Globotriaosylceramide leads to K(Ca)3.1 channel dysfunction: a new insight into endothelial dysfunction in Fabry disease. - Wikidata - wikimedia - TriplyDB

Globotriaosylceramide leads to K(Ca)3.1 channel dysfunction: a new insight into endothelial dysfunction in Fabry disease.

Globotriaosylceramide leads to K(Ca)3.1 channel dysfunction: a new insight into endothelial dysfunction in Fabry disease.

http://www.wikidata.org/entity/Q53453652

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Electrocardiographic Changes and Arrhythmia in Fabry Disease KCa3.1 channels mediate the increase of cell migration and proliferation by advanced glycation endproducts in cultured rat vascular smooth muscle cells Prevalence of chronic kidney disease in fabry disease patients: Multicenter cross sectional study in Argentina.Impaired small fiber conduction in patients with Fabry disease: a neurophysiological case-control study Isolation and in vitro culture of vascular endothelial cells from mice Distributions of Globotriaosylceramide Isoforms, and Globotriaosylsphingosine and Its Analogues in an α-Galactosidase A Knockout Mouse, a Model of Fabry Disease.Altering sphingolipid composition with aging induces contractile dysfunction of gastric smooth muscle via K(Ca) 1.1 upregulation.KCa 3.1 upregulation preserves endothelium-dependent vasorelaxation during aging and oxidative stress Reduction of Plasma Globotriaosylsphingosine Levels After Switching from Agalsidase Alfa to Agalsidase Beta as Enzyme Replacement Therapy for Fabry Disease Endothelial nitric oxide synthase uncoupling and microvascular dysfunction in the mesentery of mice deficient in α-galactosidase A.Intermediate-Conductance-Ca2-Activated K Channel IKCa1 Is Upregulated and Promotes Cell Proliferation in Cervical Cancer Role of the potassium channel KCa3.1 in diabetic nephropathy.Fabry's disease: an example of cardiorenal syndrome type 5.Development of a model system for neuronal dysfunction in Fabry disease.Changes in Ionic Conductance Signature of Nociceptive Neurons Underlying Fabry Disease Phenotype.Hyperbaric environment up-regulates CD15s expression on leukocytes, down-regulates CD77 expression on renal cells and up-regulates CD34 expression on pulmonary and cardiac cells in rat.Contradictory Effects of Superoxide and Hydrogen Peroxide on KCa3.1 in Human Endothelial Cells Early Renal Involvement in a Girl with Classic Fabry Disease.Characterization of Human Dermal Fibroblasts in Fabry Disease.Major Organic Involvement in Women with Fabry Disease in Argentina.Fabry disease

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Globotriaosylceramide leads to K(Ca)3.1 channel dysfunction: a new insight into endothelial dysfunction in Fabry disease.

http://www.wikidata.org/entity/Q53453652

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2010 nî lūn-bûn

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2010年の論文

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年学术文章

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2010年學術文章

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2010年學術文章

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2010年學術文章

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name

Globotriaosylceramide leads to K

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Globotriaosylceramide leads to ...... dysfunction in Fabry disease.

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Globotriaosylceramide leads to K

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Globotriaosylceramide leads to K

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Globotriaosylceramide leads to ...... dysfunction in Fabry disease.

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Cardiovascular Research

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Globotriaosylceramide leads to ...... dysfunction in Fabry disease.

@en

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Eun-Nam Choi

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

Ji Aee Kim

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Jung-A Shin

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Ka Young Joo

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Ki-Hwan Han

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

Seonghee Park

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

Shinkyu Choi

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Suk Hyo Suh

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P2860

The phosphatidylinositol 3-phosphate phosphatase myotubularin- related protein 6 (MTMR6) is a negative regulator of the Ca2+-activated K+ channel KCa3.1

An atypical variant of Fabry's disease with manifestations confined to the myocardium

International Union of Pharmacology. LII. Nomenclature and molecular relationships of calcium-activated potassium channels

Cardiac manifestations of Anderson-Fabry disease: results from the international Fabry outcome survey.

Phosphatidylinositol 3-phosphate indirectly activates KCa3.1 via 14 amino acids in the carboxy terminus of KCa3.1.

Adeno-associated viral vector-mediated gene transfer results in long-term enzymatic and functional correction in multiple organs of Fabry mice.

Globotriaosylceramide induces oxidative stress and up-regulates cell adhesion molecule expression in Fabry disease endothelial cells.

Decreased nitric oxide bioavailability in a mouse model of Fabry disease.

Vascular dysfunction in the alpha-galactosidase A-knockout mouse is an endothelial cell-, plasma membrane-based defect.

The intermediate-conductance Ca2+ -activated K+ channel (KCa3.1) in vascular disease.

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290-299

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10.1093/CVR/CVQ333

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2

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89

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47534519

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20971723

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