About: Vincent Probst

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researcher ORCID ID = 0000-0002-5492-8619

Attributes	Values
rdf:type	Item
description	forskare (sv) ikertzailea (eu) 연구원 (ko) wetenschapper (nl) дослідник (uk) эрдэмтэн (mn) वैज्ञानिक (hi) изилдөөчү (ky) researcher ORCID ID = 0000-0002-5492-8619 (en)
rdfs:label	Vincent Probst (en) Vincent Probst (es) Vincent Probst (nl) Vincent Probst (ast)
skos:prefLabel	Vincent Probst (en) Vincent Probst (es) Vincent Probst (nl) Vincent Probst (ast)
name	Vincent Probst (en) Vincent Probst (es) Vincent Probst (nl) Vincent Probst (ast)
given name	wds:Q57612353-B6A22EF5-FA57-4DC0-8D87-8C5A643FFD43
given name	Vincent
instance of	wds:Q57612353-E5CD5F6E-0F15-4596-8ABD-8FA95235EF7F
instance of	Homo sapiens
doctoral student	wds:Q57612353-F1C60B7E-D885-45D1-B99E-68BBFEC90B26
doctoral student	Alban-Elouen Baruteau
occupation	wds:Q57612353-79FEFBCE-6187-4EE1-B32D-2459E341B3DD
sex or gender	wds:Q57612353-D608B89B-F3A4-4431-AD5D-AEF42FB2C5F8
ISNI	wds:Q57612353-DB10FB1C-3F0D-4260-BEB8-19F89AF9ECA4
VIAF ID	wds:Q57612353-0CDF1B1A-082D-4090-A565-2B143EDA177A
IdRef ID	wds:Q57612353-E6482684-924F-42F9-B53C-2BFBD009E3D3
date of birth	wds:Q57612353-F745E784-F9B6-481B-A054-E648822968D6
VIAF ID	http://viaf.org/viaf/173371442
IdRef ID	http://www.idref.fr/088101886/id
occupation	researcher
sex or gender	male
ISNI	0000000430808983
VIAF ID	173371442
IdRef ID	088101886
date of birth	1970-01-01 00:00:00Z (xsd:dateTime)
ORCID iD	wds:Q57612353-4410FC29-E420-4F9D-B424-54D992F0876A
ORCID iD	https://orcid.org/0000-0002-5492-8619
ORCID iD	0000-0002-5492-8619
ResearcherID	wds:Q57612353-F08ACC4C-15E2-4E95-A2F0-FA77BD124866
ResearcherID	D-4996-2015
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q57612353
is author of	KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron Long-term follow-up of patients with short QT syndrome Fine-scale human genetic structure in Western France Mutations in the gene encoding filamin A as a cause for familial cardiac valvular dystrophy. Monomorphic ventricular tachycardia due to Brugada syndrome successfully treated by hydroquinidine therapy in a 3-year-old child. Response to intravenous ajmaline: a retrospective analysis of 677 ajmaline challenges. Genotype-phenotype relationship in Brugada syndrome: electrocardiographic features differentiate SCN5A-related patients from non-SCN5A-related patients Dysfunction in ankyrin-B-dependent ion channel and transporter targeting causes human sinus node disease Defects in ankyrin-based membrane protein targeting pathways underlie atrial fibrillation Variable Na(v)1.5 protein expression from the wild-type allele correlates with the penetrance of cardiac conduction disease in the Scn5a(+/-) mouse model Sodium channel β1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humans Haploinsufficiency in combination with aging causes SCN5A-linked hereditary Lenègre disease Absence of triadin, a protein of the calcium release complex, is responsible for cardiac arrhythmia with sudden death in human Common variants at SCN5A-SCN10A and HEY2 are associated with Brugada syndrome, a rare disease with high risk of sudden cardiac death MOG1: a new susceptibility gene for Brugada syndrome. Cardiac conduction defects associate with mutations in SCN5A Sudden cardiac arrest associated with early repolarization SCN5A mutations and the role of genetic background in the pathophysiology of Brugada syndrome An international compendium of mutations in the SCN5A-encoded cardiac sodium channel in patients referred for Brugada syndrome genetic testing PQ segment depression in patients with short QT syndrome: a novel marker for diagnosing short QT syndrome? Desmosomal gene analysis in arrhythmogenic right ventricular dysplasia/cardiomyopathy: spectrum of mutations and clinical impact in practice Type of SCN5A mutation determines clinical severity and degree of conduction slowing in loss-of-function sodium channelopathies Are women with severely symptomatic brugada syndrome different from men? A connexin40 mutation associated with a malignant variant of progressive familial heart block type I Drugs and Brugada syndrome patients: review of the literature, recommendations, and an up-to-date website (www.brugadadrugs.org) Inherited progressive cardiac conduction disorders Parental electrocardiographic screening identifies a high degree of inheritance for congenital and childhood nonimmune isolated atrioventricular block Characteristics and long-term outcome of non-immune isolated atrioventricular block diagnosed in utero or early childhood: a multicentre study Long-term prognosis of individuals with right precordial ST-segment-elevation Brugada syndrome Outcome after implantation of a cardioverter-defibrillator in patients with Brugada syndrome: a multicenter study Multifocal ectopic Purkinje-related premature contractions: a new SCN5A-related cardiac channelopathy Genetic association study of QT interval highlights role for calcium signaling pathways in myocardial repolarization New Family With Catecholaminergic Polymorphic Ventricular Tachycardia Linked to the Triadin Gene Ventricular fibrillation in loop recorder memories in a patient with early repolarization syndrome. Early Repolarization Disease. Valvular dystrophy associated filamin A mutations reveal a new role of its first repeats in small-GTPase regulation Screening for copy number variation in genes associated with the long QT syndrome: clinical relevance. Prevalence of early repolarization pattern in inferolateral leads in patients with Brugada syndrome Familial aggregation of calcific aortic valve stenosis in the western part of France Usefulness of fetuin-A and C-reactive protein concentrations for prediction of outcome in acute coronary syndromes (from the French Registry of Acute ST-Elevation Non-ST-Elevation Myocardial Infarction [FAST-MI]). Value of the sodium-channel blocker challenge in Brugada syndrome Molecular genetics and functional anomalies in a series of 248 Brugada cases with 11 mutations in the TRPM4 channel Characteristics of recurrent ventricular fibrillation associated with inferolateral early repolarization role of drug therapy Dysfunction of the Voltage-Gated K+ Channel β2 Subunit in a Familial Case of Brugada Syndrome Testing the burden of rare variation in arrhythmia-susceptibility genes provides new insights into molecular diagnosis for Brugada syndrome Role of electrophysiological studies in predicting risk of ventricular arrhythmia in early repolarization syndrome. Prevalence and prognostic role of various conduction disturbances in patients with the Brugada syndrome Genetic association analyses highlight biological pathways underlying mitral valve prolapse Benign vs. malignant inferolateral early repolarization: Focus on the T wave Mitral valve disease--morphology and mechanisms Predictors for short-term progressive heart failure death in New York Heart Association II patients implanted with a cardioverter defibrillator—the EVADEF study Prevalence, characteristics, and prognosis role of type 1 ST elevation in the peripheral ECG leads in patients with Brugada syndrome.

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