Ontology highlight
ABSTRACT:
PROVIDER: PRJNA559556 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A model organism for the genus Oomycetes (water molds); causes Sudden Oak death
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Project description:Whole genome shotgun sequence project for the causative agent of Sudden Oak death
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Project description:Serum samples were collected postmortem from infants dying of Sudden Infant Death Syndrome.
2018-08-02 | MSV000082713 | GNPS
Project description:Excessive O-GlcNAcylation causes heart failure and sudden death
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Project description:Sudden unexplained death in childhood (SUDC) is death of a child over one year of age that is unexplained after review of clinical history, circumstances of death, and complete autopsy with ancillary testing. Multiple etiologies may cause SUDC, with parallels to sudden unexpected death in epilepsy (SUDEP) in SUDC with a history of febrile seizures, suggesting possible abnormalities in hippocampus and cortex. To identify molecular signaling pathways underlying SUDC, we performed label-free quantitative mass spectrometry on microdissected frontal cortex, hippocampal dentate gyrus (DG), and cornu ammonis (CA1-3) in SUDC (n=19) and pediatric control cases (n=19) with an explained cause of death.
2021-12-23 | MSV000088611 | MassIVE
Project description:Sudden cardiac death is the number one cause of death worldwide. Major causes of sudden cardiac death include myocardial infarction and cardiomyopathies. To develop novel therapeutic strategies, we need to identify key factors that are required for proper cardiac function and are dysregulated in the diseased heart. Under this notion, we found T-box 5 (TBX5), a transcription factor regarded solely in the context of congenital heart disease, to be downregulated in human diseased left ventricles. To investigate the effects of TBX5 loss in the adult heart, we generated an inducible ventricular cardiomyocyte specific knock-out mouse model (vTbx5KO). We performed integrative genome-wide chromatin occupancy and transcriptomic analysis and identified 47 downregulated transcripts in vTbx5KO that contain TBX5 active enhancers. The TBX5 targets in the ventricle included genes implicated in cardiac conduction and contraction (Gja1, Kcnj5, Kcng2, Cacna1g, Chrm2), cytoskeleton organization (Fstl4, Pdlim4, Emilin2, Cmya5) as well as cardiac protection upon stress (Fhl2, Gpr22, Fgf16). In line with this analysis, vTbx5KO mice presented cardiac conduction defects and arrhythmias at baseline as well as exacerbated cardiac remodeling upon Angiotensin II-induced hypertrophy. In conclusion, this study uncovers a novel protective role of TBX5 upon cardiac remodeling and renders TBX5 as an interesting therapeutic target.
2020-07-19 | GSE101614 | GEO
Project description:These samples include exome sequences of samples from patients who suffered Sudden Unexplained Death in Epilepsy
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Project description:Pathogens that cause soybean sudden death syndrome or bean root rot
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Project description:Pathological cardiac hypertrophy is unequivocally identified as an ominous escalation of hemodynamically stressful overload, ultimately heighten risk of sudden death as heart failure (HF) ensues. Here, we explored how dysregulated mitochondrial RNA (mtRNA) metabolism remodels mitochondrial bioenergetics and controls hypertrophic-phenotype cardiopathy in mice and humans. Utilizing targeted genetic approaches and in vivo functional imaging, we describe a potent cardiac pro-hypertrophic role for serine arginine protein kinase 3 (SRPK3), which is highly induced in myocardium upon hypertrophic stimuli. Adult extended expression of SRPK3 in cardiomyocytes (CMs) leads to spontaneously concentric hypertrophy and eventuates sudden cardiac death in mice.
2024-03-05 | GSE260494 | GEO