Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency.
about
Three novel collagen VI chains, alpha4(VI), alpha5(VI), and alpha6(VI)Monoamine oxidase B prompts mitochondrial and cardiac dysfunction in pressure overloaded heartsPhysical exercise stimulates autophagy in normal skeletal muscles but is detrimental for collagen VI-deficient musclesCyclosporin A corrects mitochondrial dysfunction and muscle apoptosis in patients with collagen VI myopathiesCollagen VI related muscle disordersThe mitochondrial fission protein hFis1 requires the endoplasmic reticulum gateway to induce apoptosisThe beneficial role of proteolysis in skeletal muscle growth and stress adaptationRole of Inflammation in Muscle Homeostasis and MyogenesisA TALEN-Exon Skipping Design for a Bethlem Myopathy Model in ZebrafishRemodeling of Mitochondrial Flashes in Muscular Development and Dystrophy in ZebrafishPhoto-induction and automated quantification of reversible mitochondrial permeability transition pore opening in primary mouse myotubesMuscle-specific Drp1 overexpression impairs skeletal muscle growth via translational attenuation.Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophyInsights into the key roles of proteoglycans in breast cancer biology and translational medicineHanging on for the ride: adhesion to the extracellular matrix mediates cellular responses in skeletal muscle morphogenesis and diseaseThe OPA1-dependent mitochondrial cristae remodeling pathway controls atrophic, apoptotic, and ischemic tissue damageA novel deletion in the GTPase domain of OPA1 causes defects in mitochondrial morphology and distribution, but not in functionCOL4A1 mutations cause ocular dysgenesis, neuronal localization defects, and myopathy in mice and Walker-Warburg syndrome in humansA method for the direct identification of differentiating muscle cells by a fluorescent mitochondrial dyeA mouse model for dominant collagen VI disorders: heterozygous deletion of Col6a3 Exon 16Modulation of F0F1-ATP synthase activity by cyclophilin D regulates matrix adenine nucleotide levelsRecent advances using zebrafish animal models for muscle disease drug discoveryPhosphate is essential for inhibition of the mitochondrial permeability transition pore by cyclosporin A and by cyclophilin D ablationSelective actions of mitochondrial fission/fusion genes on metabolism-secretion coupling in insulin-releasing cellsCorrelated three-dimensional light and electron microscopy reveals transformation of mitochondria during apoptosis.Proteomics analysis of human skeletal muscle reveals novel abnormalities in obesity and type 2 diabetes.Collagen VI protects neurons against Abeta toxicity.Chronic inhibition of phosphodiesterase 5 with tadalafil attenuates mitochondrial dysfunction in type 2 diabetic hearts: potential role of NO/SIRT1/PGC-1α signaling.Monoamine oxidases as sources of oxidants in the heartAdipocyte-derived collagen VI affects early mammary tumor progression in vivo, demonstrating a critical interaction in the tumor/stroma microenvironmentHuman adipose-derived stem cell transplantation as a potential therapy for collagen VI-related congenital muscular dystrophyDistinct functions of junD in cardiac hypertrophy and heart failureMechanical and electrophysiological properties of the sarcolemma of muscle fibers in two murine models of muscle dystrophy: col6a1-/- and mdxZebrafish models of collagen VI-related myopathiesA systems biology approach identifies molecular networks defining skeletal muscle abnormalities in chronic obstructive pulmonary diseaseCancer stem cells from epithelial ovarian cancer patients privilege oxidative phosphorylation, and resist glucose deprivation.The intriguing regulators of muscle mass in sarcopenia and muscular dystrophy.Chronic treatment with long acting phosphodiesterase-5 inhibitor tadalafil alters proteomic changes associated with cytoskeletal rearrangement and redox regulation in Type 2 diabetic hearts.The collagen VI-related myopathies Ullrich congenital muscular dystrophy and Bethlem myopathy.Monoamine oxidase inhibition prevents mitochondrial dysfunction and apoptosis in myoblasts from patients with collagen VI myopathies.
P2860
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P2860
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency.
@en
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency.
@nl
type
label
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency.
@en
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency.
@nl
prefLabel
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency.
@en
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency.
@nl
P2093
P50
P356
P1433
P1476
Mitochondrial dysfunction and apoptosis in myopathic mice with collagen VI deficiency
@en
P2093
Carlo Reggiani
Dino Volpin
Giorgio M Bressan
Natascha Bergamin
Paolo Bonaldo
Patrizia Sabatelli
William A Irwin
P2888
P304
P356
10.1038/NG1270
P407
P577
2003-11-16T00:00:00Z