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Short mitochondrial ARF triggers Parkin/PINK1-dependent mitophagy
Grenier K, et al.
The Journal of Biological Chemistry (2014)
Jean-Philippe Leduc-Gaudet et al.
Oncotarget, 6(20), 17923-17937 (2015-06-09)
Skeletal muscle aging is associated with a progressive decline in muscle mass and strength, a process termed sarcopenia. Evidence suggests that accumulation of mitochondrial dysfunction plays a causal role in sarcopenia, which could be triggered by impaired mitophagy. Mitochondrial function
Yoshiyuki Ikeda et al.
Circulation research, 116(2), 264-278 (2014-10-22)
Both fusion and fission contribute to mitochondrial quality control. How unopposed fusion affects survival of cardiomyocytes and left ventricular function in the heart is poorly understood. We investigated the role of dynamin-related protein 1 (Drp1), a GTPase that mediates mitochondrial
Benjamin P Woodall et al.
JCI insight, 5 (2019-04-17)
The E3 ubiquitin ligase Parkin plays an important role in regulating clearance of dysfunctional or unwanted mitochondria in tissues, including the heart. However, whether Parkin also functions to prevent cardiac aging by maintaining a healthy population of mitochondria is still
Ana Paula Arruda et al.
Nature medicine, 20(12), 1427-1435 (2014-11-25)
Proper function of the endoplasmic reticulum (ER) and mitochondria is crucial for cellular homeostasis, and dysfunction at either site has been linked to pathophysiological states, including metabolic diseases. Although the ER and mitochondria play distinct cellular roles, these organelles also
Catharina M van Rij et al.
Cancer biotherapy & radiopharmaceuticals, 29(8), 323-329 (2014-09-17)
TROP-2 is a pancarcinoma marker that is expressed at high levels in many epithelial cancers, including prostate cancer (PC). The trivalent bispecific antibody TF12 (anti-TROP2 × anti-HSG [histamine-succinyl-glycine]) has shown to effectively target PC. In this study, the efficacy of
Lance R Todd et al.
Molecular biology of the cell, 21(7), 1225-1236 (2010-02-12)
The relationship of mitochondrial dynamics and function to pluripotency are rather poorly understood aspects of stem cell biology. Here we show that growth factor erv1-like (Gfer) is involved in preserving mouse embryonic stem cell (ESC) mitochondrial morphology and function. Knockdown
Yong-Shiou Lin et al.
Biomedicines, 10(2) (2022-02-26)
Although the effects of growth hormone (GH) therapy on spinocerebellar ataxia type 3 (SCA3) have been examined in transgenic SCA3 mice, it still poses a nonnegligible risk of cancer when used for a long term. This study investigated the efficacy
Mitsuji Moriya et al.
Human molecular genetics, 24(25), 7349-7360 (2015-10-17)
Activation of the RAS pathway has been implicated in oncogenesis and developmental disorders called RASopathies. Germline mutations in BRAF have been identified in 50-75% of patients with cardio-facio-cutaneous (CFC) syndrome, which is characterized by congenital heart defects, distinctive facial features
Takuma Uo et al.
Experimental neurology, 218(2), 274-285 (2009-05-19)
Mitochondria exist as dynamic networks that are constantly remodeled through the opposing actions of fusion and fission proteins. Changes in the expression of these proteins alter mitochondrial shape and size, and may promote or inhibit the propagation of apoptotic signals.
Martin Picard et al.
Journal of applied physiology (Bethesda, Md. : 1985), 118(9), 1161-1171 (2015-03-15)
The diaphragm is a unique skeletal muscle designed to be rhythmically active throughout life, such that its sustained inactivation by the medical intervention of mechanical ventilation (MV) represents an unanticipated physiological state in evolutionary terms. Within a short period after
Jin-Yuan Lin et al.
Frontiers in immunology, 9, 1477-1477 (2018-07-19)
This study aimed to determine whether high tidal volume (HTV) induce mitochondria damage and mitophagy, contributing to the release of mitochondrial DNA (mtDNA). Another aim of the present study was to investigate the role and mechanism of mtDNA in ventilator-induced
Chien-Min Hung et al.
Science advances, 7(15) (2021-04-09)
The serine/threonine kinase ULK1 mediates autophagy initiation in response to various cellular stresses, and genetic deletion of ULK1 leads to accumulation of damaged mitochondria. Here we identify Parkin, the core ubiquitin ligase in mitophagy, and PARK2 gene product mutated in
Yoshihiro Uchikado et al.
Frontiers in cardiovascular medicine, 8, 788655-788655 (2021-12-07)
Lectin-like oxidized low-density lipoprotein (ox-LDL) causes vascular senescence and atherosclerosis. It has been reported that ox-LDL scavenger receptor-1 (LOX-1) is associated with the angiotensin II type 1 receptor (AT1R). While mitochondria play a crucial role in the development of vascular
Makiko Kihara et al.
PloS one, 9(7), e103928-e103928 (2014-08-01)
Itm2a is a type II transmembrane protein with a BRICHOS domain. We investigated the temporospatial mRNA and protein expression patterns of Itm2a in the developing lower first molar, and examined the subcellular localization of Itm2a in murine dental epithelial (mDE6)
Benoit J Gentil et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 26(3), 1194-1203 (2011-12-14)
Intermediate filaments serve important structural roles, but other cellular functions are increasingly recognized. This study demonstrated normal function of the low-molecular-weight neurofilament protein (NFL) in mitochondrial dynamics and disruption in Charcot-Marie-Tooth disease (CMT) due to mutations in the Nefl gene.
Hideaki Tagashira et al.
Biochimica et biophysica acta, 1840(12), 3320-3334 (2014-09-02)
Amyotrophic lateral sclerosis (ALS) is a disease caused by motor neuron degeneration. Recently, a novel SIGMAR1 gene variant (p.E102Q) was discovered in some familial ALS patients. We address mechanisms underlying neurodegeneration caused by the mutation using Neuro2A cells overexpressing σ1R(E102Q)
Cecília García-Pérez et al.
American journal of physiology. Heart and circulatory physiology, 301(5), H1907-H1915 (2011-08-23)
Propagation of ryanodine receptor (RyR2)-derived Ca(2+) signals to the mitochondrial matrix supports oxidative ATP production or facilitates mitochondrial apoptosis in cardiac muscle. Ca(2+) transfer likely occurs locally at focal associations of the sarcoplasmic reticulum (SR) and mitochondria, which are secured
Mitofusin 2 expression dominates over mitofusin 1 exclusively in mouse dorsal root ganglia - a possible explanation for peripheral nervous system involvement in Charcot-Marie-Tooth 2A.
Kawalec, et al.
Folia Neuropathologica, 52, 436-442 (2019)
Jonathan P Little et al.
Journal of applied physiology (Bethesda, Md. : 1985), 111(6), 1554-1560 (2011-08-27)
Low-volume high-intensity interval training (HIT) is emerging as a time-efficient exercise strategy for improving health and fitness. This form of exercise has not been tested in type 2 diabetes and thus we examined the effects of low-volume HIT on glucose
Rajat Puri et al.
Nature communications, 10(1), 3645-3645 (2019-08-15)
Chronic mitochondrial stress associates with major neurodegenerative diseases. Recovering stressed mitochondria constitutes a critical step of mitochondrial quality control and thus energy maintenance in early stages of neurodegeneration. Here, we reveal Mul1-Mfn2 pathway that maintains neuronal mitochondrial integrity under stress
Robert H Baloh et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 27(2), 422-430 (2007-01-12)
Mutations in the mitochondrial fusion protein mitofusin 2 (MFN2) are the most commonly identified cause of Charcot-Marie-Tooth type 2 (CMT2), a dominantly inherited disease characterized by degeneration of peripheral sensory and motor axons. However, the mechanism by which mutations in
Mamta Rai et al.
Journal of cell science, 127(Pt 1), 191-203 (2013-11-08)
Mitochondrial biogenesis and morphological changes are associated with tissue-specific functional demand, but the factors and pathways that regulate these processes have not been completely identified. A lack of mitochondrial fusion has been implicated in various developmental and pathological defects. The
Gloria M Palomo et al.
EMBO molecular medicine, 10(10) (2018-08-22)
Mutant Cu/Zn superoxide dismutase (SOD1) causes mitochondrial alterations that contribute to motor neuron demise in amyotrophic lateral sclerosis (ALS). When mitochondria are damaged, cells activate mitochondria quality control (MQC) mechanisms leading to mitophagy. Here, we show that in the spinal
Shuangxi Li et al.
Cell reports, 32(5), 107989-107989 (2020-08-07)
Amyotrophic lateral sclerosis (ALS) manifests pathological changes in motor neurons and various other cell types. Compared to motor neurons, the contribution of the other cell types to the ALS phenotypes is understudied. G4C2 repeat expansion in C9ORF72 is the most
Nicholas R Wawrzyniak et al.
Oncotarget, 7(33), 52695-52709 (2016-07-23)
Fatigue is a symptom of many diseases, but it can also manifest as a unique medical condition, such as idiopathic chronic fatigue (ICF). While the prevalence of ICF increases with age, mitochondrial content and function decline with age, which may
Kiyoung Kim et al.
Life (Basel, Switzerland), 11(1) (2021-01-23)
Although mitochondrial dysfunction is associated with the development and progression of diabetic nephropathy (DN), its mechanisms are poorly understood, and it remains debatable whether mitochondrial morphological change is a cause of DN. In this study, a Drosophila DN model was
Gian-Luca McLelland et al.
eLife, 7 (2018-04-21)
Despite their importance as signaling hubs, the function of mitochondria-ER contact sites in mitochondrial quality control pathways remains unexplored. Here we describe a mechanism by which Mfn2, a mitochondria-ER tether, gates the autophagic turnover of mitochondria by PINK1 and parkin.
Hepatic HKDC1 Expression Contributes to Liver Metabolism.
Pusec, et al.
Endocrinology, 160, 313-330 (2020)
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