anti-BCL2/adenovirus E1B 19kDa Interacting Protein 3-Like (BNIP3L) Anticorps

Human BCL2/adenovirus E1B 19kDa Interacting Protein 3-Like (BNIP3L) interaction partners

1. NIX-mediated mitophagy is suppressed in proteinuric conditions and is responsible for proteinuria- induced cell apoptosis, which is consistent with previous evidence that excess albumin uptake inhibits autophagy in renal tubules and contributes to progressive tubular injury.

2. chronic obstructive pulmonary disease (COPD)patients had lower muscle mitochondrial content, higher BNIP3L and lower FUNDC1 protein, and higher Parkin protein and gene-expression. BNIP3L and Parkin protein levels inversely correlated with mtDNA/gDNA ratio and FEV1% predicted.

3. The results demonstrate that Nix can serve as an alternative mediator of mitophagy to maintain mitochondrial turnover, identifying Nix as a promising target for neuroprotective treatment in PINK1/Parkin-related Parkinson's disease.

4. Here the authors present evidence for phosphorylation-driven regulation of the Nix:LC3B interaction. Isothermal titration calorimetry and NMR indicate a ~100 fold enhanced affinity of the serine 34/35-phosphorylated Nix LC3-interacting region (LIR) to LC3B and formation of a very rigid complex compared to the non-phosphorylated sequence.

5. The authors find that KDM3A promotes anoikis through transcriptional activation of BNIP3 and BNIP3L, which encode pro-apoptotic proteins.

6. p75(NTR) and NIX may play critical roles in intracerebral hemorrhage-induced neuronal apoptosis in vitro and in vivo.

7. Data suggest that targeting BNIP3L protein in wild-type p53 tumor suppressor colon cancer cells is an anticancer strategy activating iron depletion signaling and the mitophagy-related cell death pathway.

8. regulates mitophagy during hypoxia, whereas NIX is required for mitophagy during development of the erythroid lineage.

9. Nix protein positively regulates NF-kappaB activation in gliomas

10. The physical interaction of Mieap, BNIP3 and NIX at the mitochondrial outer membrane may play a critical role in the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix.

11. mitochondrial ROS and NIX are essential factors for Mieap-induced accumulation of lysosome-like organelles within mitochondria

12. Nix functions as an autophagy receptor, which mediates mitochondrial clearance after mitochondrial damage and during erythrocyte differentiation

13. NIX binds to TSAP6 in tumor cells and has a role in apoptosis

14. The proapoptotic factor Nix is a highly regulated effector of growth during terminal erythroid maturation.

15. Bnip3L, capable of attenuating tumorigenicity, mediates p53-dependent apoptosis under hypoxia.

16. pro-apoptotic proteins BNip3 and Nix are expressed in the human placenta

17. NIX is required for the selective elimination of mitochondria, however, because mitochondrial clearance, in the absence of NIX, is arrested at the stage of mitochondrial incorporation into autophagosomes and autophagosome maturation.

18. Results report that oxygen deprivation can activate the autophagic pathway in human cancer cell lines via AMPK activity, independent of HIF-1, BNIP3, and BNIP3L.

19. Homozygous deletions in a number of biologically important genes were found in prostate cancer cell lines, including PPP2R2A and BNIP3L identified in this study.

20. Results suggest that hypoxia-induced autophagy via BNIP3 and BNIP3L is clearly a survival mechanism that promotes tumor progression.

Mouse (Murine) BCL2/adenovirus E1B 19kDa Interacting Protein 3-Like (BNIP3L) interaction partners

1. NIX-mediated mitophagy is suppressed in proteinuric conditions and is responsible for proteinuria- induced cell apoptosis, which is consistent with previous evidence that excess albumin uptake inhibits autophagy in renal tubules and contributes to progressive tubular injury.

2. Bnip3l knockout (bnip3l(-/-)) impaired mitophagy and aggravated cerebral I-R (ischemia-reperfusion) injury in mice, which can be rescued by BNIP3L overexpression. The rescuing effects of BNIP3L overexpression can be observed in park2(-/-) mice, which showed mitophagy deficiency after I-R.

3. mitophagy is dependent on the mitochondrial outer membrane receptor BNIP3L/NIX but not on mitochondrial membrane potential (DeltaPsim) dissipation and functions in an important role during the reprogramming process.

4. studies highlight a new hypoxia-induced pathway in which NANOG activates BNIP3L expression, contributing to autophagy induction in hypoxic tumor cells and their resistance to killing by CTL

5. miR-30e protects mitochondria and podocytes from aldosterone induced apoptosis by targeting BNIP3L expression.

6. Bnip3L and caspase-12 identified by the PCR arrays at both catagen stages were additionally localized using immunofluorescence and were reported in physiological hair development for the first time.

7. our study demonstrates that BNIP3L, as a substrate of PARK2, promotes mitophagy in the PINK1/PARK2 pathway associated with PD pathogenesis.

8. role in the generation of robust NK cell memory in the process of mitophagy during viral infection

9. Suggest Nix is a novel mediator of norepinephrine-induced fibrosis.

10. MicroRNA-137 has a role in inhibiting mitophagy via regulation of two mitophagy receptors FUNDC1 and NIX

11. -stimulated cytoplasmic-nuclear shuttling of the alternately spliced non-mitochondrial Nix isoform and uncover a role for sNix as a modulator of TNFalpha/NFkappaB-stimulated cardiac gene expression

12. BNIP3L activity localizes to a small region in its cytoplasmic domain, the minimal essential region (MER).

13. These results establish Nix as a critical mediator of beta cell apoptosis and programmed necrosis in Pdx1-deficient diabetes.

14. molecular events responsible for the different phases of mitophagy and placed Nix upstream of the events

15. Mitochondrial Nix activates Bax/Bak- and caspase-dependent apoptosis, whereas ER-Nix activates Bax/Bak-independent, MPTP-dependent necrosis.

16. Nix functions as an autophagy receptor, which mediates mitochondrial clearance after mitochondrial damage and during erythrocyte differentiation

17. induced in cardiac hypertrophy and triggers apoptotic cardiomyopathy

18. Up-regulation of myocardial Nix and BNip3 is associated with apoptosis in cardiac hypertrophy and ischemia, respectively.

19. Nix promotes cell death via interaction with POSH and activation of the JNK/c-Jun pathway and that Nix protein is induced and contributes to cell death in a cellular model of Parkinson disease

20. Nix is identified as the critical proapoptotic mediator within the erythrocyte lineage; Nix null mice are viable and fertile.