cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.15157240.v2
title: Anillin/Mid1p interacts with the ESCRT-associated protein Vps4p and mitotic kinases to regulate cytokinesis in fission yeast

description: Cytokinesis is the final stage of the cell cycle which separates cellular constituents to produce two daughter cells. Using the fission yeast <i>Schizosaccharomyces pombe</i> we have investigated the role of various classes of proteins involved in this process. Central to these is anillin/Mid1p which forms a ring-like structure at the cell equator that predicts the site of cell separation through septation in fission yeast. Here we demonstrate a direct physical interaction between Mid1p and the endosomal sorting complex required for transport (ESCRT)-associated protein Vps4p, a genetic interaction of the <i>mid1</i> and <i>vps4</i> genes essential for cell viability, and a requirement of Vps4p for the correct cellular localization of Mid1p. Furthermore, we show that Mid1p is phosphorylated by aurora kinase, a genetic interaction of the <i>mid1</i> and the aurora kinase <i>ark1</i> genes is essential for cell viability, and that Ark1p is also required for the correct cellular localization of Mid1p. We mapped the sites of phosphorylation of Mid1p by human aurora A and the polo kinase Plk1 and assessed their importance in fission yeast by mutational analysis. Such analysis revealed serine residues S332, S523 and S531 to be required for Mid1p function and its interaction with Vps4p, Ark1p and Plo1p. Combined these data suggest a physical interaction between Mid1p and Vps4p important for cytokinesis, and identify phosphorylation of Mid1p by aurora and polo kinases as being significant for this process.
DOI: 10.6084/m9.figshare.16432554.v1
title: Ketamine enhances autophagy and endoplasmic reticulum stress in rats and SV-HUC-1 cells via activating IRE1-TRAF2-ASK1-JNK pathway

description: Background Ketamine-related cystitis (KC) has been researched in many clinical studies, but its exact mechanism is ambiguous and needs further research. Methods We established a KC rat model and analyzed physiological, biochemical, and urodynamic parameters of ketamine (KET)-related bladder injury. Bladder histologic feature, reactive oxygen species (ROS), autophagy-, apoptosis-, and endoplasmic reticulum stress (ERS)-related markers were examined by hematoxylin and eosin staining, Masson staining, ROS kit, quantitative real-time polymerase chain reaction, and western blot. <i>In vitro</i>, effects of 0.01, 0.1, and 1 mM KET on cell vitality, apoptosis, ROS level, autophagy-, apoptosis-, and ERS-related markers were examined again. Effects of KET-1 and salubrinal on complex formation, autophagy-, apoptosis-, and ERS-related markers were examined by Co-Immunoprecipitation and western blot. After transfection with shIRE1, complex formation, cell biological behaviors, ROS level, autophagy-, apoptosis-, and ERS-related markers were examined again. Results KET induced bladder hyperactivity and injury. KET facilitated urinary frequency, ROS production, and induced bladder histologic injury by activating autophagy-, apoptosis-, and ERS-related markers in rats. <i>In vitro</i>, KET (0.01, 0.1, and 1 mM) restrained cell vitality and elevated apoptosis and ROS level via activating autophagy-, apoptosis-, and ERS-related markers. Moreover, salubrinal reversed the promotion of KET-1 on complex formation, autophagy-, apoptosis-, and ERS-related marker expressions. After transfection with shIRE1, shIRE1 weakened complex formation induced by KET-1, and the effects of KET-1 on cells were offset by shIRE1. Conclusion KET enhanced autophagy and ERS <i>in vivo</i> and <i>in vitro</i> via restraining IRE1-TRAF2-ASK1-JNK pathway.
DOI: 10.6084/m9.figshare.16432554
title: Ketamine enhances autophagy and endoplasmic reticulum stress in rats and SV-HUC-1 cells via activating IRE1-TRAF2-ASK1-JNK pathway

description: Background Ketamine-related cystitis (KC) has been researched in many clinical studies, but its exact mechanism is ambiguous and needs further research. Methods We established a KC rat model and analyzed physiological, biochemical, and urodynamic parameters of ketamine (KET)-related bladder injury. Bladder histologic feature, reactive oxygen species (ROS), autophagy-, apoptosis-, and endoplasmic reticulum stress (ERS)-related markers were examined by hematoxylin and eosin staining, Masson staining, ROS kit, quantitative real-time polymerase chain reaction, and western blot. <i>In vitro</i>, effects of 0.01, 0.1, and 1 mM KET on cell vitality, apoptosis, ROS level, autophagy-, apoptosis-, and ERS-related markers were examined again. Effects of KET-1 and salubrinal on complex formation, autophagy-, apoptosis-, and ERS-related markers were examined by Co-Immunoprecipitation and western blot. After transfection with shIRE1, complex formation, cell biological behaviors, ROS level, autophagy-, apoptosis-, and ERS-related markers were examined again. Results KET induced bladder hyperactivity and injury. KET facilitated urinary frequency, ROS production, and induced bladder histologic injury by activating autophagy-, apoptosis-, and ERS-related markers in rats. <i>In vitro</i>, KET (0.01, 0.1, and 1 mM) restrained cell vitality and elevated apoptosis and ROS level via activating autophagy-, apoptosis-, and ERS-related markers. Moreover, salubrinal reversed the promotion of KET-1 on complex formation, autophagy-, apoptosis-, and ERS-related marker expressions. After transfection with shIRE1, shIRE1 weakened complex formation induced by KET-1, and the effects of KET-1 on cells were offset by shIRE1. Conclusion KET enhanced autophagy and ERS <i>in vivo</i> and <i>in vitro</i> via restraining IRE1-TRAF2-ASK1-JNK pathway.
DOI: 10.6084/m9.figshare.15157240.v1
title: Anillin/Mid1p interacts with the ESCRT-associated protein Vps4p and mitotic kinases to regulate cytokinesis in fission yeast

description: Cytokinesis is the final stage of the cell cycle which separates cellular constituents to produce two daughter cells. Using the fission yeast <i>Schizosaccharomyces pombe</i> we have investigated the role of various classes of proteins involved in this process. Central to these is anillin/Mid1p which forms a ring-like structure at the cell equator that predicts the site of cell separation through septation in fission yeast. Here we demonstrate a direct physical interaction between Mid1p and the endosomal sorting complex required for transport (ESCRT)-associated protein Vps4p, a genetic interaction of the <i>mid1</i> and <i>vps4</i> genes essential for cell viability, and a requirement of Vps4p for the correct cellular localization of Mid1p. Furthermore, we show that Mid1p is phosphorylated by aurora kinase, a genetic interaction of the <i>mid1</i> and the aurora kinase <i>ark1</i> genes is essential for cell viability, and that Ark1p is also required for the correct cellular localization of Mid1p. We mapped the sites of phosphorylation of Mid1p by human aurora A and the polo kinase Plk1 and assessed their importance in fission yeast by mutational analysis. Such analysis revealed serine residues S332, S523 and S531 to be required for Mid1p function and its interaction with Vps4p, Ark1p and Plo1p. Combined these data suggest a physical interaction between Mid1p and Vps4p important for cytokinesis, and identify phosphorylation of Mid1p by aurora and polo kinases as being significant for this process.
DOI: 10.6084/m9.figshare.15157245
title: NAD<sup>+</sup> metabolism controls growth inhibition by HIF1 in normoxia and determines differential sensitivity of normal and cancer cells

description: The hypoxia-induced transcription factor HIF1 inhibits cell growth in normoxia through poorly understood mechanisms. A constitutive upregulation of hypoxia response is associated with increased malignancy, indicating a loss of antiproliferative effects of HIF1 in cancer cells. To understand these differences, we examined the control of cell cycle in primary human cells with activated hypoxia response in normoxia. Activated HIF1 caused a global slowdown of cell cycle progression through G1, S and G2 phases leading to the loss of mitotic cells. Cell cycle inhibition required a prolonged HIF1 activation and was not associated with upregulation of p53 or the CDK inhibitors p16, p21 or p27. Growth inhibition by HIF1 was independent of its Asn803 hydroxylation or the presence of HIF2. Antiproliferative effects of hypoxia response were alleviated by inhibition of lactate dehydrogenase and, more effectively, by boosting cellular production of NAD<sup>+</sup>, which was decreased by HIF1 activation. In comparison to normal cells, various cancer lines showed several fold-higher expressions of NAMPT, which is a rate-limiting enzyme in the main biosynthetic pathway for NAD<sup>+</sup>. Inhibition of NAMPT activity in overexpressor cancer cells sensitized them to antigrowth effects of HIF1. Thus, metabolic changes in cancer cells, such as enhanced NAD<sup>+</sup> production, create resistance to growth-inhibitory activity of HIF1 permitting manifestation of its tumor-promoting properties.<b>Abbreviations</b>: DMOG: dimethyloxalylglycine, DM-NOFD: dimethyl N-oxalyl-D-phenylalanine, NMN: β-nicotinamide mononucleotide
DOI: 10.6084/m9.figshare.15142420
title: CircTYW1 serves as a sponge for microRNA-380 in accelerating neurological recovery following spinal cord injury via regulating FGF9

description: As one of the most severe kinds of neurological damage, spinal cord injury (SCI) contributes to persistent motor dysfunction and involves a large repertoire of gene alterations. The participation of circular RNAs (circRNAs) in neurological recovery following SCI needs to be clarified. In the current work, we attempted to assess the function of hsa_circRNA_0003962/circTYW1 and its underlying mechanism in SCI. By accessing the GEO repository, the expression of circTYW1, microRNA-380 (miR-380), and FGF9 in SCI and sham-operated rats was evaluated. PC12 cells after oxygen-glucose deprivation (OGD) treatment were prepared to mimic the SCI model. circTYW1 and FGF9 were poorly expressed, whereas miR-380 was highly expressed in the spinal cord tissues of SCI rats. circTYW1 promoted neurological recovery in SCI rats and inhibited apoptosis in spinal cord tissues. In PC12 cells exposed to OGD, circTYW1 suppressed PC12 cell apoptosis; however, miR-380 overexpression reversed the protective effect of circTYW1 on PC12 cells. Also, circTYW1 promoted FGF9 expression through competitively binding to miR-380, which activated the ERK1/2 signaling. In summary, our results demonstrated that declines in circTYW1 prevented SCI rats from neurological recovery by regulating the miR-380/FGF9/ERK1/2 axis, which might provide new understanding for SCI treatment.
DOI: 10.6084/m9.figshare.15157245.v2
title: NAD<sup>+</sup> metabolism controls growth inhibition by HIF1 in normoxia and determines differential sensitivity of normal and cancer cells

description: The hypoxia-induced transcription factor HIF1 inhibits cell growth in normoxia through poorly understood mechanisms. A constitutive upregulation of hypoxia response is associated with increased malignancy, indicating a loss of antiproliferative effects of HIF1 in cancer cells. To understand these differences, we examined the control of cell cycle in primary human cells with activated hypoxia response in normoxia. Activated HIF1 caused a global slowdown of cell cycle progression through G1, S and G2 phases leading to the loss of mitotic cells. Cell cycle inhibition required a prolonged HIF1 activation and was not associated with upregulation of p53 or the CDK inhibitors p16, p21 or p27. Growth inhibition by HIF1 was independent of its Asn803 hydroxylation or the presence of HIF2. Antiproliferative effects of hypoxia response were alleviated by inhibition of lactate dehydrogenase and, more effectively, by boosting cellular production of NAD<sup>+</sup>, which was decreased by HIF1 activation. In comparison to normal cells, various cancer lines showed several fold-higher expressions of NAMPT, which is a rate-limiting enzyme in the main biosynthetic pathway for NAD<sup>+</sup>. Inhibition of NAMPT activity in overexpressor cancer cells sensitized them to antigrowth effects of HIF1. Thus, metabolic changes in cancer cells, such as enhanced NAD<sup>+</sup> production, create resistance to growth-inhibitory activity of HIF1 permitting manifestation of its tumor-promoting properties.<b>Abbreviations</b>: DMOG: dimethyloxalylglycine, DM-NOFD: dimethyl N-oxalyl-D-phenylalanine, NMN: β-nicotinamide mononucleotide
DOI: 10.6084/m9.figshare.15157245.v1
title: NAD<sup>+</sup> metabolism controls growth inhibition by HIF1 in normoxia and determines differential sensitivity of normal and cancer cells

description: The hypoxia-induced transcription factor HIF1 inhibits cell growth in normoxia through poorly understood mechanisms. A constitutive upregulation of hypoxia response is associated with increased malignancy, indicating a loss of antiproliferative effects of HIF1 in cancer cells. To understand these differences, we examined a control of cell cycle in primary human cells with activated hypoxia response in normoxia. Activated HIF1 caused a global slowdown of cell cycle progression through G1, S and G2 phases leading to the loss of mitotic cells. Cell cycle inhibition required a prolonged HIF1 activation and was not associated with upregulation of p53 or the CDK inhibitors p16, p21 or p27. Growth inhibition by HIF1 was independent of its Asn803 hydroxylation or the presence of HIF2. Antiproliferative effects of hypoxia response were alleviated by inhibition of lactate dehydrogenase and more effectively, by boosting cellular production of NAD<sup>+</sup>, which was decreased by HIF1 activation. In comparison to normal cells, various cancer lines showed several fold-higher expression of NAMPT which is a rate-limiting enzyme in the main biosynthetic pathway for NAD<sup>+</sup>. Inhibition of NAMPT activity in overexpressor cancer cells sensitized them to antigrowth effects of HIF1. Thus, metabolic changes in cancer cells, such as enhanced NAD<sup>+</sup> production, create resistance to growth-inhibitory activity of HIF1 permitting manifestation of its tumor-promoting properties. <b>Abbreviations</b> DMOG: dimethyloxalylglycine, DM-NOFD: dimethyl N-oxalyl-D-phenylalanine, NMN: β-nicotinamide mononucleotide
DOI: 10.6084/m9.figshare.15142420.v2
title: CircTYW1 serves as a sponge for microRNA-380 in accelerating neurological recovery following spinal cord injury via regulating FGF9

description: As one of the most severe kinds of neurological damage, spinal cord injury (SCI) contributes to persistent motor dysfunction and involves a large repertoire of gene alterations. The participation of circular RNAs (circRNAs) in neurological recovery following SCI needs to be clarified. In the current work, we attempted to assess the function of hsa_circRNA_0003962/circTYW1 and its underlying mechanism in SCI. By accessing the GEO repository, the expression of circTYW1, microRNA-380 (miR-380), and FGF9 in SCI and sham-operated rats was evaluated. PC12 cells after oxygen-glucose deprivation (OGD) treatment were prepared to mimic the SCI model. circTYW1 and FGF9 were poorly expressed, whereas miR-380 was highly expressed in the spinal cord tissues of SCI rats. circTYW1 promoted neurological recovery in SCI rats and inhibited apoptosis in spinal cord tissues. In PC12 cells exposed to OGD, circTYW1 suppressed PC12 cell apoptosis; however, miR-380 overexpression reversed the protective effect of circTYW1 on PC12 cells. Also, circTYW1 promoted FGF9 expression through competitively binding to miR-380, which activated the ERK1/2 signaling. In summary, our results demonstrated that declines in circTYW1 prevented SCI rats from neurological recovery by regulating the miR-380/FGF9/ERK1/2 axis, which might provide new understanding for SCI treatment.
DOI: 10.6073/pasta/1aede6fb20c4870079fd754b77d13711
title: Sonadora elevational plots: long-term monitoring of air temperature

description: This is a long-term monitoring of air temperature at each elevation plot along the Sonadora gradient. At each plot a HOBO sensor is located close to the middle of the plot: at 1m above ground: and placed inside a radiation shield (a plastic cup). Sensors are programmed to sample and store air temperature every hour. A daily average is computed from hourly readings. Sensors are downloaded twice a year: thus blanks represent sensor malfunction: loss of battery: or memory full. Initial blanks were due to lack of enough sensors to cover the gradient
DOI: 10.6084/m9.figshare.9208979
title: 1000 genomes (phase 3) files with SNPs in common with HapMap3 and UK Biobank

description: This provides 2490 (mostly unrelated) individuals of the 1000 genomes project (phase 3) in PLINK bed/bim/fam format. The SNPs are restricted to the ones in common with HapMap3 and UK Biobank (~1.7M).<br><br>The R code that has been used to generate these data is also provided.<br><br>Do not forget to cite the 1000 genomes project.<br>TODO: add citation + mine<br>
DOI: 10.25810/4c3b-b819.42
title: World Newspaper Coverage of Climate Change or Global Warming, 2004-2021 - September 2021

description:         The Media and Climate Change Observatory Data monitors 127 sources (across newspapers, radio and TV) in 59 countries in seven different regions around the world. Data is assembled by accessing archives through the Lexis Nexis, Proquest and Factiva databases via the University of Colorado libraries. More information may be found at: http://mecco.colorado.edu.
DOI: 10.6073/pasta/c91626f1171bb1a9668cee8dabfe3c52
title: Sonadora elevational plots: long-term monitoring of air temperature

description: This is a long-term monitoring of air temperature at each elevation plot along the Sonadora gradient. At each plot a HOBO sensor is located close to the middle of the plot: at 1m above ground: and placed inside a radiation shield (a plastic cup). Sensors are programmed to sample and store air temperature every hour. A daily average is computed from hourly readings. Sensors are downloaded twice a year: thus blanks represent sensor malfunction: loss of battery: or memory full. Initial blanks were due to lack of enough sensors to cover the gradient
DOI: 10.5519/qd.rduc98cw
title: Query on the Natural History Museum Data Portal (data.nhm.ac.uk) (3 records)
DOI: 10.5281/zenodo.5567746
title: Ara militaris decontaminated FSCR

description: .
DOI: 10.5281/zenodo.5567745
title: Ara militaris decontaminated FSCR

description: .
DOI: 10.25810/k55w-7a04.42
title: World Radio Coverage of Climate Change or Global Warming, 2000-2021 - September 2021

description:         The Media and Climate Change Observatory Data monitors 127 sources (across newspapers, radio and TV) in 59 countries in seven different regions around the world. Data is assembled by accessing archives through the Lexis Nexis, Proquest and Factiva databases via the University of Colorado libraries. More information may be found at: http://mecco.colorado.edu.
DOI: 10.6084/m9.figshare.16807150
title: IDBA-UD Assemblies of 16 Arctic Ocean Metagenomes from Cao et al 2020

description: This datapack contains anvi'o contigs databases for 16 metagenome samples from the Cao et al 2020 paper (https://doi.org/10.1186/s40168-020-00826-9) that were assembled using IDBA-UD as part of the anvi'o metagenomic workflow. <br>It also contains a tab-delimited metadata file derived from data provided in the Cao et al paper, describing the depth, sampling location, and public database accession numbers of each Cao et al sample (including the 16 assemblies within this datapack).<br>The database names do not correspond to the original sample names from the Cao et al paper. You can find the original sample names in the metadata file.<br>The size of the unzipped datapack is 6.5 GB.
DOI: 10.5517/ccdc.csd.cc1ltcpg
title: CCDC 1484146: Experimental Crystal Structure Determination

description: Related Article: Aaron Sandleben|2016|CSD Communication|||
description: Related Article: Aaron Sandleben, Nicolas Vogt, Gerald Hörner, Axel Klein|2018|Organometallics|37|3332|doi:10.1021/acs.organomet.8b00559
DOI: 10.5517/ccdc.csd.cc1lyhbc
title: CCDC 1488103: Experimental Crystal Structure Determination

description: Related Article: Aaron Sandleben|2016|CSD Communication|||
DOI: 10.5517/ccdc.csd.cc1lyhcd
title: CCDC 1488104: Experimental Crystal Structure Determination

description: Related Article: Aaron Sandleben, Nicolas Vogt, Gerald Hörner, Axel Klein|2018|Organometallics|37|3332|doi:10.1021/acs.organomet.8b00559
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DOI: 10.5517/ccdc.csd.cc1lyhfg
title: CCDC 1488106: Experimental Crystal Structure Determination

description: Related Article: Aaron Sandleben, Nicolas Vogt, Gerald Hörner, Axel Klein|2018|Organometallics|37|3332|doi:10.1021/acs.organomet.8b00559
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DOI: 10.5517/ccdc.csd.cc1lyhhj
title: CCDC 1488108: Experimental Crystal Structure Determination

description: Related Article: Aaron Sandleben, Nicolas Vogt, Gerald Hörner, Axel Klein|2018|Organometallics|37|3332|doi:10.1021/acs.organomet.8b00559
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DOI: 10.5517/ccdc.csd.cc1mdtys
title: CCDC 1501886: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1phg2q
title: CCDC 1563983: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1pwk04
title: CCDC 1575606: Experimental Crystal Structure Determination

description: Related Article: Aaron Sandleben|2017|CSD Communication|||
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DOI: 10.5517/ccdc.csd.cc1pwk15
title: CCDC 1575607: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1pxc65
title: CCDC 1576387: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1q71mm
title: CCDC 1585700: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1q7ypl
title: CCDC 1586570: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1ytm8n
title: CCDC 1812082: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1ytm9p
title: CCDC 1812083: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1ytmbq
title: CCDC 1812084: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1ytmcr
title: CCDC 1812085: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1ytdqw
title: CCDC 1811879: Experimental Crystal Structure Determination

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DOI: 10.5517/ccdc.csd.cc1ytqfx
title: CCDC 1812180: Experimental Crystal Structure Determination

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