Results 41 to 50 of about 13,811 (214)
Cerebral Ischemic Preconditioning Aggravates Death of Oligodendrocytes
Biomolecules, 2022 Neurodegeneration can benefit from ischemic preconditioning, a natural adaptive reaction to sublethal noxious stimuli. Although there is growing interest in advancing preconditioning to preserve brain function, preconditioning is not yet considered ...
Teng Guan +7 more
doaj +1 more source
BNIP3 promotes calcium and calpain-dependent cell death [PDF]
Life Sciences, 2015 Loss of cardiac muscle by programmed cell death contributes to the progression of ischemic heart disease. Hypoxia, metabolite waste buildup and energy depletion are components of ischemia which may initiate caspase dependent and independent cell death pathways.
Regina M, Graham +2 more
openaire +2 more sources
Regulation of Mitochondrial Integrity, Autophagy and Cell Survival by BNIP3 [PDF]
Autophagy, 2007 Understanding the role of BNIP3 in the systemic response to hypoxia has been complicated by conflicting results that indicate on the one hand that BNIP3 promotes cell death, and other data, including our own that BNIP3 is not sufficient for cell death, but rather plays a critical role in hypoxia-induced autophagy.
Kristin, Tracy, Kay F, Macleod
openaire +2 more sources
BNIP3 Upregulation Characterizes Cancer Cell Subpopulation With Increased Fitness and Proliferation
Frontiers in Oncology, 2022 BNIP3 is a BH3-only protein with both pro-apoptotic and pro-survival roles depending on the cellular context. It remains unclear how BNIP3 RNA level dictates cell fate decisions of cancer cells.
Yanyan Zhu +9 more
doaj +1 more source
Cloning of BNIP3h, a member of proapoptotic BNIP3 family genes [PDF]
Experimental & Molecular Medicine, 2001 Apoptosis is regulated by interaction of antiapoptotic Bcl-2 family proteins with various proapoptotic proteins, several of which are also members of the Bcl-2 family. BNIP3 (formerly NIP3) is a proapoptotic mitochondrial protein classified in the Bcl-2 family based on limited sequence homology-3 (BH3) domain and COOH-terminal transmembrane domain ...
M, Farooq +7 more
openaire +2 more sources
BMC Cancer, 2009 Background Bcl-2/adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) is a pro-apoptotic member of the Bcl-2 family induced under hypoxia. Low or absent expression has recently been described in human tumors, including gastrointestinal tumors, resulting ...
de Weger Roel A +5 more
doaj +1 more source
The ER membrane protein complex restricts mitophagy by controlling BNIP3 turnover
The EMBO Journal, 2023 Lysosomal degradation of autophagy receptors is a common proxy for selective autophagy. However, we find that two established mitophagy receptors, BNIP3 and BNIP3L/NIX, are constitutively delivered to lysosomes in an autophagy-independent manner.
Jose M Delgado +4 more
doaj +1 more source
C-terminal BNIP3 phosphorylation inhibits BNIP3-induced cell death.
, 2015 (A) Quantification of the percent of Annexin V positive cells 24 hr after induction of BNIP3 expression, analyzed by flow cytometry. Data is expressed as the average of 4 independent experiments.
William A. Frazier (759144) +1 more
core +1 more source
Bnip3-mediated defects in oxidative phosphorylation promote mitophagy [PDF]
Autophagy, 2011 The Bcl-2 proteins are best known as regulators of the intrinsic mitochondrial pathway of apoptosis. However, recent studies have demonstrated that they can also regulate autophagy. For many years, autophagy was considered to be a nonselective process where the autophagosomes randomly sequestered contents in the cytosol to supply the cells with amino ...
Robert L, Thomas +2 more
openaire +2 more sources
Methylated BNIP3 gene in colorectal cancer prognosis
Oncology Letters, 2010 The DNA methylation of apoptosis-related genes in various cancers contributes to the disruption of the apoptotic pathway and results in resistance to chemotherapeutic agents. Irinotecan (CPT-11) is one of the key chemotherapy drugs used to treat metastatic colorectal cancer (CRC).
Sayaka, Shimizu +12 more
openaire +3 more sources