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BNIP3L is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. Additionally we are shipping BCL2/adenovirus E1B 19kDa Interacting Protein 3-Like Antibodies (113) and BCL2/adenovirus E1B 19kDa Interacting Protein 3-Like Kits (1) and many more products for this protein.
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Data suggest that targeting BNIP3L protein in wild-type p53 tumor suppressor (show TP53 Proteins) colon cancer cells is an anticancer strategy activating iron depletion signaling and the mitophagy-related cell death pathway.
regulates mitophagy during hypoxia, whereas NIX is required for mitophagy during development of the erythroid lineage.
Nix protein positively regulates NF-kappaB (show NFKB1 Proteins) activation in gliomas
The physical interaction of Mieap (show SPATA18 Proteins), BNIP3 (show BNIP3 Proteins) 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.
mitochondrial ROS (show ROS1 Proteins) and NIX are essential factors for Mieap (show SPATA18 Proteins)-induced accumulation of lysosome-like organelles within mitochondria
Nix functions as an autophagy receptor, which mediates mitochondrial clearance after mitochondrial damage and during erythrocyte differentiation
NIX binds to TSAP6 (show STEAP3 Proteins) in tumor cells and has a role in apoptosis
The proapoptotic factor Nix is a highly regulated effector of growth during terminal erythroid maturation.
Bnip3L, capable of attenuating tumorigenicity, mediates p53 (show TP53 Proteins)-dependent apoptosis under hypoxia.
pro-apoptotic proteins BNip3 (show BNIP3 Proteins) and Nix are expressed in the human placenta
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.
our study demonstrates that BNIP3L, as a substrate of PARK2 (show PARK2 Proteins), promotes mitophagy in the PINK1 (show PINK1 Proteins)/PARK2 (show PARK2 Proteins) pathway associated with PD pathogenesis.
Suggest Nix is a novel mediator of norepinephrine-induced fibrosis.
MicroRNA-137 has a role in inhibiting mitophagy via regulation of two mitophagy receptors FUNDC1 (show FUNDC1 Proteins) and NIX
-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
BNIP3L activity localizes to a small region in its cytoplasmic domain, the minimal essential region (MER (show ERH Proteins)).
These results establish Nix as a critical mediator of beta cell apoptosis and programmed necrosis in Pdx1 (show PDX1 Proteins)-deficient diabetes.
molecular events responsible for the different phases of mitophagy and placed Nix upstream of the events
Mitochondrial Nix activates Bax (show BAX Proteins)/Bak (show BAK1 Proteins)- and caspase (show CASP3 Proteins)-dependent apoptosis, whereas ER-Nix activates Bax (show BAX Proteins)/Bak (show BAK1 Proteins)-independent, MPTP (show PTPN2 Proteins)-dependent necrosis.
This gene is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. It interacts with the E1B 19 kDa protein, which protects cells from virally-induced cell death. The encoded protein also interacts with E1B 19 kDa-like sequences of BCL2, another apoptotic protector. This protein counteracts the apoptotic inducer BNIP3 and may play a role in tumor suppression.
BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like
, BCL2/adenovirus E1B 19 kDa protein-interacting protein 3A
, BCL2/adenovirus E1B 19-kd protein-interacting protein 3a
, NIP3-like protein X
, adenovirus E1B19k-binding protein B5
, BCL2/adenovirus E1B 19kD-interacting protein 3-like
, BCL2/adenovirus E1B 19 kDa-interacting protein 3-like
, BCL2/adenovirus E1B 19kDa-interacting protein 3-like