cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.7680359
title: The role of PAK1 in the sensitivity of kidney epithelial cells to ischemia-like conditions

description: Kidney ischemia, characterized by insufficient supply of oxygen and nutrients to renal epithelial cells, is the main cause of acute kidney injury and an important contributor to mortality world-wide. Earlier research implicated a G-protein coupled receptor (NK1R) in the death of kidney epithelial cells in ischemia-like conditions. P21-associated kinase 1 (PAK1) is involved in signalling by several G-proteins. We explored the consequences of PAK1 inhibition for cell survival under the conditions of reduced glucose and oxygen. Inhibition of PAK1 by RNA interference, expression of a dominant-negative mutant or treatment with small molecule inhibitors greatly reduced the death of cultured kidney epithelial cells. Similar protection was achieved by treating the cells with inhibitors of MEK1, in agreement with the prior reports on PAK1-MEK1 connection. Concomitant inhibition of NK1R and PAK1 offered no better protection than inhibition of NK1R alone, consistent with the two proteins being members of the same pathway. Furthermore, NK1R, PAK and MEK inhibitors reduced the induction of TRAIL in ischemia-like conditions. Considering the emerging role of TRAIL in ischemia-mediated cell death, this phenomenon may contribute to the protective effects of these small molecules. Our findings support further exploration of PAK and MEK inhibitors as possible agents to avert ischemic kidney injury.
DOI: 10.6084/m9.figshare.7776797
title: RETRACTED ARTICLE: Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-β1/Smads signaling pathway by targeting TRPM6

description: We, the Editors and Publisher of the journal <i>Cell Cycle</i>, have retracted the following article: Hui-Ying Wu, Jian-Li Wu, and Zhan-Ling Ni. Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-β1/Smads signaling pathway by targeting TRPM6. Cell Cycle. 2019;18(5):621-637. doi: 10.1080/15384101.2019.1580494. Since publication, concerns have been raised about the integrity of the data in the article. When approached for an explanation, the authors have been unable to address the concerns raised and have not been able to provide their original data or supporting information. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. The corresponding author listed in this publication has been informed. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions.
DOI: 10.6084/m9.figshare.7680359.v3
title: The role of PAK1 in the sensitivity of kidney epithelial cells to ischemia-like conditions

description: Kidney ischemia, characterized by insufficient supply of oxygen and nutrients to renal epithelial cells, is the main cause of acute kidney injury and an important contributor to mortality world-wide. Earlier research implicated a G-protein coupled receptor (NK1R) in the death of kidney epithelial cells in ischemia-like conditions. P21-associated kinase 1 (PAK1) is involved in signalling by several G-proteins. We explored the consequences of PAK1 inhibition for cell survival under the conditions of reduced glucose and oxygen. Inhibition of PAK1 by RNA interference, expression of a dominant-negative mutant or treatment with small molecule inhibitors greatly reduced the death of cultured kidney epithelial cells. Similar protection was achieved by treating the cells with inhibitors of MEK1, in agreement with the prior reports on PAK1-MEK1 connection. Concomitant inhibition of NK1R and PAK1 offered no better protection than inhibition of NK1R alone, consistent with the two proteins being members of the same pathway. Furthermore, NK1R, PAK and MEK inhibitors reduced the induction of TRAIL in ischemia-like conditions. Considering the emerging role of TRAIL in ischemia-mediated cell death, this phenomenon may contribute to the protective effects of these small molecules. Our findings support further exploration of PAK and MEK inhibitors as possible agents to avert ischemic kidney injury.
DOI: 10.6084/m9.figshare.7731113
title: DYRK1A regulates the recruitment of 53BP1 to the sites of DNA damage in part through interaction with RNF169

description: Human Dual-specificity tyrosine (Y) Regulated Kinase 1A (DYRK1A) is encoded by a dosage dependent gene whereby either trisomy or haploinsufficiency result in developmental abnormalities. However, the function and regulation of this important protein kinase are not fully understood. Here, we report proteomic analysis of DYRK1A in human cells that revealed a novel role of DYRK1A in DNA double-strand breaks (DSBs) repair, mediated in part by its interaction with the ubiquitin-binding protein RNF169 that accumulates at the DSB sites and promotes homologous recombination repair (HRR) by displacing 53BP1, a key mediator of non-homologous end joining (NHEJ). We found that overexpression of active, but not the kinase inactive DYRK1A in U-2 OS cells inhibits accumulation of 53BP1 at the DSB sites in the RNF169-dependent manner. DYRK1A phosphorylates RNF169 at two sites that influence its ability to displace 53BP1 from the DSBs. Although DYRK1A is not required for the recruitment of RNF169 to the DSB sites and 53BP1 displacement, inhibition of DYRK1A or mutation of the DYRK1A phosphorylation sites in RNF169 decreases its ability to block accumulation of 53BP1 at the DSB sites. Interestingly, CRISPR-Cas9 knockout of DYRK1A in human and mouse cells also diminished the 53BP1 DSB recruitment in a manner that did not require RNF169, suggesting that dosage of DYRK1A can influence the DNA repair processes through both RNF169-dependent and independent mechanisms. Human U-2 OS cells devoid of DYRK1A display an increased HRR efficiency and resistance to DNA damage, therefore our findings implicate DYRK1A in the DNA repair processes.
DOI: 10.6084/m9.figshare.7776797.v2
title: RETRACTED ARTICLE: Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-β1/Smads signaling pathway by targeting TRPM6

description: We, the Editors and Publisher of the journal <i>Cell Cycle</i>, have retracted the following article: Hui-Ying Wu, Jian-Li Wu, and Zhan-Ling Ni. Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-β1/Smads signaling pathway by targeting TRPM6. Cell Cycle. 2019;18(5):621-637. doi: 10.1080/15384101.2019.1580494. Since publication, concerns have been raised about the integrity of the data in the article. When approached for an explanation, the authors have been unable to address the concerns raised and have not been able to provide their original data or supporting information. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. The corresponding author listed in this publication has been informed. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions.
DOI: 10.6084/m9.figshare.7680359.v2
title: The role of PAK1 in the sensitivity of kidney epithelial cells to ischemia-like conditions

description: Kidney ischemia, characterized by insufficient supply of oxygen and nutrients to renal epithelial cells, is the main cause of acute kidney injury and an important contributor to mortality world-wide. Earlier research implicated a G-protein coupled receptor (NK1R) in the death of kidney epithelial cells in ischemia-like conditions. P21-associated kinase 1 (PAK1) is involved in signalling by several G-proteins. We explored the consequences of PAK1 inhibition for cell survival under the conditions of reduced glucose and oxygen. Inhibition of PAK1 by RNA interference, expression of a dominant-negative mutant or treatment with small molecule inhibitors greatly reduced the death of cultured kidney epithelial cells. Similar protection was achieved by treating the cells with inhibitors of MEK1, in agreement with the prior reports on PAK1-MEK1 connection. Concomitant inhibition of NK1R and PAK1 offered no better protection than inhibition of NK1R alone, consistent with the two proteins being members of the same pathway. Furthermore, NK1R, PAK and MEK inhibitors reduced the induction of TRAIL in ischemia-like conditions. Considering the emerging role of TRAIL in ischemia-mediated cell death, this phenomenon may contribute to the protective effects of these small molecules. Our findings support further exploration of PAK and MEK inhibitors as possible agents to avert ischemic kidney injury.
DOI: 10.6084/m9.figshare.7731113.v2
title: DYRK1A regulates the recruitment of 53BP1 to the sites of DNA damage in part through interaction with RNF169

description: Human Dual-specificity tyrosine (Y) Regulated Kinase 1A (DYRK1A) is encoded by a dosage dependent gene whereby either trisomy or haploinsufficiency result in developmental abnormalities. However, the function and regulation of this important protein kinase are not fully understood. Here, we report proteomic analysis of DYRK1A in human cells that revealed a novel role of DYRK1A in DNA double-strand breaks (DSBs) repair, mediated in part by its interaction with the ubiquitin-binding protein RNF169 that accumulates at the DSB sites and promotes homologous recombination repair (HRR) by displacing 53BP1, a key mediator of non-homologous end joining (NHEJ). We found that overexpression of active, but not the kinase inactive DYRK1A in U-2 OS cells inhibits accumulation of 53BP1 at the DSB sites in the RNF169-dependent manner. DYRK1A phosphorylates RNF169 at two sites that influence its ability to displace 53BP1 from the DSBs. Although DYRK1A is not required for the recruitment of RNF169 to the DSB sites and 53BP1 displacement, inhibition of DYRK1A or mutation of the DYRK1A phosphorylation sites in RNF169 decreases its ability to block accumulation of 53BP1 at the DSB sites. Interestingly, CRISPR-Cas9 knockout of DYRK1A in human and mouse cells also diminished the 53BP1 DSB recruitment in a manner that did not require RNF169, suggesting that dosage of DYRK1A can influence the DNA repair processes through both RNF169-dependent and independent mechanisms. Human U-2 OS cells devoid of DYRK1A display an increased HRR efficiency and resistance to DNA damage, therefore our findings implicate DYRK1A in the DNA repair processes.
DOI: 10.6084/m9.figshare.7731113.v1
title: DYRK1A regulates the recruitment of 53BP1 to the sites of DNA damage in part through interaction with RNF169

description: Human Dual-specificity tyrosine (Y) Regulated Kinase 1A (DYRK1A) is encoded by a dosage dependent gene whereby either trisomy or haploinsufficiency result in developmental abnormalities. However, the function and regulation of this important protein kinase are not fully understood. Here, we report proteomic analysis of DYRK1A in human cells that revealed a novel role of DYRK1A in DNA double-strand breaks (DSBs) repair, mediated in part by its interaction with the ubiquitin-binding protein RNF169 that accumulates at the DSB sites and promotes homologous recombination repair (HRR) by displacing 53BP1, a key mediator of non-homologous end joining (NHEJ). We found that overexpression of active, but not the kinase inactive DYRK1A in U-2 OS cells inhibits accumulation of 53BP1 at the DSB sites in the RNF169-dependent manner. DYRK1A phosphorylates RNF169 at two sites that influence its ability to displace 53BP1 from the DSBs. Although DYRK1A is not required for the recruitment of RNF169 to the DSB sites and 53BP1 displacement, inhibition of DYRK1A or mutation of the DYRK1A phosphorylation sites in RNF169 decreases its ability to block accumulation of 53BP1 at the DSB sites. Interestingly, CRISPR-Cas9 knockout of DYRK1A in human and mouse cells also diminished the 53BP1 DSB recruitment in a manner that did not require RNF169, suggesting that dosage of DYRK1A can influence the DNA repair processes through both RNF169-dependent and independent mechanisms. Human U-2 OS cells devoid of DYRK1A display an increased HRR efficiency and resistance to DNA damage, therefore our findings implicate DYRK1A in the DNA repair processes.
DOI: 10.6084/m9.figshare.7776797.v1
title: Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-β1/Smads signaling pathway by targeting TRPM6

description: MicroRNAs (miRNAs) have been found to act as key regulators in the pathogenesis of myocardial ischemic-reperfusion (I/R) injury. In this study, we explore the role and mechanism of microRNA-202-3p (miR-202-3p) in regulating cardiomyocyte apoptosis, in respective of the TGF-β1/Smads signaling pathway by targeting the transient receptor potential cation channel, subfamily M, member 6 (TRPM6). The targeting relationship between miR-202-3p and TRPM6 was verified by a dual-luciferase reporter gene assay. Sprague-Dawley rat models of myocardial I/R injury were initially established and treated with different mimics, inhibitors and siRNAs to test the effects of miR-202-3p and TRPM6 on myocardial I/R injury. The levels of inflammatory factors; IL-1β, IL-6, TNF-α as well as the degree of myocardial fibrosis and cardiomyocyte apoptosis were determined in rats transfected with different plasmids. TRPM6 was found to be the target of miR-202-3p. Up-regulated miR-202-3p or knockdown of TRPM-6 alleviated oxidative stress and inflammatory response, reduced ventricular mass, altered cardiac hemodynamics, suppressed myocardial infarction, attenuated cell apoptosis, and inhibited myocardial fibrosis. MiR-202-3p overexpression activates the TGF-β1/Smads signaling pathway by negatively regulating TRPM6 expression. Taken together, these findings suggest that miR-202-3p offers protection against ventricular remodeling after myocardial I/R injury via activation of the TGF-β1/Smads signaling pathway.
DOI: 10.6084/m9.figshare.14454133
title: Inference on Multi-level Partial Correlations Based on Multi-subject Time Series Data

description: Partial correlations are commonly used to analyze the conditional dependence among variables. In this work, we propose a hierarchical model to study both the subject- and population-level partial correlations based on multi-subject time-series data. Multiple testing procedures adaptive to temporally dependent data with false discovery proportion control are proposed to identify the nonzero partial correlations in both the subject and population levels. A computationally feasible algorithm is developed. Theoretical results and simulation studies demonstrate the good properties of the proposed procedures. We illustrate the application of the proposed methods in a real example of brain connectivity on fMRI data from normal healthy persons and patients with Parkinson’s disease. Supplementary materials for this article are available online.
DOI: 10.6084/m9.figshare.14454133.v2
title: Inference on Multi-level Partial Correlations Based on Multi-subject Time Series Data

description: Partial correlations are commonly used to analyze the conditional dependence among variables. In this work, we propose a hierarchical model to study both the subject- and population-level partial correlations based on multi-subject time-series data. Multiple testing procedures adaptive to temporally dependent data with false discovery proportion control are proposed to identify the nonzero partial correlations in both the subject and population levels. A computationally feasible algorithm is developed. Theoretical results and simulation studies demonstrate the good properties of the proposed procedures. We illustrate the application of the proposed methods in a real example of brain connectivity on fMRI data from normal healthy persons and patients with Parkinson’s disease. Supplementary materials for this article are available online.
DOI: 10.6084/m9.figshare.14454133.v1
title: Inference on Multi-level Partial Correlations based on Multi-subject Time Series Data

description: Partial correlations are commonly used to analyze the conditional dependence among variables. In this work, we propose a hierarchical model to study both the subject and population level partial correlations based on multi-subject time series data. Multiple testing procedures adaptive to temporally dependent data with false discovery proportion control are proposed to identify the nonzero partial correlations in both the subject and population levels. A computationally feasible algorithm is developed. Theoretical results and simulation studies demonstrate the good properties of the proposed procedures. We illustrate the application of the proposed methods in a real example of brain connectivity on fMRI data from normal healthy persons and patients with Parkinson’s disease.
DOI: 10.6084/m9.figshare.13566900
title: Preparation and characterization of epichlorohydrin treated Putranjiva roxburghii seeds as a novel adsorbent: removal of Ni(II) from the artificial and real electroplating wastewaters

description: In the present study, preparation and characterization of an adsorbent made from the chemically modified <i>Putranjiva roxburghii</i> seeds and its applicability toward removing Ni(II) abatement from water and electroplating wastewater have been thoroughly investigated. For process optimization, various physicochemical factors affecting the adsorption process were examined. The equilibrium was achieved in 60 min for the experimental conditions accompanying the Ni(II) concentration of 50 mg L<sup>−1</sup> with the adsorbent dose of 0.2 g in 20 mL solution. The practical utility and cost-efficiency of the adsorbent have been analyzed. The present adsorbent was proved to be efficient for the decontamination of laboratory prepared polluted water and real wastewater (electroplating wastewater of the lock industry) containing Ni(II) ions. The additional advantages of facile synthesis, low-cost, and reusability of the present adsorbent make it a novel.
DOI: 10.6084/m9.figshare.13566900.v1
title: Preparation and characterization of epichlorohydrin treated Putranjiva roxburghii seeds as a novel adsorbent: removal of Ni(II) from the artificial and real electroplating wastewaters

description: In the present study, preparation and characterization of an adsorbent made from the chemically modified <i>Putranjiva roxburghii</i> seeds and its applicability toward removing Ni(II) abatement from water and electroplating wastewater have been thoroughly investigated. For process optimization, various physicochemical factors affecting the adsorption process were examined. The equilibrium was achieved in 60 min for the experimental conditions accompanying the Ni(II) concentration of 50 mg L<sup>−1</sup> with the adsorbent dose of 0.2 g in 20 mL solution. The practical utility and cost-efficiency of the adsorbent have been analyzed. The present adsorbent was proved to be efficient for the decontamination of laboratory prepared polluted water and real wastewater (electroplating wastewater of the lock industry) containing Ni(II) ions. The additional advantages of facile synthesis, low-cost, and reusability of the present adsorbent make it a novel.
DOI: 10.6084/m9.figshare.12853026.v1
title: Potato tuber metabolomics-based prediction of chip color quality and application using gas chromatography/flame ionization detector

description: Potato (<i>Solanum tuberosum</i> L.) tubers are usually harvested once a year; thus, long-term storage is required to supply quality-assured tubers throughout the year. Further, an applicable method to predict tuber quality during storage is needed. In this study, gas chromatography-mass spectrometry (GC/MS) metabolomics was applied to identify applicable biomarkers for prediction of potato chip color based on 3 years’ field-grown tubers. The projections to latent structures (PLS) prediction model, calculated from a metabolome data set obtained before storage, was consistent with actual measured chip color values. Additionally, GC with frame ionization detector (GC/FID) metabolite fingerprinting simultaneously re-constructed more reliable and relevant prediction models for chip color quality compared to GC/MS. Moreover, nine metabolites detected by GC/MS analysis were further validated as applicable prediction markers. This strategy will provide a practical and cost-effective quality-control tool for potato processing manufacturers on an industrial scale. GC/MS and GC/FID metabolomics was applied to identify applicable biomarkers for prediction of potato chip color.
DOI: 10.6084/m9.figshare.12853026
title: Potato tuber metabolomics-based prediction of chip color quality and application using gas chromatography/flame ionization detector

description: Potato (<i>Solanum tuberosum</i> L.) tubers are usually harvested once a year; thus, long-term storage is required to supply quality-assured tubers throughout the year. Further, an applicable method to predict tuber quality during storage is needed. In this study, gas chromatography-mass spectrometry (GC/MS) metabolomics was applied to identify applicable biomarkers for prediction of potato chip color based on 3 years’ field-grown tubers. The projections to latent structures (PLS) prediction model, calculated from a metabolome data set obtained before storage, was consistent with actual measured chip color values. Additionally, GC with frame ionization detector (GC/FID) metabolite fingerprinting simultaneously re-constructed more reliable and relevant prediction models for chip color quality compared to GC/MS. Moreover, nine metabolites detected by GC/MS analysis were further validated as applicable prediction markers. This strategy will provide a practical and cost-effective quality-control tool for potato processing manufacturers on an industrial scale. GC/MS and GC/FID metabolomics was applied to identify applicable biomarkers for prediction of potato chip color.
DOI: 10.6084/m9.figshare.12854992
title: Public Opinion Towards Gene Drive as a Pest Control Approach for Biodiversity Conservation and the Association of Underlying Worldviews

description: Synthetic gene drive approaches are nascent technologies with potential applicability for pest control for conservation purposes. Responsible science mandates that society be engaged in a dialogue over new technology, particularly where there exist global ramifications as with gene drive. We hypothesize that public attitudes towards gene drive are not formed on scientific knowledge or demographics alone, but are heavily influenced by underlying worldviews, which encapsulate a broad and interactive system of attitudes, beliefs, and values. To test this, we conducted a national survey in New Zealand (<i>n</i> = 8199) and found that respondents clustered into four distinct segments with underlying worldviews, better able to explain attitudes toward gene drive than either the participants' scientific knowledge or other explanatory factors such demographics, political ideology or religiosity. We found that the use of gene drive for biodiversity conservation currently has moderate (32%) levels of support in New Zealand but that varied substantially across the four segments. Should gene drive become a technically viable approach for pest control, understanding the worldviews that shape public decision-making can guide a more empathetic engagement process and empower society to participate in informed decision-making about if and how gene drive should be used for conservation purposes.