Parkin and PINK1 Patient iPSC-Derived Midbrain Dopamine Neurons Exhibit Mitochondrial Dysfunction and α-Synuclein Accumulation. - Wikidata - wikimedia - TriplyDB

Parkin and PINK1 Patient iPSC-Derived Midbrain Dopamine Neurons Exhibit Mitochondrial Dysfunction and α-Synuclein Accumulation.

Parkin and PINK1 Patient iPSC-Derived Midbrain Dopamine Neurons Exhibit Mitochondrial Dysfunction and α-Synuclein Accumulation.

http://www.wikidata.org/entity/Q37337917

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PINK1/Parkin-Dependent Mitochondrial Surveillance: From Pleiotropy to Parkinson's Disease.Induced Pluripotent Stem Cell Neuronal Models for the Study of Autophagy Pathways in Human Neurodegenerative Disease.Parkin-phosphoubiquitin complex reveals cryptic ubiquitin-binding site required for RBR ligase activity.Ubiquitin and Parkinson's disease through the looking glass of genetics.The Endoplasmic Reticulum Unfolded Protein Response in Neurodegenerative Disorders and Its Potential Therapeutic Significance Inappropriate trafficking of damaged mitochondria in Parkinson's disease.Oxidative stress and cellular pathologies in Parkinson's disease.Shatavarin IV elicits lifespan extension and alleviates Parkinsonism in Caenorhabditis elegans.iPS cells in the study of PD molecular pathogenesis.MicroRNA‑138‑5p regulates neural stem cell proliferation and differentiation in vitro by targeting TRIP6 expression.SLP-2 interacts with Parkin in mitochondria and prevents mitochondrial dysfunction in Parkin-deficient human iPSC-derived neurons and Drosophila.Age-Related Epigenetic Derangement upon Reprogramming and Differentiation of Cells from the Elderly.A Comprehensive Atlas of E3 Ubiquitin Ligase Mutations in Neurological Disorders.Current perspective of mitochondrial biology in Parkinson's disease.Modeling Neuropsychiatric and Neurodegenerative Diseases With Induced Pluripotent Stem Cells.Dysregulation of the autophagic-lysosomal pathway in Gaucher and Parkinson's disease.Mfn2 ubiquitination by PINK1/parkin gates the p97-dependent release of ER from mitochondria to drive mitophagy.HSP90-incorporating chaperome networks as biosensor for disease-related pathways in patient-specific midbrain dopamine neurons T-type Calcium Channels Determine the Vulnerability of Dopaminergic Neurons to Mitochondrial Stress in Familial Parkinson Disease Modeling Parkinson's Disease Using Patient-specific Induced Pluripotent Stem Cells

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Parkin and PINK1 Patient iPSC-Derived Midbrain Dopamine Neurons Exhibit Mitochondrial Dysfunction and α-Synuclein Accumulation.

http://www.wikidata.org/entity/Q37337917

description

article científic

@ca

article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 15 September 2016

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

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name

Parkin and PINK1 Patient iPSC- ...... and α-Synuclein Accumulation.

@en

Parkin and PINK1 Patient iPSC- ...... and α-Synuclein Accumulation.

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type

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Parkin and PINK1 Patient iPSC- ...... and α-Synuclein Accumulation.

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Parkin and PINK1 Patient iPSC- ...... and α-Synuclein Accumulation.

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prefLabel

Parkin and PINK1 Patient iPSC- ...... and α-Synuclein Accumulation.

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Parkin and PINK1 Patient iPSC- ...... and α-Synuclein Accumulation.

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J.STEMCR.2016.08.012

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Stem Cell Reports

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Parkin and PINK1 Patient iPSC- ...... and α-Synuclein Accumulation.

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Ana Mrejeru

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Dimitri Krainc

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Eugene V Mosharov

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Jae-Won Shim

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John Graziotto

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Joseph R Mazzulli

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Lesly Puspita

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Parvin Valiulahi

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Sarah Kishinevsky

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Sun Young Chung

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P2860

PINK1 is selectively stabilized on impaired mitochondria to activate Parkin

Parkinson's disease: from monogenic forms to genetic susceptibility factors

LRRK2 mutant iPSC-derived DA neurons demonstrate increased susceptibility to oxidative stress

Mitochondrial Parkin recruitment is impaired in neurons derived from mutant PINK1 induced pluripotent stem cells

Parkin controls dopamine utilization in human midbrain dopaminergic neurons derived from induced pluripotent stem cells

Gaucher disease glucocerebrosidase and α-synuclein form a bidirectional pathogenic loop in synucleinopathies

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

Hereditary early-onset Parkinson's disease caused by mutations in PINK1

Pharmacological rescue of mitochondrial deficits in iPSC-derived neural cells from patients with familial Parkinson's disease.

α-Synuclein occurs physiologically as a helically folded tetramer that resists aggregation

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664-677

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scholarly article

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10.1016/J.STEMCR.2016.08.012

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4

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