Results 11 to 20 of about 19,187 (211)

BNIP3 in melanoma: isn’t it IRONic? [PDF]

open access: yesMolecular & Cellular Oncology, 2021
Melanoma cells exploit mitophagy and hypoxia signaling to promote their growth. In a recent study, we found that loss of B-cell lymphoma 2 (BCL-2)/adenovirus E1B 19kDa protein-interacting protein 3 (BNIP3) curbed Hypoxia Inducible Factor 1 alpha (HIF-1α)
Mónica Vara-Pérez, Patrizia Agostinis
doaj   +3 more sources

ULK1 promotes mitophagy via phosphorylation and stabilization of BNIP3 [PDF]

open access: yesScientific Reports, 2021
UNC51-like kinase-1 (ULK1) is the catalytic component of the autophagy pre-initiation complex that stimulates autophagy via phosphorylation of ATG14, BECLN1 and other autophagy proteins.
Logan P. Poole   +3 more
doaj   +4 more sources

Enhancing lysosome biogenesis attenuates BNIP3-induced cardiomyocyte death [PDF]

open access: yesAutophagy, 2012
Hypoxia-inducible pro-death protein BNIP3 (BCL-2/adenovirus E1B 19-kDa interacting protein 3), provokes mitochondrial permeabilization causing cardiomyocyte death in ischemia-reperfusion injury.
Diwan, Abhinav   +3 more
core   +6 more sources

TAp73 transcriptionally represses BNIP3 expression [PDF]

open access: yesCell Cycle, 2015
TAp73 is a tumor suppressor transcriptional factor, belonging to p53 family. Alteration of TAp73 in tumors might lead to reduced DNA damage response, cell cycle arrest and apoptosis. Carcinogen-induced TAp73−/− tumors display also increased angiogenesis, associated to hyperactivition of hypoxia inducible factor signaling.
Petrova, V   +7 more
openaire   +4 more sources

BNIP3-Dependent Mitophagy via PGC1α Promotes Cartilage Degradation [PDF]

open access: yesCells, 2021
Since mitochondria are suggested to be important regulators in maintaining cartilage homeostasis, turnover of mitochondria through mitochondrial biogenesis and mitochondrial degradation may play an important role in the pathogenesis of osteoarthritis (OA).
Deokha Kim, Jinsoo Song, Eun-Jung Jin
openaire   +3 more sources

EIF4A3-Induced circ-BNIP3 Aggravated Hypoxia-Induced Injury of H9c2 Cells by Targeting miR-27a-3p/BNIP3 [PDF]

open access: yesMolecular Therapy - Nucleic Acids, 2020
Acute myocardial infarction (AMI) results from long-term diminished blood supply diminishment (ischemia) to the heart, and the main reason for ischemia is hypoxia. BCL2 interaction protein 3 (BNIP3) can be upregulated by hypoxia and participates in the mediation of hypoxia-activated apoptosis in cardiac myocyte death.
Li, Yansong   +4 more
openaire   +2 more sources

BNIP3 phosphorylation by JNK1/2 promotes mitophagy via enhancing its stability under hypoxia

open access: yesCell Death and Disease, 2022
Mitophagy is an important metabolic mechanism that modulates mitochondrial quality and quantity by selectively removing damaged or unwanted mitochondria.
Yun-Ling He   +11 more
doaj   +1 more source

Tumor suppressor functions of BNIP3 and mitophagy [PDF]

open access: yesAutophagy, 2015
There is a growing realization that tumor cells rely on healthy mitochondria to promote their growth under changing microenvironmental stresses and do so by dynamically modulating both their mitochondrial mass and state of mitochondrial fusion. Our recent work adds to this appreciation by showing that the mitophagy receptor BNIP3 functions as a tumor ...
Aparajita H, Chourasia, Kay F, Macleod
openaire   +2 more sources

IGF-1 Signalling Regulates Mitochondria Dynamics and Turnover through a Conserved GSK-3β–Nrf2–BNIP3 Pathway

open access: yesCells, 2020
The Insulin-like Growth Factor I (IGF-1) signalling pathway is essential for cell growth and facilitates tumourogenic processes. We recently reported that IGF-1 induces a transcriptional programme for mitochondrial biogenesis, while also inducing ...
Sarah Riis   +2 more
doaj   +1 more source

Phosphorylation of the BNIP3 C-Terminus Inhibits Mitochondrial Damage and Cell Death without Blocking Autophagy. [PDF]

open access: yesPLoS ONE, 2015
BNIP3 is a dual function protein, able to activate autophagy and induce cell death. Upon expression of BNIP3, which is upregulated by hypoxia, the protein induces mitochondrial dysfunction, often leading to cell death.
Katherine E Liu, William A Frazier
doaj   +1 more source

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