cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.22091527.v1
title: Reduced secretion of LCN2 (lipocalin 2) from reactive astrocytes through autophagic and proteasomal regulation alleviates inflammatory stress and neuronal damage

description: LCN2/neutrophil gelatinase-associated lipocalin/24p3 (lipocalin 2) is a secretory protein that acts as a mammalian bacteriostatic molecule. Under neuroinflammatory stress conditions, LCN2 is produced and secreted by activated microglia and reactive astrocytes, resulting in neuronal apoptosis. However, it remains largely unknown whether inflammatory stress and neuronal loss can be minimized by modulating LCN2 production and secretion. Here, we first demonstrated that LCN2 was secreted from reactive astrocytes, which were stimulated by treatment with lipopolysaccharide (LPS) as an inflammatory stressor. Notably, we found two effective conditions that led to the reduction of induced LCN2 levels in reactive astrocytes: proteasome inhibition and macroautophagic/autophagic flux activation. Mechanistically, proteasome inhibition suppresses NFKB/NF-κB activation through NFKBIA/IκBα stabilization in primary astrocytes, even under inflammatory stress conditions, resulting in the downregulation of <i>Lcn2</i> expression. In contrast, autophagic flux activation via MTOR inhibition reduced the intracellular levels of LCN2 through its pre-secretory degradation. In addition, we demonstrated that the N-terminal signal peptide of LCN2 is critical for its secretion and degradation, suggesting that these two pathways may be mechanistically coupled. Finally, we observed that LPS-induced and secreted LCN2 levels were reduced in the astrocyte-cultured medium under the above-mentioned conditions, resulting in increased neuronal viability, even under inflammatory stress. <b>Abbreviations:</b> ACM, astrocyte-conditioned medium; ALP, autophagy-lysosome pathway; BAF, bafilomycin A<sub>1</sub>; BTZ, bortezomib; CHX, cycloheximide; CNS, central nervous system; ER, endoplasmic reticulum; GFAP, glial fibrillary acidic protein; GFP, green fluorescent protein; JAK, Janus kinase; KD, knockdown; LCN2, lipocalin 2; LPS, lipopolysaccharide; MACS, magnetic-activated cell sorting; MAP1LC3/LC3, microtubule-associated protein 1 light chain 3; MTOR, mechanistic target of rapamycin kinase; NFKB/NF-κB, nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105; NFKBIA/IκBα, nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha; OVEX, overexpression; SLC22A17, solute carrier family 22 member 17; SP, signal peptide; SQSTM1, sequestosome 1; STAT3, signal transducer and activator of transcription 3; TNF/TNF-α, tumor necrosis factor; TUBA, tubulin, alpha; TUBB3/β3-TUB, tubulin, beta 3 class III; UB, ubiquitin; UPS, ubiquitin-proteasome system
DOI: 10.6084/m9.figshare.22140840
title: Identifying a selective inhibitor of autophagy that targets ATG12-ATG3 protein-protein interaction

description: Macroautophagy/autophagy is a catabolic process by which cytosolic content is engulfed, degraded and recycled. It has been implicated as a critical pathway in advanced stages of cancer, as it maintains tumor cell homeostasis and continuous growth by nourishing hypoxic or nutrient-starved tumors. Autophagy also supports alternative cellular trafficking pathways, providing a mechanism of non-canonical secretion of inflammatory cytokines. This opens a significant therapeutic opportunity for using autophagy inhibitors in cancer and acute inflammatory responses. Here we developed a high throughput compound screen to identify inhibitors of protein-protein interaction (PPI) in autophagy, based on the protein-fragment complementation assay (PCA). We chose to target the ATG12-ATG3 PPI, as this interaction is indispensable for autophagosome formation, and the analyzed structure of the interaction interface predicts that it may be amenable to inhibition by small molecules. We screened 41,161 compounds yielding 17 compounds that effectively inhibit the ATG12-ATG3 interaction in the PCA platform, and which were subsequently filtered by their ability to inhibit autophagosome formation in viable cells. We describe a lead compound (#189) that inhibited GFP-fused MAP1LC3B/LC3B (microtubule associated protein 1 light chain 3 beta) puncta formation in cells with IC50 value corresponding to 9.3 μM. This compound displayed a selective inhibitory effect on the growth of autophagy addicted tumor cells and inhibited secretion of IL1B/IL-1β (interleukin 1 beta) by macrophage-like cells. Compound 189 has the potential to be developed into a therapeutic drug and its discovery documents the power of targeting PPIs for acquiring specific and selective compound inhibitors of autophagy. <b>Abbreviations:</b> ANOVA: analysis of variance; ATG: autophagy related; CQ: chloroquine; GFP: green fluorescent protein; GLuc: <i>Gaussia</i> Luciferase; HEK: human embryonic kidney; IL1B: interleukin 1 beta; LPS: lipopolysaccharide; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; PCA: protein-fragment complementation assay; PDAC: pancreatic ductal adenocarcinoma; PMA: phorbol 12-myristate 13-acetate; PPI: protein-protein interaction. VCL: vinculin.
DOI: 10.6084/m9.figshare.22140840.v1
title: Identifying a selective inhibitor of autophagy that targets ATG12-ATG3 protein-protein interaction

description: Macroautophagy/autophagy is a catabolic process by which cytosolic content is engulfed, degraded and recycled. It has been implicated as a critical pathway in advanced stages of cancer, as it maintains tumor cell homeostasis and continuous growth by nourishing hypoxic or nutrient-starved tumors. Autophagy also supports alternative cellular trafficking pathways, providing a mechanism of non-canonical secretion of inflammatory cytokines. This opens a significant therapeutic opportunity for using autophagy inhibitors in cancer and acute inflammatory responses. Here we developed a high throughput compound screen to identify inhibitors of protein-protein interaction (PPI) in autophagy, based on the protein-fragment complementation assay (PCA). We chose to target the ATG12-ATG3 PPI, as this interaction is indispensable for autophagosome formation, and the analyzed structure of the interaction interface predicts that it may be amenable to inhibition by small molecules. We screened 41,161 compounds yielding 17 compounds that effectively inhibit the ATG12-ATG3 interaction in the PCA platform, and which were subsequently filtered by their ability to inhibit autophagosome formation in viable cells. We describe a lead compound (#189) that inhibited GFP-fused MAP1LC3B/LC3B (microtubule associated protein 1 light chain 3 beta) puncta formation in cells with IC50 value corresponding to 9.3 μM. This compound displayed a selective inhibitory effect on the growth of autophagy addicted tumor cells and inhibited secretion of IL1B/IL-1β (interleukin 1 beta) by macrophage-like cells. Compound 189 has the potential to be developed into a therapeutic drug and its discovery documents the power of targeting PPIs for acquiring specific and selective compound inhibitors of autophagy. <b>Abbreviations:</b> ANOVA: analysis of variance; ATG: autophagy related; CQ: chloroquine; GFP: green fluorescent protein; GLuc: <i>Gaussia</i> Luciferase; HEK: human embryonic kidney; IL1B: interleukin 1 beta; LPS: lipopolysaccharide; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; PCA: protein-fragment complementation assay; PDAC: pancreatic ductal adenocarcinoma; PMA: phorbol 12-myristate 13-acetate; PPI: protein-protein interaction. VCL: vinculin.
DOI: 10.6084/m9.figshare.22145359
title: The LC3B FRET biosensor monitors the modes of action of ATG4B during autophagy in living cells

description: Although several mechanisms of macroautophagy/autophagy have been dissected in the last decade, following this pathway in real time remains challenging. Among the early events leading to its activation, the ATG4B protease primes the key autophagy player MAP1LC3B/LC3B. Given the lack of reporters to follow this event in living cells, we developed a Förster’s resonance energy transfer (FRET) biosensor responding to the priming of LC3B by ATG4B. The biosensor was generated by flanking LC3B within a pH-resistant donor-acceptor FRET pair, Aquamarine-tdLanYFP. We here showed that the biosensor has a dual readout. First, FRET indicates the priming of LC3B by ATG4B and the resolution of the FRET image makes it possible to characterize the spatial heterogeneity of the priming activity. Second, quantifying the number of Aquamarine-LC3B puncta determines the degree of autophagy activation. We then showed that there are pools of unprimed LC3B upon <i>ATG4B</i> downregulation, and the priming of the biosensor is abolished in <i>ATG4B</i> knockout cells. The lack of priming can be rescued with the wild-type ATG4B or with the partially active W142A mutant, but not with the catalytically dead C74S mutant. Moreover, we screened for commercially-available ATG4B inhibitors, and illustrated their differential mode of action by implementing a spatially-resolved, broad-to-sensitive analysis pipeline combining FRET and the quantification of autophagic puncta. Finally, we uncovered the CDK1-dependent regulation of the ATG4B-LC3B axis at mitosis. Therefore, the LC3B FRET biosensor paves the way for a highly-quantitative monitoring of the ATG4B activity in living cells and in real time, with unprecedented spatiotemporal resolution. <b>Abbreviations:</b> Aqua: aquamarine; ATG: autophagy related; AURKA: aurora kinase A; BafA<sub>1</sub>: bafilomycin A<sub>1</sub>; CDK1: cyclin dependent kinase 1; DKO: double knockout; FLIM: fluorescence lifetime imaging microscopy; FP: fluorescence protein; FRET: Förster’s resonance energy transfer; GABARAP: GABA type A receptor-associated protein; HBSS: Hanks’ balanced salt solution; KO: knockout; LAMP2: lysosomal associated membrane protein 2; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; NSC: NSC 185058; PE: phosphatidylethanolamine; SKO: single knockout; TKO: triple knockout; ULK1: unc-51 like autophagy activating kinase 1; WT: wild-type; ZPCK: <i>Z-L</i>-phe chloromethyl ketone
DOI: 10.6084/m9.figshare.22145359.v1
title: The LC3B FRET biosensor monitors the modes of action of ATG4B during autophagy in living cells

description: Although several mechanisms of macroautophagy/autophagy have been dissected in the last decade, following this pathway in real time remains challenging. Among the early events leading to its activation, the ATG4B protease primes the key autophagy player MAP1LC3B/LC3B. Given the lack of reporters to follow this event in living cells, we developed a Förster’s resonance energy transfer (FRET) biosensor responding to the priming of LC3B by ATG4B. The biosensor was generated by flanking LC3B within a pH-resistant donor-acceptor FRET pair, Aquamarine-tdLanYFP. We here showed that the biosensor has a dual readout. First, FRET indicates the priming of LC3B by ATG4B and the resolution of the FRET image makes it possible to characterize the spatial heterogeneity of the priming activity. Second, quantifying the number of Aquamarine-LC3B puncta determines the degree of autophagy activation. We then showed that there are pools of unprimed LC3B upon <i>ATG4B</i> downregulation, and the priming of the biosensor is abolished in <i>ATG4B</i> knockout cells. The lack of priming can be rescued with the wild-type ATG4B or with the partially active W142A mutant, but not with the catalytically dead C74S mutant. Moreover, we screened for commercially-available ATG4B inhibitors, and illustrated their differential mode of action by implementing a spatially-resolved, broad-to-sensitive analysis pipeline combining FRET and the quantification of autophagic puncta. Finally, we uncovered the CDK1-dependent regulation of the ATG4B-LC3B axis at mitosis. Therefore, the LC3B FRET biosensor paves the way for a highly-quantitative monitoring of the ATG4B activity in living cells and in real time, with unprecedented spatiotemporal resolution. <b>Abbreviations:</b> Aqua: aquamarine; ATG: autophagy related; AURKA: aurora kinase A; BafA<sub>1</sub>: bafilomycin A<sub>1</sub>; CDK1: cyclin dependent kinase 1; DKO: double knockout; FLIM: fluorescence lifetime imaging microscopy; FP: fluorescence protein; FRET: Förster’s resonance energy transfer; GABARAP: GABA type A receptor-associated protein; HBSS: Hanks’ balanced salt solution; KO: knockout; LAMP2: lysosomal associated membrane protein 2; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; NSC: NSC 185058; PE: phosphatidylethanolamine; SKO: single knockout; TKO: triple knockout; ULK1: unc-51 like autophagy activating kinase 1; WT: wild-type; ZPCK: <i>Z-L</i>-phe chloromethyl ketone
DOI: 10.5281/zenodo.8147664
title: psolus_chitonoides_spades_01.fasta.gz

description: .
DOI: 10.5281/zenodo.8147663
title: psolus_chitonoides_spades_01.fasta.gz

description: .
DOI: 10.5281/zenodo.8010310
title: Data for: "Unlocking the potential of LC-MS through an XIC-based algorithm for chromatographic optimisation"

description: This dataset is for upload of supplementary info and data for my master research thesis at the University of Amsterdam. All the compounds in each pesticide mix of the RESTEK multiresidue kit can be found along with some descriptors. For easy use of the developed algorithm without having to generate any mzxml files, a few files are included on which SAFD and CompCreate have already been performed using three different LC methods, Their gradients are also provided. To run the code, a package has been developed and is ready for installation at: https://github.com/tobihul/LC_MS_Resolved_Peaks.
DOI: 10.5281/zenodo.8010309
title: Data for: "Unlocking the potential of LC-MS through an XIC-based algorithm for chromatographic optimisation"

description: This dataset is for upload of supplementary info and data for my master research thesis at the University of Amsterdam. All the compounds in each pesticide mix of the RESTEK multiresidue kit can be found along with some descriptors. For easy use of the developed algorithm without having to generate any mzxml files, a few files are included on which SAFD and CompCreate have already been performed using three different LC methods, Their gradients are also provided. To run the code, a package has been developed and is ready for installation at: https://github.com/tobihul/LC_MS_Resolved_Peaks.
DOI: 10.6084/m9.figshare.23686413
title: Field input values for the Simple excel depth-irradiance primary producution model for ICES station 7 and 13 in the North Sea

description: Dataset for field value input for a Simple excel depth-irradiance primary prodcution model. Data was obtained from copernicus satellite observations with chlorophyll from : https://doi.org/10.48670/moi-00284 and Kd was from: https://doi.org/10.48670/moi-00278. Irradinace was obtained from an ERA5 download found here ECMWF Reanalysis v5 | ECMWF.
DOI: 10.6084/m9.figshare.23686413.v3
title: Field input values for the Simple excel depth-irradiance primary producution model for ICES station 7 and 13 in the North Sea

description: Dataset for field value input for a Simple excel depth-irradiance primary prodcution model. Data was obtained from copernicus satellite observations with chlorophyll from : https://doi.org/10.48670/moi-00284 and Kd was from: https://doi.org/10.48670/moi-00278. Irradinace was obtained from an ERA5 download found here ECMWF Reanalysis v5 | ECMWF.
DOI: 10.6084/m9.figshare.23686413.v2
title: Field input values for the Simple excel depth-irradiance primary prodcution model for ICES station 7 and 13 in the North Sea

description: Dataset for field value input for a Simple excel depth-irradiance primary prodcution model. Data was obtained from copernicus satellite observations with chlorophyll from : https://doi.org/10.48670/moi-00284 and Kd was from: https://doi.org/10.48670/moi-00278. Irradinace was obtained from an ERA5 download found here ECMWF Reanalysis v5 | ECMWF.
DOI: 10.5281/zenodo.8147695
title: sarracenia_flava_spades_01.fasta.gz

description: .
DOI: 10.5281/zenodo.8147694
title: sarracenia_flava_spades_01.fasta.gz

description: .
DOI: 10.6084/m9.figshare.23686107
title: When Worlds Collide, Context Matters: Merging Distinct Datasets Built for Different Purposes

description: This poster presents the workflow/motivations of the joining of two distinct Earth science datasets built for different purposes (Macrostrat database of rocks and the Paleobiology Database of fossil occurrences), the intended applications of both data platforms, and how their unique data structures shaped interpretations of results generated from their merged dataset.
DOI: 10.6084/m9.figshare.23686107.v1
title: When Worlds Collide, Context Matters: Merging Distinct Datasets Built for Different Purposes

description: This poster presents the workflow/motivations of the joining of two distinct Earth science datasets built for different purposes (Macrostrat database of rocks and the Paleobiology Database of fossil occurrences), the intended applications of both data platforms, and how their unique data structures shaped interpretations of results generated from their merged dataset.
DOI: 10.5281/zenodo.8147723
title: heliamphora_pulchella_spades_01.fasta.gz

description: .
DOI: 10.5281/zenodo.8147722
title: heliamphora_pulchella_spades_01.fasta.gz

description: .
DOI: 10.5281/zenodo.8010478
title: Expecting Brexit and UK migration: Should I go? - Replication file

description: This folder contains the data and codes used for the article: Di Iasio, V. and Wahba, J. (2023) Expecting Brexit and UK migration: Should I go? <em>European Economic Review, </em>157:104484. A previous version of the article: Di Iasio, V. and Wahba, J. (2021) Brexit uncertainty and UK migration: Should I go? <em>QuantMig Project Deliverable D3.2</em>. University of Southampton. Included is a read_me,pdf file containing basic information for the replication and a data_files_location.pdf file that lists all the data files used in the analysis and their location.
DOI: 10.5281/zenodo.8010479
title: Expecting Brexit and UK migration: Should I go? - Replication file

description: This folder contains the data and codes used for the article: Di Iasio, V. and Wahba, J. (2023) Expecting Brexit and UK migration: Should I go? <em>European Economic Review, </em>157:104484. A previous version of the article: Di Iasio, V. and Wahba, J. (2021) Brexit uncertainty and UK migration: Should I go? <em>QuantMig Project Deliverable D3.2</em>. University of Southampton. Included is a read_me,pdf file containing basic information for the replication and a data_files_location.pdf file that lists all the data files used in the analysis and their location.
DOI: 10.6084/m9.figshare.23687094.v1
title: Transcripciones proyecto "<strong>Encuentros y tensiones en la construcción de cuerpos y sexualidades juveniles: las representaciones del mundo joven y del sistema de salud en el Chile actual"</strong>

description: <strong>Encuentros y tensiones en la construcción de cuerpos y sexualidades juveniles: las representaciones del mundo joven y del sistema de salud en el Chile actual</strong>
DOI: 10.3217/psrys-yep17
title: COFREND23 conference: Supplementary data to the manuscript

description: Data sets and technical description of the data sets presented in the manuscript. JOURNEES DE COFREND 2023 (Marseille, FR)
DOI: 10.3217/g0myc-fd571
title: DGZfP Jahrestagung 2023: Datenbasis zum Manuskript

description: Datenbasis und technische Beschreibung der Datensätze, die für die Analyse verwendet wurden und im Manuskript für die DGZfP Jahrestagung 2023 dargestellt sind.
DOI: 10.6084/m9.figshare.21893046
title: Yellow warbler Galapagos data

description: Animals across diverse lineages use referential calls to warn of and respond to specific threats, though the ability to understand these calls may be dependent on experience with the threat being referenced. Yellow warblers (<em>Setophaga petechia</em>) produce referential ‘seet’ calls towards brood parasitic brown-headed cowbirds (<em>Molothrus ater</em>), which threaten the warblers’ reproductive success. Seet calls are produced frequently in populations sympatric with cowbirds, but rarely in allopatric populations, even when those populations are genetically similar, begging the question of the role of personal experience in anti-parasitic responsiveness in aggression and propensity to seet call towards brood parasites. Here we tested for seet call responses from a yellow warbler population on the Galapagos Islands (subspecies <em>aureola</em>), which has been geographically isolated from the mainland and brood parasites for ~300,000 years. We presented playbacks of brown-headed cowbird calls (allopatric brood parasite), seet calls (North American yellow warbler’s referential anti-parasitic call), chip calls (yellow warbler’s general alarm call), sympatric predator calls, and harmless allopatric and sympatric control songs to breeding yellow warblers, and compared behavioral and vocal responses between treatments. We found that in response to playbacks signaling brood parasitic risk (seet and cowbird calls), Galapagos yellow warblers showed aggression comparable to controls, and much lower compared to chip or predator playbacks. Galapagos yellow warblers never produced any seet calls in response to the playbacks. Our results suggest that in geographic isolation from cowbirds, Galapagos yellow warblers do not produce or respond to referential alarm calls indicating mainland brood parasitic nest threats.
DOI: 10.6084/m9.figshare.23681868.v1
title: Nutrient

description: Input nutrient data for loadest
DOI: 10.6084/m9.figshare.23681868.v2
title: loadestInput_nutrient

description: Input nutrient data for loadest
DOI: 10.5281/zenodo.8147760
title: sarracenia_psittacina_spades_01.fasta.gz

description: .
DOI: 10.5281/zenodo.8147759
title: sarracenia_psittacina_spades_01.fasta.gz

description: .
DOI: 10.5066/p9wa2m2y
title: Greater Sage-Grouse Adult and Nest Observations Before and After Wildfire in Northwest Nevada (2008-2019)

description: Wildfire events are becoming more frequent and severe on a global scale. Rising temperatures, prolonged drought, and the presence of pyrophytic invasive grasses are contributing to the degradation of native vegetation communities. Within the Great Basin region of the Western United States, increasing wildfire frequency is transforming the ecosystem toward a higher degree of homogeneity, one dominated by invasive annual grasses and declining landscape productivity. Greater sage-grouse (Centrocercus urophasianus; hereafter sage-grouse) are a species of conservation concern that rely on large tracts of structurally and functionally diverse sagebrush (Artemisia spp.) communities. Using a 12-year (2008-2019) telemetry dataset, we documented immediate impacts of wildfire on demographic rates of a population of sage-grouse that were exposed to two large wildfire events (Virginia Mountains Fire Complex - 2016; Long Valley Fire - 2017) near the border of California and Nevada. Spatiotemporal heterogeneity in demographic rates were accounted for using a Before-After Control-Impact Paired Series (BACIPS) study design. These data support the following publication: Tyrrell, E.A., Coates, P.S., Prochazka, B.G., Brussee, B.E., Espinosa, S.P. and Hull, J.M., 2023. Wildfire immediately reduces nest and adult survival of greater sage-grouse. Scientific Reports, 13(1), p.10970.