Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway - sprookjes - yvandenbroek - TriplyDB

Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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Recent advances in understanding the role of lamins in health and disease Repression of the Antioxidant NRF2 Pathway in Premature Aging The "inherent vice" in the anti-angiogenic theory may cause the highly metastatic cancer to spread more aggressively.LMNA Sequences of 60,706 Unrelated Individuals Reveal 132 Novel Missense Variants in A-Type Lamins and Suggest a Link between Variant p.G602S and Type 2 Diabetes A Drosophila model of dominant inclusion body myopathy type 3 shows diminished myosin kinetics that reduce muscle power and yield myofibrillar defects.Activation of the Keap1/Nrf2 stress response pathway in autophagic vacuolar myopathies Isolation of Intermediate Filament Proteins from Multiple Mouse Tissues to Study Aging-associated Post-translational Modifications.Responses to reductive stress in the cardiovascular system.Reductive Stress in Inflammation-Associated Diseases and the Pro-Oxidant Effect of Antioxidant Agents.Expression Profiling of Differentiating Emerin-Null Myogenic Progenitor Identifies Molecular Pathways Implicated in Their Impaired Differentiation.Messages from the voices within: regulation of signaling by proteins of the nuclear lamina.Protein sequestration at the nuclear periphery as a potential regulatory mechanism in premature aging.Increasing autophagy and blocking Nrf2 suppress laminopathy-induced age-dependent cardiac dysfunction and shortened lifespan.Invertebrate models of lamin diseases.Defective protein repair under methionine sulfoxide A deletion drives autophagy and ARE-dependent gene transcription.Non-farnesylated B-type lamin can tether chromatin inside the nucleus and its chromatin interaction requires the Ig-fold region.Phosphorylated TDP-43 (pTDP-43) aggregates in the axial skeletal muscle of patients with sporadic and familial amyotrophic lateral sclerosis.Skeletal Muscle Dystrophy mutant of lamin A alters the structure and dynamics of the Ig fold domain

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P2860

Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

http://www.wikidata.org/entity/Q28547400

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2015年の論文

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2015年論文

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2015年論文

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Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

@ast

Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

@ast

Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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JOURNAL.PGEN.1005231

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Myopathic lamin mutations cause reductive stress and activate the nrf2/keap-1 pathway

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Dylan A Thiemann

http://www.w3.org/2001/XMLSchema#string

George Dialynas

http://www.w3.org/2001/XMLSchema#string

Grant H Young

http://www.w3.org/2001/XMLSchema#string

Jan Lammerding

http://www.w3.org/2001/XMLSchema#string

Jessica M Ponce

http://www.w3.org/2001/XMLSchema#string

Monika Zwerger

http://www.w3.org/2001/XMLSchema#string

Om K Shrestha

http://www.w3.org/2001/XMLSchema#string

P2860

The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1

p62/SQSTM1 is a target gene for transcription factor NRF2 and creates a positive feedback loop by inducing antioxidant response element-driven gene transcription

Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts

Regulation of Drosophila metamorphosis by xenobiotic response regulators

The Ig-like structure of the C-terminal domain of lamin A/C, mutated in muscular dystrophies, cardiomyopathy, and partial lipodystrophy

Structure of the lamin A/C R482W mutant responsible for dominant familial partial lipodystrophy (FPLD)

Using NMRView to visualize and analyze the NMR spectra of macromolecules

NMRPipe: a multidimensional spectral processing system based on UNIX pipes

Laminopathies and the long strange trip from basic cell biology to therapy

The nuclear envelope at a glance

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e1005231

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scholarly article

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2738357

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10.1371/JOURNAL.PGEN.1005231

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5

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Lori L Wallrath

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2015-05-21T00:00:00Z

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275892870

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25996830

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4440730

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