cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7872236
title: gVCF_HG00231

description: 1000 Genomes gVCF mapped to hs37d5 for HG00231.
DOI: 10.6084/m9.figshare.7872236.v1
title: gVCF_HG00231

description: 1000 Genomes gVCF mapped to hs37d5 for HG00231.
DOI: 10.6084/m9.figshare.7872242.v1
title: Right Heart Catheterization During Exercise in Patients with COPD—An Overview of Clinical Results and Methodological Aspects

description: While right heart catheterization (RHC) at rest is the gold standard to assess pulmonary hemodynamics in patients with chronic obstructive pulmonary disease (COPD) and pulmonary hypertension (PH), the invasive measurement of exercise hemodynamics is less well established in this group. Since exercise hemodynamics are increasingly recognized as important clinical information in patients with PH, our goal was to review the literature in this field to provide a basis for clinical use, further studies, and future recommendations. We identified 69 studies (published since 1968) reporting RHC data in 2819 patients with COPD, of whom 2561 underwent exercise testing. Few studies simultaneously measured gas exchange during exercise. Overall, these studies showed large variations in the patient populations and research questions studied and the methods and definitions employed. Despite these limitations, the data consistently demonstrated the presence of precapillary PH at rest in up to 38% of patients with COPD. With exercise, a relevant proportion of patients developed an abnormal hemodynamic response, depending on the definition used. Furthermore, some studies assessed right ventricular function during exercise and showed a blunted increase in right ventricular ejection fraction. Drug effects and the impact of interventional procedures were also studied. Again, due to large variations in the patients studied and the methods used, firm conclusions are difficult to derive. Despite the limitations of this dataset, several recommendations with respect to technical aspects (body position, exercise protocol, and data acquisition) can be inferred for this challenging patient population and may be helpful for further studies or recommendations.
DOI: 10.6084/m9.figshare.7872224
title: gVCF_HG00141

description: 1000 Genomes gVCF mapped to hs37d5 for HG00141.
DOI: 10.6084/m9.figshare.7872227
title: gVCF_HG00189

description: 1000 Genomes gVCF mapped to hs37d5 for HG00189.
DOI: 10.6084/m9.figshare.7872230.v1
title: gVCF_HG00190

description: 1000 Genomes gVCF mapped to hs37d5 for HG00190.
DOI: 10.6084/m9.figshare.7872203
title: gVCF_HG00140

description: 1000 Genomes gVCF mapped to hs37d5 for HG00140.
DOI: 10.6084/m9.figshare.7872221
title: gVCF_HG00188

description: 1000 Genomes gVCF mapped to hs37d5 for HG00188.
DOI: 10.6084/m9.figshare.7872224.v1
title: gVCF_HG00141

description: 1000 Genomes gVCF mapped to hs37d5 for HG00141.
DOI: 10.6084/m9.figshare.7872227.v1
title: gVCF_HG00189

description: 1000 Genomes gVCF mapped to hs37d5 for HG00189.
DOI: 10.6084/m9.figshare.7872221.v1
title: gVCF_HG00188

description: 1000 Genomes gVCF mapped to hs37d5 for HG00188.
DOI: 10.6084/m9.figshare.7872143
title: gVCF_HG00186

description: 1000 Genomes gVCF mapped to hs37d5 for HG00186.
DOI: 10.6084/m9.figshare.7872149
title: gVCF_HG00187

description: 1000 Genomes gVCF mapped to hs37d5 for HG00187.
DOI: 10.6084/m9.figshare.7872203.v1
title: gVCF_HG00140

description: 1000 Genomes gVCF mapped to hs37d5 for HG00140.
DOI: 10.6084/m9.figshare.7872137
title: gVCF_HG00185

description: 1000 Genomes gVCF mapped to hs37d5 for HG00185.
DOI: 10.6084/m9.figshare.7872140
title: gVCF_HG00139

description: 1000 Genomes gVCF mapped to hs37d5 for HG00139.
DOI: 10.6084/m9.figshare.7872149.v1
title: gVCF_HG00187

description: 1000 Genomes gVCF mapped to hs37d5 for HG00187.
DOI: 10.6084/m9.figshare.7872137.v1
title: gVCF_HG00185

description: 1000 Genomes gVCF mapped to hs37d5 for HG00185.
DOI: 10.6084/m9.figshare.7872140.v1
title: gVCF_HG00139

description: 1000 Genomes gVCF mapped to hs37d5 for HG00139.
DOI: 10.6084/m9.figshare.7872143.v1
title: gVCF_HG00186

description: 1000 Genomes gVCF mapped to hs37d5 for HG00186.
DOI: 10.6084/m9.figshare.7872125
title: gVCF_HG00182

description: 1000 Genomes gVCF mapped to hs37d5 for HG00182.
DOI: 10.6084/m9.figshare.7872128
title: gVCF_HG00137

description: 1000 Genomes gVCF mapped to hs37d5 for HG00137.
DOI: 10.6084/m9.figshare.7872131
title: gVCF_HG00183

description: 1000 Genomes gVCF mapped to hs37d5 for HG00183.
DOI: 10.6084/m9.figshare.7872122
title: gVCF_HG00136

description: 1000 Genomes gVCF mapped to hs37d5 for HG00136.
DOI: 10.6084/m9.figshare.7872122.v1
title: gVCF_HG00136

description: 1000 Genomes gVCF mapped to hs37d5 for HG00136.
DOI: 10.6084/m9.figshare.7872125.v1
title: gVCF_HG00182

description: 1000 Genomes gVCF mapped to hs37d5 for HG00182.
DOI: 10.6084/m9.figshare.7872134
title: gVCF_HG00138

description: 1000 Genomes gVCF mapped to hs37d5 for HG00138.
DOI: 10.6084/m9.figshare.7872128.v1
title: gVCF_HG00137

description: 1000 Genomes gVCF mapped to hs37d5 for HG00137.
DOI: 10.6084/m9.figshare.7872131.v1
title: gVCF_HG00183

description: 1000 Genomes gVCF mapped to hs37d5 for HG00183.
DOI: 10.6084/m9.figshare.7872134.v1
title: gVCF_HG00138

description: 1000 Genomes gVCF mapped to hs37d5 for HG00138.
DOI: 10.6084/m9.figshare.7872116
title: gVCF_HG00133

description: 1000 Genomes gVCF mapped to hs37d5 for HG00133.
DOI: 10.6084/m9.figshare.7872119
title: gVCF_HG00181

description: 1000 Genomes gVCF mapped to hs37d5 for HG00181.
DOI: 10.6084/m9.figshare.7872107
title: gVCF_HG00180

description: 1000 Genomes gVCF mapped to hs37d5 for HG00180.
DOI: 10.6084/m9.figshare.7872116.v1
title: gVCF_HG00133

description: 1000 Genomes gVCF mapped to hs37d5 for HG00133.
DOI: 10.6084/m9.figshare.7872119.v1
title: gVCF_HG00181

description: 1000 Genomes gVCF mapped to hs37d5 for HG00181.
DOI: 10.6084/m9.figshare.7872104
title: gVCF_HG00132

description: 1000 Genomes gVCF mapped to hs37d5 for HG00132.
DOI: 10.6084/m9.figshare.7872107.v1
title: gVCF_HG00180

description: 1000 Genomes gVCF mapped to hs37d5 for HG00180.
DOI: 10.6084/m9.figshare.7872092
title: gVCF_HG00178

description: 1000 Genomes gVCF mapped to hs37d5 for HG00178.
DOI: 10.6084/m9.figshare.7872095
title: gVCF_HG00130

description: 1000 Genomes gVCF mapped to hs37d5 for HG00130.
DOI: 10.6084/m9.figshare.7872098
title: gVCF_HG00131

description: 1000 Genomes gVCF mapped to hs37d5 for HG00131.
DOI: 10.6084/m9.figshare.7872095.v1
title: gVCF_HG00130

description: 1000 Genomes gVCF mapped to hs37d5 for HG00130.
DOI: 10.6084/m9.figshare.7872101
title: gVCF_HG00179

description: 1000 Genomes gVCF mapped to hs37d5 for HG00179.
DOI: 10.6084/m9.figshare.7872101.v1
title: gVCF_HG00179

description: 1000 Genomes gVCF mapped to hs37d5 for HG00179.
DOI: 10.6084/m9.figshare.7872104.v1
title: gVCF_HG00132

description: 1000 Genomes gVCF mapped to hs37d5 for HG00132.
DOI: 10.6084/m9.figshare.7872098.v1
title: gVCF_HG00131

description: 1000 Genomes gVCF mapped to hs37d5 for HG00131.
DOI: 10.6084/m9.figshare.7872077
title: gVCF_HG00128

description: 1000 Genomes gVCF mapped to hs37d5 for HG00128.
DOI: 10.6084/m9.figshare.7872080
title: gVCF_HG00129

description: 1000 Genomes gVCF mapped to hs37d5 for HG00129.
DOI: 10.6084/m9.figshare.7872083
title: gVCF_HG00177

description: 1000 Genomes gVCF mapped to hs37d5 for HG00177.
DOI: 10.6084/m9.figshare.7872092.v1
title: gVCF_HG00178

description: 1000 Genomes gVCF mapped to hs37d5 for HG00178.
DOI: 10.6084/m9.figshare.7872080.v1
title: gVCF_HG00129

description: 1000 Genomes gVCF mapped to hs37d5 for HG00129.
DOI: 10.6084/m9.figshare.7872083.v1
title: gVCF_HG00177

description: 1000 Genomes gVCF mapped to hs37d5 for HG00177.
DOI: 10.6084/m9.figshare.7872065
title: gVCF_HG00127

description: 1000 Genomes gVCF mapped to hs37d5 for HG00127.
DOI: 10.6084/m9.figshare.7872074
title: gVCF_HG00176

description: 1000 Genomes gVCF mapped to hs37d5 for HG00176.
DOI: 10.6084/m9.figshare.7872077.v1
title: gVCF_HG00128

description: 1000 Genomes gVCF mapped to hs37d5 for HG00128.
DOI: 10.6084/m9.figshare.7872062
title: gVCF_HG00174

description: 1000 Genomes gVCF mapped to hs37d5 for HG00174.
DOI: 10.6084/m9.figshare.7872062.v1
title: gVCF_HG00174

description: 1000 Genomes gVCF mapped to hs37d5 for HG00174.
DOI: 10.6084/m9.figshare.7872065.v1
title: gVCF_HG00127

description: 1000 Genomes gVCF mapped to hs37d5 for HG00127.
DOI: 10.6084/m9.figshare.7872074.v1
title: gVCF_HG00176

description: 1000 Genomes gVCF mapped to hs37d5 for HG00176.
DOI: 10.26180/5c92f6146f040
title: Online Supplement.pdf

description: Online supplement to "Coagulation factor XII may drive idiopathic pulmonary fibrosis by inducing pro-fibrotic changes in lung fibroblasts".<br>
DOI: 10.6084/m9.figshare.7872041
title: gVCF_HG00160

description: 1000 Genomes gVCF mapped to hs37d5 for HG00160.
DOI: 10.6084/m9.figshare.7872050
title: gVCF_HG00171

description: 1000 Genomes gVCF mapped to hs37d5 for HG00171.
DOI: 10.6084/m9.figshare.7872053
title: gVCF_HG00126

description: 1000 Genomes gVCF mapped to hs37d5 for HG00126.
DOI: 10.6084/m9.figshare.7872059
title: gVCF_HG00173

description: 1000 Genomes gVCF mapped to hs37d5 for HG00173.
DOI: 10.6084/m9.figshare.7872041.v1
title: gVCF_HG00160

description: 1000 Genomes gVCF mapped to hs37d5 for HG00160.
DOI: 10.6084/m9.figshare.7872050.v1
title: gVCF_HG00171

description: 1000 Genomes gVCF mapped to hs37d5 for HG00171.
DOI: 10.6084/m9.figshare.7872053.v1
title: gVCF_HG00126

description: 1000 Genomes gVCF mapped to hs37d5 for HG00126.
DOI: 10.6084/m9.figshare.7872059.v1
title: gVCF_HG00173

description: 1000 Genomes gVCF mapped to hs37d5 for HG00173.
DOI: 10.6084/m9.figshare.7872032
title: gVCF_HG00125

description: 1000 Genomes gVCF mapped to hs37d5 for HG00125.
DOI: 10.6084/m9.figshare.7872035
title: Human activity can influence the gut microbiota of Darwin’s finches in the Galapagos Islands

description: The gut microbiota in animal hosts is influenced by environmental factors, including those that affect food resource availability. For example, humans can alter dietary resources by introducing novel food items. Over the past 30 years, human presence has grown exponentially in the Galapagos Islands, which are home to endemic Darwin’s finches. Consequently, humans have changed the environment and diet of Darwin’s finches, which in turn, could affect their gut microbiota. In this study, we compared the gut microbiota of two species of Darwin’s finches, small ground finches (<i>Geospiza fuliginosa</i>) and medium ground finches (<i>Geospiza fortis</i>), across sites with and without human presence, where finches prefer human-processed and natural food, respectively. We predicted that: 1) finch microbiota would differ between sites with and without humans due to differences in diet, and 2) gut microbiota of each finch species would be most similar where finches have the highest niche overlap (areas with humans) compared to the lowest niche overlap (areas without humans).We found that gut bacterial community structure differed across sites and host species. Gut bacterial diversity was most distinct between the two species at the site with human presence compared to the site without human presence, which contradicted our predictions. Within host species, medium ground finches had lower bacterial diversity at the site with human presence compared to the site without human presence and bacterial diversity of small ground finches did not differ between sites. Our results show that the gut microbiota of Darwin’s finches is affected differently across sites with varying human presence.
DOI: 10.6084/m9.figshare.7872029
title: <i>Atg14</i> protects the intestinal epithelium from TNF-triggered villus atrophy

description: Regulation of intestinal epithelial turnover is a key component of villus maintenance in the intestine. The balance of cell turnover can be perturbed by various extrinsic factors including the cytokine TNF, a cell signaling protein that mediates both proliferative and cytotoxic outcomes. Under conditions of infection and damage, defects in autophagy are associated with TNF-mediated cell death and tissue damage in the intestinal epithelium. However, a direct role of autophagy within the context of enterocyte cell death during homeostasis is lacking. Here, we generated mice lacking ATG14 (autophagy related 14) within the intestinal epithelium [<i>Atg14<sup>f/f</sup> Vil1-</i>Cre (<i>VC</i>)<i><sup>+</sup></i>]. These mice developed spontaneous villus loss and intestinal epithelial cell death within the small intestine. Based on marker studies, the increased cell death in these mice was due to apoptosis. <i>Atg14<sup>f/f</sup> VC<sup>+</sup></i> intestinal epithelial cells demonstrated sensitivity to TNF-triggered apoptosis. Correspondingly, both TNF blocking antibody and genetic deletion of <i>Tnfrsf1a/Tnfr1</i> rescued villus loss and cell death phenotype in <i>Atg14<sup>f/f</sup> VC<sup>+</sup></i> mice. Lastly, we identified a similar pattern of spontaneous villus atrophy and cell death when <i>Rb1cc1</i>/<i>Fip200</i> was conditionally deleted from the intestinal epithelium (<i>Rb1cc1<sup>f/f</sup> VC<sup>+</sup></i>). Overall, these findings are consistent with the hypothesis that factors that control entry into the autophagy pathway are also required during homeostasis to prevent TNF triggered death in the intestine. <b>Abbreviations:</b> ANOVA: analysis of variance; <i>Atg14</i>: autophagy related 14; <i>Atg16l1</i>: autophagy related 16-like 1 (S. cerevisiae); <i>Atg5</i>: autophagy related 5; cCASP3: cleaved CASP3/caspase-3; cCASP8: cleaved CASP8/caspase-8; CHX: cycloheximide; EdU: 5-ethynyl-2´-deoxyuridine thymidine; f/f: flox/flox; H&E: hematoxylin and eosin; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Nec-1: necrostatin-1; <i>Rb1cc1/Fip200</i>: RB1-inducible coiled-coil 1; <i>Ripk1</i>: receptor (TNFRSF)-interacting serine-threonine kinase 1; <i>Ripk3</i>: receptor (TNFRSF)-interacting serine-threonine kinase 3; <i>Tnfrsf1a/Tnfr1</i>: tumor necrosis factor receptor superfamily, member 1a; <i>Tnf/ Tnfsf1a</i>: tumor necrosis factor; VC: <i>Vil1/villin 1</i>-Cre
DOI: 10.6084/m9.figshare.7872038
title: Sputum vs. OPS

description: The data showed the head-to-head compatison between sputum and oropharyngeal swab specimens collected from 440 hospitalized LRTI children which were tested by GeXP-based multiplex-PCR.
DOI: 10.6084/m9.figshare.7872032.v1
title: gVCF_HG00125

description: 1000 Genomes gVCF mapped to hs37d5 for HG00125.
DOI: 10.6084/m9.figshare.7872029.v3
title: <i>Atg14</i> protects the intestinal epithelium from TNF-triggered villus atrophy

description: Regulation of intestinal epithelial turnover is a key component of villus maintenance in the intestine. The balance of cell turnover can be perturbed by various extrinsic factors including the cytokine TNF, a cell signaling protein that mediates both proliferative and cytotoxic outcomes. Under conditions of infection and damage, defects in autophagy are associated with TNF-mediated cell death and tissue damage in the intestinal epithelium. However, a direct role of autophagy within the context of enterocyte cell death during homeostasis is lacking. Here, we generated mice lacking ATG14 (autophagy related 14) within the intestinal epithelium [<i>Atg14<sup>f/f</sup> Vil1-</i>Cre (<i>VC</i>)<i><sup>+</sup></i>]. These mice developed spontaneous villus loss and intestinal epithelial cell death within the small intestine. Based on marker studies, the increased cell death in these mice was due to apoptosis. <i>Atg14<sup>f/f</sup> VC<sup>+</sup></i> intestinal epithelial cells demonstrated sensitivity to TNF-triggered apoptosis. Correspondingly, both TNF blocking antibody and genetic deletion of <i>Tnfrsf1a/Tnfr1</i> rescued villus loss and cell death phenotype in <i>Atg14<sup>f/f</sup> VC<sup>+</sup></i> mice. Lastly, we identified a similar pattern of spontaneous villus atrophy and cell death when <i>Rb1cc1</i>/<i>Fip200</i> was conditionally deleted from the intestinal epithelium (<i>Rb1cc1<sup>f/f</sup> VC<sup>+</sup></i>). Overall, these findings are consistent with the hypothesis that factors that control entry into the autophagy pathway are also required during homeostasis to prevent TNF triggered death in the intestine. <b>Abbreviations:</b> ANOVA: analysis of variance; <i>Atg14</i>: autophagy related 14; <i>Atg16l1</i>: autophagy related 16-like 1 (S. cerevisiae); <i>Atg5</i>: autophagy related 5; cCASP3: cleaved CASP3/caspase-3; cCASP8: cleaved CASP8/caspase-8; CHX: cycloheximide; EdU: 5-ethynyl-2´-deoxyuridine thymidine; f/f: flox/flox; H&E: hematoxylin and eosin; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Nec-1: necrostatin-1; <i>Rb1cc1/Fip200</i>: RB1-inducible coiled-coil 1; <i>Ripk1</i>: receptor (TNFRSF)-interacting serine-threonine kinase 1; <i>Ripk3</i>: receptor (TNFRSF)-interacting serine-threonine kinase 3; <i>Tnfrsf1a/Tnfr1</i>: tumor necrosis factor receptor superfamily, member 1a; <i>Tnf/ Tnfsf1a</i>: tumor necrosis factor; VC: <i>Vil1/villin 1</i>-Cre
DOI: 10.6084/m9.figshare.7872029.v2
title: <i>Atg14</i> protects the intestinal epithelium from TNF-triggered villus atrophy

description: Regulation of intestinal epithelial turnover is a key component of villus maintenance in the intestine. The balance of cell turnover can be perturbed by various extrinsic factors including the cytokine TNF, a cell signaling protein that mediates both proliferative and cytotoxic outcomes. Under conditions of infection and damage, defects in autophagy are associated with TNF-mediated cell death and tissue damage in the intestinal epithelium. However, a direct role of autophagy within the context of enterocyte cell death during homeostasis is lacking. Here, we generated mice lacking ATG14 (autophagy related 14) within the intestinal epithelium [<i>Atg14<sup>f/f</sup> Vil1-</i>Cre (<i>VC</i>)<i><sup>+</sup></i>]. These mice developed spontaneous villus loss and intestinal epithelial cell death within the small intestine. Based on marker studies, the increased cell death in these mice was due to apoptosis. <i>Atg14<sup>f/f</sup> VC<sup>+</sup></i> intestinal epithelial cells demonstrated sensitivity to TNF-triggered apoptosis. Correspondingly, both TNF blocking antibody and genetic deletion of <i>Tnfrsf1a/Tnfr1</i> rescued villus loss and cell death phenotype in <i>Atg14<sup>f/f</sup> VC<sup>+</sup></i> mice. Lastly, we identified a similar pattern of spontaneous villus atrophy and cell death when <i>Rb1cc1</i>/<i>Fip200</i> was conditionally deleted from the intestinal epithelium (<i>Rb1cc1<sup>f/f</sup> VC<sup>+</sup></i>). Overall, these findings are consistent with the hypothesis that factors that control entry into the autophagy pathway are also required during homeostasis to prevent TNF triggered death in the intestine. <b>Abbreviations:</b> ANOVA: analysis of variance; <i>Atg14</i>: autophagy related 14; <i>Atg16l1</i>: autophagy related 16-like 1 (S. cerevisiae); <i>Atg5</i>: autophagy related 5; cCASP3: cleaved CASP3/caspase-3; cCASP8: cleaved CASP8/caspase-8; CHX: cycloheximide; EdU: 5-ethynyl-2´-deoxyuridine thymidine; f/f: flox/flox; H&E: hematoxylin and eosin; MTT: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; Nec-1: necrostatin-1; <i>Rb1cc1/Fip200</i>: RB1-inducible coiled-coil 1; <i>Ripk1</i>: receptor (TNFRSF)-interacting serine-threonine kinase 1; <i>Ripk3</i>: receptor (TNFRSF)-interacting serine-threonine kinase 3; <i>Tnfrsf1a/Tnfr1</i>: tumor necrosis factor receptor superfamily, member 1a; <i>Tnf/ Tnfsf1a</i>: tumor necrosis factor; VC: <i>Vil1/villin 1</i>-Cre
DOI: 10.6084/m9.figshare.7872002
title: gVCF_HG00124

description: 1000 Genomes gVCF mapped to hs37d5 for HG00124.
DOI: 10.6084/m9.figshare.7872005
title: gVCF_HG00159

description: 1000 Genomes gVCF mapped to hs37d5 for HG00159.
DOI: 10.6084/m9.figshare.7872005.v1
title: gVCF_HG00159

description: 1000 Genomes gVCF mapped to hs37d5 for HG00159.
DOI: 10.6084/m9.figshare.7872002.v1
title: gVCF_HG00124

description: 1000 Genomes gVCF mapped to hs37d5 for HG00124.
DOI: 10.6084/m9.figshare.7871999
title: gVCF_HG00158

description: 1000 Genomes gVCF mapped to hs37d5 for HG00158.
DOI: 10.6084/m9.figshare.7871990
title: gVCF_HG00157

description: 1000 Genomes gVCF mapped to hs37d5 for HG00157.
DOI: 10.6084/m9.figshare.7871990.v1
title: gVCF_HG00157

description: 1000 Genomes gVCF mapped to hs37d5 for HG00157.
DOI: 10.6084/m9.figshare.7871999.v1
title: gVCF_HG00158

description: 1000 Genomes gVCF mapped to hs37d5 for HG00158.
DOI: 10.6084/m9.figshare.7871978
title: The anti-cancer drug 5-fluorouracil affects cell cycle regulators and potential regulatory long non-coding RNAs in yeast

description: 5-fluorouracil (5-FU) was isolated as an inhibitor of thymidylate synthase, which is important for DNA synthesis. The drug was later found to also affect the conserved 3ʹ-5ʹ exoribonuclease EXOSC10/Rrp6, a catalytic subunit of the RNA exosome that degrades and processes protein-coding and non-coding transcripts. Work on 5-FU’s cytotoxicity has been focused on mRNAs and non-coding transcripts such as rRNAs, tRNAs and snoRNAs. However, the effect of 5-FU on long non-coding RNAs (lncRNAs), which include regulatory transcripts important for cell growth and differentiation, is poorly understood. RNA profiling of synchronized 5-FU treated yeast cells and protein assays reveal that the drug specifically inhibits a set of cell cycle regulated genes involved in mitotic division, by decreasing levels of the paralogous Swi5 and Ace2 transcriptional activators. We also observe widespread accumulation of different lncRNA types in treated cells, which are typically present at high levels in a strain lacking EXOSC10/Rrp6. 5-FU responsive lncRNAs include potential regulatory antisense transcripts that form double-stranded RNAs (dsRNAs) with overlapping sense mRNAs. Some of these transcripts encode proteins important for cell growth and division, such as the transcription factor Ace2, and the RNA exosome subunit EXOSC6/Mtr3. In addition to revealing a transcriptional effect of 5-FU action via DNA binding regulators involved in cell cycle progression, our results have implications for the function of putative regulatory lncRNAs in 5-FU mediated cytotoxicity. The data raise the intriguing possibility that the drug deregulates lncRNAs/dsRNAs involved in controlling eukaryotic cell division, thereby highlighting a new class of promising therapeutical targets.
DOI: 10.6084/m9.figshare.7871975
title: gVCF_HG00155

description: 1000 Genomes gVCF mapped to hs37d5 for HG00155.
DOI: 10.6084/m9.figshare.7871975.v1
title: gVCF_HG00155

description: 1000 Genomes gVCF mapped to hs37d5 for HG00155.