasmic reticulum and mitochondria, IRBIT facilitates massive Ca(2+) transfer to mitochondria and promotes apoptosis.

4. we describe the identification of a structural genetic variant segregating with affective psychosis in a family with multiple members suffering from bipolar I disorder. Using whole-genome sequencing, we delineated the translocation breakpoints as corresponding intragenic events disrupting BCL2L10 and PNLDC1. These data warrant further consideration for BCL2L10 and PNLDC1 as novel candidates for affective psychosis.

5. Results found that BCL2L10 was down-regulated in human hepatocellular carcinoma (HCC) tissues; its overexpression suppresses cell growth and migration of HCC cell lines. These results suggested that BCL2L10 functions as a tumor-suppressor in HCC.

6. BCLB expression was a starvation stress sensor inducing apoptosis and autophagy simultaneously in HCC cells through the adenosine monophosphate-activated protein kinase AMPK-mTOR signaling cascade.

7. Identification of a variant in the BCL2L10 gene as a protective factor for the development of therapy-related myeloid neoplasms and de novo myelodysplastic syndrome.

8. polyubiquitination and proteasomal turnover dictate the expression level and anti-apoptotic capacity of Bcl-B

9. Data suggest that BCL2L10 is localized predominantly to mitochondria in high-quality preimplantation embryos/blastocysts; in contrast, abnormal embryos/blastocysts exhibit extra-mitochondrial localization (cytoplasm/cell nucleus) of BCL2L10.

10. Bcl-B in complex with the BH3 motif of Bim protected cells from Bax-dependent apoptotic pathways.

11. Bcl-B interacts with the BH3 domain of BECN1 and Bcl-B overexpression reduces autophagy triggered by a variety of pro-autophagic stimuli.

12. expression is predictive of azacitidine-resistance in myelodysplastic syndrome patients

13. Ubqln stabilizes BCLb protein, while also promoting monoubiquitination on multiple lysine residues and relocation to the cytosol.

14. BCL2L10 methylation is associated with myelodysplastic syndromes.

15. Loss of BCL2L10 protein expression predicts poor clinical outcome in gastric carcinoma.

16. The apoptotic gene BCL2L10 is a frequent target for aberrant promoter methylation in patients with acute leukemia, de novo and therapy-related.

17. The pro-apoptotic effect of BCL2L10 and growth promotion by BCL2L10 siRNA in gastric cancer cells suggest that it may be a tumour suppressor.

18. study evaluates 3D structure of Bcl-2L10 protein using homology modeling and aims to understand plausible functional and binding interactions between Bcl-2L10 with BH3 domain of BAX using protein - protein docking

19. BCL2L10 is frequently silenced by promoter hypermethylation in gastric cancer.

20. Thus, these results indicate the existence of a previously undiscovered mechanism by which NM23-H2 involves in the regulation of Diva-mediated apoptosis.

Mouse (Murine) BCL2-Like 10 (Apoptosis Facilitator) (BCL2L10) interaction partners

1. The knockdown of BCL-B resulted in increased apoptosis and mitophagy in hepatic stellate cells, while the overexpression of BCL-B caused the opposite effects.

2. role for Bcl-B in B cell proliferation and plasmocyte differentiation through its ability to impair B cell death and drive multiple myeloma progression.

3. Bcl2l10, Tpx2, and Aurka co-localized on the meiotic spindles, and Bcl2l10 was present in the same complex with Tpx2.

4. Protein-protein interactions involving apoptosis regulator Diva (Boo) and the BH3 domain of proapoptotic Bcl-2 members.

5. analysis of a novel interaction between Bcl-2 members Diva and Harakiri

6. Structure and sequence alignment of mouse pro-survival Bcl-2 family members reveals Boo/Diva as a divergent Bcl-2 protein.

7. The role of Bcl2l10 is strongly associated with oocyte maturation, especially at the MI-MII transition.

8. BCL2L10 is a novel and prime candidate related to oocyte maturation, fertility, and embryo developmental competence

Zebrafish BCL2-Like 10 (Apoptosis Facilitator) (BCL2L10) interaction partners

1. Nrz phosphorylation is necessary for the generation of IP3-mediated Ca2+ transients and the formation of circumferential actin-myosin cables required for epiboly.

2. In the yolk syncytial layer, Nrz appears to prevent the release of Ca(2+) from the endoplasmic reticulum by directly interacting with the IP3R1 Ca(2+) channel.

3. data suggest that Nrz, in addition to its effect on apoptosis, contributes to cell movements during gastrulation by negatively regulating the expression of Snail-1, a transcription factor that controls cell adhesion