cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1314131.v1
title: Single-cell analysis challenges the connection between autophagy and senescence induced by DNA damage

description: Autophagy and senescence have been described as central features of cell biology, but the interplay between these mechanisms remains obscure. Using a therapeutically relevant model of DNA damage-induced senescence in human glioma cells, we demonstrated that acute treatment with temozolomide induces DNA damage, a transitory activation of PRKAA/AMPK-ULK1 and MAPK14/p38 and the sustained inhibition of AKT-MTOR. This produced a transient induction of autophagy, which was followed by senescence. However, at the single cell level, this coordinated transition was not observed, and autophagy and senescence were triggered in a very heterogeneous manner. Indeed, at a population level, autophagy was highly negatively correlated with senescence markers, while in single cells this correlation did not exist. The inhibition of autophagy triggered apoptosis and decreased senescence, while its activation increased temozolomide-induced senescence, showing that DNA damage-induced autophagy acts by suppressing apoptosis.
DOI: 10.6084/m9.figshare.1314132.v3
title: <i>Purranisaurus potens</i> Rusconi, an enigmatic metriorhynchid from the Late Jurassic–Early Cretaceous of the Neuquén Basin

description: ABSTRACTThe Tithonian record from northwestern Patagonia (Neuquén Basin) documents a complete succession of lower, middle, and late Tithonian marine reptiles. From the late Tithonian–early Berriasian of Patagonia, three marine crocodyliforms have been recorded: <i>Dakosaurus andiniensis</i>, <i>Cricosaurus araucanensis</i>, and <i>Purranisaurus potens</i>. Although <i>P. potens</i> includes the first metriorhynchid skull described from Patagonia, no detailed description and/or illustrations have been published. Since the mid-20th century, several authors have discussed the validity of <i>P. potens</i>. Recent preparation of the type material allowed a detailed description as well as exploration of its phylogenetic relationships. We consider <i>P. potens</i> as a valid taxon characterized by a unique combination of characters, such as medial and posterolateral processes of the frontal forming an angle of 60°; supratemporal fossae reaching the minimum interorbital distance, with the dorsal margin of the supratemporal arch being slightly concave in lateral view; thin bony lamina projecting from the lateral and medial alveolar margins of the maxilla; occipital surface ventral to occipital condyle parallel to transverse plane of skull; well-developed crest that extends along the entire height of the supraoccipital; and orbital process of the quadrate very conspicuous and acute, horizontal, and without bony attachment. Phylogenetic analysis recovers <i>P. potens</i> as deeply nested within Geosaurini and, contrary to previous proposals, not closely related to ‘<i>Metriorhynchus</i>’ <i>casamiquelai</i> and ‘<i>M.</i>’ <i>westermanni</i>. Internal relationships within Geosaurini are unresolved. <i>Purranisaurus</i>, as a monotypic genus, is restricted to the late Tithonian–early Berriasian.http://zoobank.org/urn:lsid:zoobank.org:pub:CDB288F2-087C-4E19-A897-8AB94BD60EC2SUPPLEMENTAL DATA—Supplemental materials are available for this article for free at www.tandfonline.com/UJVP
DOI: 10.6084/m9.figshare.1314132.v2
title: <i>Purranisaurus potens</i> Rusconi, an enigmatic metriorhynchid from the Late Jurassic–Early Cretaceous of the Neuquén Basin

description: ABSTRACTThe Tithonian record from northwestern Patagonia (Neuquén Basin) documents a complete succession of lower, middle, and late Tithonian marine reptiles. From the late Tithonian–early Berriasian of Patagonia, three marine crocodyliforms have been recorded: <i>Dakosaurus andiniensis</i>, <i>Cricosaurus araucanensis</i>, and <i>Purranisaurus potens</i>. Although <i>P. potens</i> includes the first metriorhynchid skull described from Patagonia, no detailed description and/or illustrations have been published. Since the mid-20th century, several authors have discussed the validity of <i>P. potens</i>. Recent preparation of the type material allowed a detailed description as well as exploration of its phylogenetic relationships. We consider <i>P. potens</i> as a valid taxon characterized by a unique combination of characters, such as medial and posterolateral processes of the frontal forming an angle of 60°; supratemporal fossae reaching the minimum interorbital distance, with the dorsal margin of the supratemporal arch being slightly concave in lateral view; thin bony lamina projecting from the lateral and medial alveolar margins of the maxilla; occipital surface ventral to occipital condyle parallel to transverse plane of skull; well-developed crest that extends along the entire height of the supraoccipital; and orbital process of the quadrate very conspicuous and acute, horizontal, and without bony attachment. Phylogenetic analysis recovers <i>P. potens</i> as deeply nested within Geosaurini and, contrary to previous proposals, not closely related to ‘<i>Metriorhynchus</i>’ <i>casamiquelai</i> and ‘<i>M.</i>’ <i>westermanni</i>. Internal relationships within Geosaurini are unresolved. <i>Purranisaurus</i>, as a monotypic genus, is restricted to the late Tithonian–early Berriasian.http://zoobank.org/urn:lsid:zoobank.org:pub:CDB288F2-087C-4E19-A897-8AB94BD60EC2SUPPLEMENTAL DATA—Supplemental materials are available for this article for free at www.tandfonline.com/UJVP
DOI: 10.6084/m9.figshare.1314128
title: SIRT5 regulation of ammonia-induced autophagy and mitophagy

description: In liver the mitochondrial sirtuin, SIRT5, controls ammonia detoxification by regulating CPS1, the first enzyme of the urea cycle. However, while SIRT5 is ubiquitously expressed, urea cycle and CPS1 are only present in the liver and, to a minor extent, in the kidney. To address the possibility that SIRT5 is involved in ammonia production also in nonliver cells, clones of human breast cancer cell lines MDA-MB-231 and mouse myoblast C2C12, overexpressing or silenced for SIRT5 were produced. Our results show that ammonia production increased in SIRT5-silenced and decreased in SIRT5-overexpressing cells. We also obtained the same ammonia increase when using a new specific inhibitor of SIRT5 called MC3482. SIRT5 regulates ammonia production by controlling glutamine metabolism. In fact, in the mitochondria, glutamine is transformed in glutamate by the enzyme glutaminase, a reaction producing ammonia. We found that SIRT5 and glutaminase coimmunoprecipitated and that SIRT5 inhibition resulted in an increased succinylation of glutaminase. We next determined that autophagy and mitophagy were increased by ammonia by measuring autophagic proteolysis of long-lived proteins, increase of autophagy markers MAP1LC3B, GABARAP, and GABARAPL2, mitophagy markers BNIP3 and the PINK1-PARK2 system as well as mitochondrial morphology and dynamics. We observed that autophagy and mitophagy increased in SIRT5-silenced cells and in WT cells treated with MC3482 and decreased in SIRT5-overexpressing cells. Moreover, glutaminase inhibition or glutamine withdrawal completely prevented autophagy. In conclusion we propose that the role of SIRT5 in nonliver cells is to regulate ammonia production and ammonia-induced autophagy by regulating glutamine metabolism.
DOI: 10.6084/m9.figshare.1314128.v2
title: SIRT5 regulation of ammonia-induced autophagy and mitophagy

description: In liver the mitochondrial sirtuin, SIRT5, controls ammonia detoxification by regulating CPS1, the first enzyme of the urea cycle. However, while SIRT5 is ubiquitously expressed, urea cycle and CPS1 are only present in the liver and, to a minor extent, in the kidney. To address the possibility that SIRT5 is involved in ammonia production also in nonliver cells, clones of human breast cancer cell lines MDA-MB-231 and mouse myoblast C2C12, overexpressing or silenced for SIRT5 were produced. Our results show that ammonia production increased in SIRT5-silenced and decreased in SIRT5-overexpressing cells. We also obtained the same ammonia increase when using a new specific inhibitor of SIRT5 called MC3482. SIRT5 regulates ammonia production by controlling glutamine metabolism. In fact, in the mitochondria, glutamine is transformed in glutamate by the enzyme glutaminase, a reaction producing ammonia. We found that SIRT5 and glutaminase coimmunoprecipitated and that SIRT5 inhibition resulted in an increased succinylation of glutaminase. We next determined that autophagy and mitophagy were increased by ammonia by measuring autophagic proteolysis of long-lived proteins, increase of autophagy markers MAP1LC3B, GABARAP, and GABARAPL2, mitophagy markers BNIP3 and the PINK1-PARK2 system as well as mitochondrial morphology and dynamics. We observed that autophagy and mitophagy increased in SIRT5-silenced cells and in WT cells treated with MC3482 and decreased in SIRT5-overexpressing cells. Moreover, glutaminase inhibition or glutamine withdrawal completely prevented autophagy. In conclusion we propose that the role of SIRT5 in nonliver cells is to regulate ammonia production and ammonia-induced autophagy by regulating glutamine metabolism.
DOI: 10.6084/m9.figshare.1314131.v2
title: Single-cell analysis challenges the connection between autophagy and senescence induced by DNA damage

description: Autophagy and senescence have been described as central features of cell biology, but the interplay between these mechanisms remains obscure. Using a therapeutically relevant model of DNA damage-induced senescence in human glioma cells, we demonstrated that acute treatment with temozolomide induces DNA damage, a transitory activation of PRKAA/AMPK-ULK1 and MAPK14/p38 and the sustained inhibition of AKT-MTOR. This produced a transient induction of autophagy, which was followed by senescence. However, at the single cell level, this coordinated transition was not observed, and autophagy and senescence were triggered in a very heterogeneous manner. Indeed, at a population level, autophagy was highly negatively correlated with senescence markers, while in single cells this correlation did not exist. The inhibition of autophagy triggered apoptosis and decreased senescence, while its activation increased temozolomide-induced senescence, showing that DNA damage-induced autophagy acts by suppressing apoptosis.
DOI: 10.6084/m9.figshare.1314459
title: Portal Project Teaching Database

description: The Portal Project Teaching Database is a simplified version of the Portal Project Database designed for teaching. It provides a real world example of life-history, population, and ecological data, with sufficient complexity to teach many aspects of data analysis and management, but with many complexities removed to allow students to focus on the core ideas and skills being taught. The database is currently available in csv, json, and sqlite. This database is not designed for research as it intentionally removes some of the real-world complexities. The original database is published at Ecological Archives(http://esapubs.org/archive/ecol/E090/118/) and this version of the database should be used for research purposes. The Python code used for converting the original database to this teach version is included as 'create_portal_teach_dataset.py'. Suggested changes or additions to this dataset can be requested or contributed in the project GitHub repository(https://github.com/weecology/portal-teachingdb).
DOI: 10.6084/m9.figshare.1314128.v1
title: SIRT5 regulation of ammonia-induced autophagy and mitophagy

description: In liver the mitochondrial sirtuin, SIRT5, controls ammonia detoxification by regulating CPS1, the first enzyme of the urea cycle. However, while SIRT5 is ubiquitously expressed, urea cycle and CPS1 are only present in the liver and, to a minor extent, in the kidney. To address the possibility that SIRT5 is involved in ammonia production also in nonliver cells, clones of human breast cancer cell lines MDA-MB-231 and mouse myoblast C2C12, overexpressing or silenced for SIRT5 were produced. Our results show that ammonia production increased in SIRT5-silenced and decreased in SIRT5-overexpressing cells. We also obtained the same ammonia increase when using a new specific inhibitor of SIRT5 called MC3482. SIRT5 regulates ammonia production by controlling glutamine metabolism. In fact, in the mitochondria, glutamine is transformed in glutamate by the enzyme glutaminase, a reaction producing ammonia. We found that SIRT5 and glutaminase coimmunoprecipitated and that SIRT5 inhibition resulted in an increased succinylation of glutaminase. We next determined that autophagy and mitophagy were increased by ammonia by measuring autophagic proteolysis of long-lived proteins, increase of autophagy markers MAP1LC3B, GABARAP, and GABARAPL2, mitophagy markers BNIP3 and the PINK1-PARK2 system as well as mitochondrial morphology and dynamics. We observed that autophagy and mitophagy increased in SIRT5-silenced cells and in WT cells treated with MC3482 and decreased in SIRT5-overexpressing cells. Moreover, glutaminase inhibition or glutamine withdrawal completely prevented autophagy. In conclusion we propose that the role of SIRT5 in nonliver cells is to regulate ammonia production and ammonia-induced autophagy by regulating glutamine metabolism.
DOI: 10.6084/m9.figshare.1314126
title: A novel mechanism of autophagic cell death in dystrophic muscle regulated by P2RX7 receptor large-pore formation and HSP90

description: P2RX7 is an ATP-gated ion channel, which can also exhibit an open state with a considerably wider permeation. However, the functional significance of the movement of molecules through the large pore (LP) and the intracellular signaling events involved are not known. Here, analyzing the consequences of P2RX7 activation in primary myoblasts and myotubes from the <i>Dmd<sup>mdx</sup></i> mouse model of Duchenne muscular dystrophy, we found ATP-induced P2RX7-dependent autophagic flux, leading to CASP3-CASP7-independent cell death. P2RX7-evoked autophagy was triggered by LP formation but not Ca<sup>2+</sup> influx or MAPK1-MAPK3 phosphorylation, 2 canonical P2RX7-evoked signals. Phosphoproteomics, protein expression inference and signaling pathway prediction analysis of P2RX7 signaling mediators pointed to HSPA2 and HSP90 proteins. Indeed, specific HSP90 inhibitors prevented LP formation, LC3-II accumulation, and cell death in myoblasts and myotubes but not in macrophages. Pharmacological blockade or genetic ablation of <i>p2rx7</i> also proved protective against ATP-induced death of muscle cells, as did inhibition of autophagy with 3-MA. The functional significance of the P2RX7 LP is one of the great unknowns of purinergic signaling. Our data demonstrate a novel outcome—autophagy—and show that molecules entering through the LP can be targeted to phagophores. Moreover, we show that in muscles but not in macrophages, autophagy is needed for the formation of this LP. Given that P2RX7-dependent LP and HSP90 are critically interacting in the ATP-evoked autophagic death of dystrophic muscles, treatments targeting this axis could be of therapeutic benefit in this debilitating and incurable form of muscular dystrophy.
DOI: 10.6084/m9.figshare.1314131.v3
title: Single-cell analysis challenges the connection between autophagy and senescence induced by DNA damage

description: Autophagy and senescence have been described as central features of cell biology, but the interplay between these mechanisms remains obscure. Using a therapeutically relevant model of DNA damage-induced senescence in human glioma cells, we demonstrated that acute treatment with temozolomide induces DNA damage, a transitory activation of PRKAA/AMPK-ULK1 and MAPK14/p38 and the sustained inhibition of AKT-MTOR. This produced a transient induction of autophagy, which was followed by senescence. However, at the single cell level, this coordinated transition was not observed, and autophagy and senescence were triggered in a very heterogeneous manner. Indeed, at a population level, autophagy was highly negatively correlated with senescence markers, while in single cells this correlation did not exist. The inhibition of autophagy triggered apoptosis and decreased senescence, while its activation increased temozolomide-induced senescence, showing that DNA damage-induced autophagy acts by suppressing apoptosis.
DOI: 10.6084/m9.figshare.1314124
title: Qualitative Report

description: This report contains the findings of qualitative research which was conducted in 7 districts of Uttar Pradesh and Bihar in India to understand and assess community's recognition of pneumonia and its danger signs, when and where do they seek health care and what was their perception regarding risk due to delayed treatment.
DOI: 10.6084/m9.figshare.1314126.v1
title: A novel mechanism of autophagic cell death in dystrophic muscle regulated by P2RX7 receptor large-pore formation and HSP90

description: P2RX7 is an ATP-gated ion channel, which can also exhibit an open state with a considerably wider permeation. However, the functional significance of the movement of molecules through the large pore (LP) and the intracellular signaling events involved are not known. Here, analyzing the consequences of P2RX7 activation in primary myoblasts and myotubes from the <i>Dmd<sup>mdx</sup></i> mouse model of Duchenne muscular dystrophy, we found ATP-induced P2RX7-dependent autophagic flux, leading to CASP3-CASP7-independent cell death. P2RX7-evoked autophagy was triggered by LP formation but not Ca<sup>2+</sup> influx or MAPK1-MAPK3 phosphorylation, 2 canonical P2RX7-evoked signals. Phosphoproteomics, protein expression inference and signaling pathway prediction analysis of P2RX7 signaling mediators pointed to HSPA2 and HSP90 proteins. Indeed, specific HSP90 inhibitors prevented LP formation, LC3-II accumulation, and cell death in myoblasts and myotubes but not in macrophages. Pharmacological blockade or genetic ablation of <i>p2rx7</i> also proved protective against ATP-induced death of muscle cells, as did inhibition of autophagy with 3-MA. The functional significance of the P2RX7 LP is one of the great unknowns of purinergic signaling. Our data demonstrate a novel outcome—autophagy—and show that molecules entering through the LP can be targeted to phagophores. Moreover, we show that in muscles but not in macrophages, autophagy is needed for the formation of this LP. Given that P2RX7-dependent LP and HSP90 are critically interacting in the ATP-evoked autophagic death of dystrophic muscles, treatments targeting this axis could be of therapeutic benefit in this debilitating and incurable form of muscular dystrophy.
DOI: 10.6084/m9.figshare.1314124.v1
title: Qualitative Report

description: This report contains the findings of qualitative research which was conducted in 7 districts of Uttar Pradesh and Bihar in India to understand and assess community's recognition of pneumonia and its danger signs, when and where do they seek health care and what was their perception regarding risk due to delayed treatment.
DOI: 10.6084/m9.figshare.1314099
title: Human behavior in contextual multi-armed bandit problems - Experimental data

description: This is raw data from the experiment described in the following article: Stojic, H., Analytis, P. P., & Speekenbrink, M. (2015). Human behavior in contextual multi-armed bandit problems. Proceedings of the 37th Annual Conference of the Cognitive Science Society. Austin, TX: Cognitive Science Society. See exp1_Readme.pdf file for more detailed instructions, descriptions of variables and licencse. The experiment itself can be tried out at the following URL: http://experimentnext.com/CMABvsMABexp1
DOI: 10.6084/m9.figshare.1314131.v4
title: Single-cell analysis challenges the connection between autophagy and senescence induced by DNA damage

description: Autophagy and senescence have been described as central features of cell biology, but the interplay between these mechanisms remains obscure. Using a therapeutically relevant model of DNA damage-induced senescence in human glioma cells, we demonstrated that acute treatment with temozolomide induces DNA damage, a transitory activation of PRKAA/AMPK-ULK1 and MAPK14/p38 and the sustained inhibition of AKT-MTOR. This produced a transient induction of autophagy, which was followed by senescence. However, at the single cell level, this coordinated transition was not observed, and autophagy and senescence were triggered in a very heterogeneous manner. Indeed, at a population level, autophagy was highly negatively correlated with senescence markers, while in single cells this correlation did not exist. The inhibition of autophagy triggered apoptosis and decreased senescence, while its activation increased temozolomide-induced senescence, showing that DNA damage-induced autophagy acts by suppressing apoptosis.
DOI: 10.6084/m9.figshare.1313972
title: #MikeBrown.12.26-1.23.xlsx

description: Twitter data on #MikeBrown. See Project Descritpion for details.
DOI: 10.6084/m9.figshare.1314102.v1
title: 12 January 2015 Field Notes

description: Field notes including image and/or video records.
DOI: 10.6084/m9.figshare.1313951
title: #MikeBrown12.17-12.26.xlsx

description: Twitter data on #MikeBrown. See Project Descritpion for details.
DOI: 10.6084/m9.figshare.1313924
title: #MikeBrown.12.10-12.17.xlsx

description: Twitter data on #MikeBrown. See Project Descritpion for details.
DOI: 10.6084/m9.figshare.1313951.v1
title: #MikeBrown12.17-12.26.xlsx

description: Twitter data on #MikeBrown. See Project Descritpion for details.
DOI: 10.6084/m9.figshare.1313924.v1
title: #MikeBrown.12.10-12.17.xlsx

description: Twitter data on #MikeBrown. See Project Descritpion for details.
DOI: 10.6084/m9.figshare.1314131.v5
title: Single-cell analysis challenges the connection between autophagy and senescence induced by DNA damage

description: Autophagy and senescence have been described as central features of cell biology, but the interplay between these mechanisms remains obscure. Using a therapeutically relevant model of DNA damage-induced senescence in human glioma cells, we demonstrated that acute treatment with temozolomide induces DNA damage, a transitory activation of PRKAA/AMPK-ULK1 and MAPK14/p38 and the sustained inhibition of AKT-MTOR. This produced a transient induction of autophagy, which was followed by senescence. However, at the single cell level, this coordinated transition was not observed, and autophagy and senescence were triggered in a very heterogeneous manner. Indeed, at a population level, autophagy was highly negatively correlated with senescence markers, while in single cells this correlation did not exist. The inhibition of autophagy triggered apoptosis and decreased senescence, while its activation increased temozolomide-induced senescence, showing that DNA damage-induced autophagy acts by suppressing apoptosis.
DOI: 10.6084/m9.figshare.1313905
title: #MikeBrown.12.6-12.10.xlsx

description: Twitter data on #MikeBrown. See Project Descritpion for details.
DOI: 10.6084/m9.figshare.1314102.v2
title: 12 January 2015 Field Notes

description: Field notes including image and/or video records.
DOI: 10.6084/m9.figshare.1313875
title: #MikeBrown12.4-12.6.xlsx

description: Twitter data on #MikeBrown. See Project Descritpion for details.
DOI: 10.6084/m9.figshare.1314099.v4
title: Human behavior in contextual multi-armed bandit problems

description: This is raw data from the experiment described in the following article: Stojic, H., Analytis, P. P., & Speekenbrink, M. (2015). Human behavior in contextual multi-armed bandit problems. Proceedings of the 37th Annual Conference of the Cognitive Science Society. Austin, TX: Cognitive Science Society. See exp1_Readme.pdf file for more detailed instructions, descriptions of variables and licencse. The experiment itself can be tried out at the following URL: http://experimentnext.com/CMABvsMABexp1