The Quest for the Identification of Genetic Variants in Unexplained Cardiac Arrest and Idiopathic Ventricular Fibrillation
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Vyšlo v časopise:
The Quest for the Identification of Genetic Variants in Unexplained Cardiac Arrest and Idiopathic Ventricular Fibrillation. PLoS Genet 9(4): e32767. doi:10.1371/journal.pgen.1003480
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Perspective
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.pgen.1003480
Souhrn
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Zdroje
1. NakanoY, ChayamaK, OchiH, ToshishigeM, HayashidaY, et al. (2013) A nonsynonymous polymorphism in Semaphorin 3A as a risk factor for human unexplained cardiac arrest with documented ventricular fibrillation. PLoS Genet 9: e1003364 doi:10.1371/journal.pgen.1003364.
2. BezzinaCR, PazokiR, BardaiA, MarsmanRF, De JongJS, et al. (2010) Genome-wide association study identifies a susceptibility locus at 21q21 for ventricular fibrillation in acute myocardial infarction. Nat Genet 42: 688–691.
3. ArkingDE, JunttilaMJ, GoyetteP, Huertas-VazquezA, EijgelsheimM, et al. (2011) Identification of a sudden cardiac death susceptibility locus at 2q24.2 through genome-wide association in European ancestry individuals. PLoS Genet 7: e1002158 doi:10.1371/journal.pgen.1002158.
4. Van der WerfC, Van LangenIM, WildeAA (2010) Sudden death in the young: what do we know about it and how to prevent? Circ Arrhythm Electrophysiol 3: 96–104.
5. AldersM, KoopmannTT, ChristiaansI, PostemaPG, BeekmanL, et al. (2009) Haplotype-sharing analysis implicates chromosome 7q36 harboring DPP6 in familial idiopathic ventricular fibrillation. Am J Hum Genet 84: 468–476.
6. IedaM, KanazawaH, KimuraK, HattoriF, IedaY, et al. (2007) Sema3a maintains normal heart rhythm through sympathetic innervation patterning. Nat Med 13: 604–612.
7. KanekoS, IwanamiA, NakamuraM, KishinoA, KikuchiK, et al. (2006) A selective Sema3A inhibitor enhances regenerative responses and functional recovery of the injured spinal cord. Nat Med 12: 1380–1389.
8. HanchateNK, GiacobiniP, LhuillierP, ParkashJ, EspyC, et al. (2012) SEMA3A, a gene involved in axonal pathfinding, is mutated in patients with Kallmann syndrome. PLoS Genet 8: e1002896 doi:10.1371/journal.pgen.1002896.
Štítky
Genetika Reprodukčná medicínaČlánok vyšiel v časopise
PLOS Genetics
2013 Číslo 4
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