cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.6754103
title: PARK7 modulates autophagic proteolysis through binding to the N-terminally arginylated form of the molecular chaperone HSPA5

description: Macroautophagy is induced under various stresses to remove cytotoxic materials, including misfolded proteins and their aggregates. These protein cargoes are collected by specific autophagic receptors such as SQSTM1/p62 (sequestosome 1) and delivered to phagophores for lysosomal degradation. To date, little is known about how cells sense and react to diverse stresses by inducing the activity of SQSTM1. Here, we show that the peroxiredoxin-like redox sensor PARK7/DJ-1 modulates the activity of SQSTM1 and the targeting of ubiquitin (Ub)-conjugated proteins to macroautophagy under oxidative stress caused by TNFSF10/TRAIL (tumor necrosis factor [ligand] superfamily, member 10). In this mechanism, TNFSF10 induces the N-terminal arginylation (Nt-arginylation) of the endoplasmic reticulum (ER)-residing molecular chaperone HSPA5/BiP/GRP78, leading to cytosolic accumulation of Nt-arginylated HSPA5 (R-HSPA5). In parallel, TNFSF10 induces the oxidation of PARK7. Oxidized PARK7 acts as a co-chaperone-like protein that binds the ER-derived chaperone R-HSPA5, a member of the HSPA/HSP70 family. By forming a complex with PARK7 (and possibly misfolded protein cargoes), R-HSPA5 binds SQSTM1 through its Nt-Arg, facilitating self-polymerization of SQSTM1 and the targeting of SQSTM1-cargo complexes to phagophores. The 3-way interaction among PARK7, R-HSPA5, and SQSTM1 is stabilized by the Nt-Arg residue of R-HSPA5. PARK7-deficient cells are impaired in the targeting of R-HSPA5 and SQSTM1 to phagophores and the removal of Ub-conjugated cargoes. Our results suggest that PARK7 functions as a co-chaperone for R-HSPA5 to modulate autophagic removal of misfolded protein cargoes generated by oxidative stress.
DOI: 10.6084/m9.figshare.6754103.v2
title: PARK7 modulates autophagic proteolysis through binding to the N-terminally arginylated form of the molecular chaperone HSPA5

description: Macroautophagy is induced under various stresses to remove cytotoxic materials, including misfolded proteins and their aggregates. These protein cargoes are collected by specific autophagic receptors such as SQSTM1/p62 (sequestosome 1) and delivered to phagophores for lysosomal degradation. To date, little is known about how cells sense and react to diverse stresses by inducing the activity of SQSTM1. Here, we show that the peroxiredoxin-like redox sensor PARK7/DJ-1 modulates the activity of SQSTM1 and the targeting of ubiquitin (Ub)-conjugated proteins to macroautophagy under oxidative stress caused by TNFSF10/TRAIL (tumor necrosis factor [ligand] superfamily, member 10). In this mechanism, TNFSF10 induces the N-terminal arginylation (Nt-arginylation) of the endoplasmic reticulum (ER)-residing molecular chaperone HSPA5/BiP/GRP78, leading to cytosolic accumulation of Nt-arginylated HSPA5 (R-HSPA5). In parallel, TNFSF10 induces the oxidation of PARK7. Oxidized PARK7 acts as a co-chaperone-like protein that binds the ER-derived chaperone R-HSPA5, a member of the HSPA/HSP70 family. By forming a complex with PARK7 (and possibly misfolded protein cargoes), R-HSPA5 binds SQSTM1 through its Nt-Arg, facilitating self-polymerization of SQSTM1 and the targeting of SQSTM1-cargo complexes to phagophores. The 3-way interaction among PARK7, R-HSPA5, and SQSTM1 is stabilized by the Nt-Arg residue of R-HSPA5. PARK7-deficient cells are impaired in the targeting of R-HSPA5 and SQSTM1 to phagophores and the removal of Ub-conjugated cargoes. Our results suggest that PARK7 functions as a co-chaperone for R-HSPA5 to modulate autophagic removal of misfolded protein cargoes generated by oxidative stress.
DOI: 10.5281/zenodo.8196962
title: RDM dataset

description: This dataset contains images of the CNR-STIIMA ReDeManufacturing Lab, focusing on three classes of objects: conveyor, pallet, PCB. The dataset comprises real data as pictures of real assets and synthetic data generated using the VR digital twin of the lab.
DOI: 10.6084/m9.figshare.6754103.v1
title: PARK7 modulates autophagic proteolysis through binding to the N-terminally arginylated form of the molecular chaperone HSPA5

description: Macroautophagy is induced under various stresses to remove cytotoxic materials, including misfolded proteins and their aggregates. These protein cargoes are collected by specific autophagic receptors such as SQSTM1/p62 (sequestosome 1) and delivered to phagophores for lysosomal degradation. To date, little is known about how cells sense and react to diverse stresses by inducing the activity of SQSTM1. Here, we show that the peroxiredoxin-like redox sensor PARK7/DJ-1 modulates the activity of SQSTM1 and the targeting of ubiquitin (Ub)-conjugated proteins to macroautophagy under oxidative stress caused by TNFSF10/TRAIL (tumor necrosis factor [ligand] superfamily, member 10). In this mechanism, TNFSF10 induces the N-terminal arginylation (Nt-arginylation) of the endoplasmic reticulum (ER)-residing molecular chaperone HSPA5/BiP/GRP78, leading to cytosolic accumulation of Nt-arginylated HSPA5 (R-HSPA5). In parallel, TNFSF10 induces the oxidation of PARK7. Oxidized PARK7 acts as a co-chaperone-like protein that binds the ER-derived chaperone R-HSPA5, a member of the HSPA/HSP70 family. By forming a complex with PARK7 (and possibly misfolded protein cargoes), R-HSPA5 binds SQSTM1 through its Nt-Arg, facilitating self-polymerization of SQSTM1 and the targeting of SQSTM1-cargo complexes to phagophores. The 3-way interaction among PARK7, R-HSPA5, and SQSTM1 is stabilized by the Nt-Arg residue of R-HSPA5. PARK7-deficient cells are impaired in the targeting of R-HSPA5 and SQSTM1 to phagophores and the removal of Ub-conjugated cargoes. Our results suggest that PARK7 functions as a co-chaperone for R-HSPA5 to modulate autophagic removal of misfolded protein cargoes generated by oxidative stress.
DOI: 10.6084/m9.figshare.6973877
title: 6-Hydroxydopamine induces secretion of PARK7/DJ-1 via autophagy-based unconventional secretory pathway

description: PARK7/DJ-1 is a Parkinson disease- and cancer-associated protein that functions as a multifunctional protein involved in gene transcription regulation and anti-oxidative defense. Although PARK7 lacks the secretory signal sequence, it is secreted and plays important physiological and pathophysiological roles. Whereas secretory proteins that lack the endoplasmic reticulum-targeting signal sequence are secreted from cells by way of what is called the unconventional secretion mechanism, the specific processes responsible for causing PARK7 to be secreted across the plasma membrane have remained unclear. In the present study, we found that PARK7 secretion was increased by treatment with 6-OHDA via the unconventional secretory pathway in human neuroblastoma SH-SY5Y cells and MEF cells. We also found that 6-OHDA-induced PARK7 secretion was suppressed in <i>Atg5-, Atg9</i>-, or <i>Atg16l1</i>-deficient MEF cells or ATG16L1 knockdown SH-SY5Y cells, indicating that the autophagy-based unconventional secretory pathway is involved in PARK7 secretion. We moreover observed that 6-OHDA-derived electrophilic quinone induced oxidative stress as indicated by a decrease in glutathione levels, and that this was suppressed by pretreatment with antioxidant NAC. We further found that NAC treatment suppressed autophagy and PARK7 secretion. We also observed that 6-OHDA-induced autophagy was associated with activation of AMPK and ULK1 via a pathway which was independent of MTOR. Collectively these results suggest that electrophilic 6-OHDA quinone enhances oxidative stress, and that this is followed by AMPK-ULK1 pathway activation and induction of secretory autophagy to produce unconventional secretion of PARK7. <b>Abbreviations:</b> 6-OHDA: 6-hydroxydopamine; AMPK: AMP-activated protein kinase; ATG: autophagy related; CAV1: caveolin 1; ER: endoplasmic reticulum; FN1: fibronectin 1; GSH: glutathione; IDE: insulin degrading enzyme; IL: interleukin; LDH: lactate dehydrogenase; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MEF: mouse embryonic fibroblast; MTOR: mechanistic target of rapamycin kinase; NAC: N-acetyl-L-cysteine; PARK7/DJ-1: Parkinsonism associated deglycase; PD: Parkinson disease; RPS6KB1/p70S6K: ribosomal protein S6 kinase B1; RPN1: ribophorin I; ROS: reactive oxygen species; ULK1: unc-51 like autophagy activating kinase 1; WT: wild-type
DOI: 10.6084/m9.figshare.6973877.v1
title: 6-Hydroxydopamine induces secretion of PARK7/DJ-1 via autophagy-based unconventional secretory pathway

description: PARK7/DJ-1 is a Parkinson disease- and cancer-associated protein that functions as a multifunctional protein involved in gene transcription regulation and anti-oxidative defense. Although PARK7 lacks the secretory signal sequence, it is secreted and plays important physiological and pathophysiological roles. Whereas secretory proteins that lack the endoplasmic reticulum-targeting signal sequence are secreted from cells by way of what is called the unconventional secretion mechanism, the specific processes responsible for causing PARK7 to be secreted across the plasma membrane have remained unclear. In the present study, we found that PARK7 secretion was increased by treatment with 6-OHDA via the unconventional secretory pathway in human neuroblastoma SH-SY5Y cells and MEF cells. We also found that 6-OHDA-induced PARK7 secretion was suppressed in <i>Atg5-, Atg9</i>-, or <i>Atg16l1</i>-deficient MEF cells or ATG16L1 knockdown SH-SY5Y cells, indicating that the autophagy-based unconventional secretory pathway is involved in PARK7 secretion. We moreover observed that 6-OHDA-derived electrophilic quinone induced oxidative stress as indicated by a decrease in glutathione levels, and that this was suppressed by pretreatment with antioxidant NAC. We further found that NAC treatment suppressed autophagy and PARK7 secretion. We also observed that 6-OHDA-induced autophagy was associated with activation of AMPK and ULK1 via a pathway which was independent of MTOR. Collectively these results suggest that electrophilic 6-OHDA quinone enhances oxidative stress, and that this is followed by AMPK-ULK1 pathway activation and induction of secretory autophagy to produce unconventional secretion of PARK7. <b>Abbreviations:</b> 6-OHDA: 6-hydroxydopamine; AMPK: AMP-activated protein kinase; ATG: autophagy related; CAV1: caveolin 1; ER: endoplasmic reticulum; FN1: fibronectin 1; GSH: glutathione; IDE: insulin degrading enzyme; IL: interleukin; LDH: lactate dehydrogenase; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MEF: mouse embryonic fibroblast; MTOR: mechanistic target of rapamycin kinase; NAC: N-acetyl-L-cysteine; PARK7/DJ-1: Parkinsonism associated deglycase; PD: Parkinson disease; RPS6KB1/p70S6K: ribosomal protein S6 kinase B1; RPN1: ribophorin I; ROS: reactive oxygen species; ULK1: unc-51 like autophagy activating kinase 1; WT: wild-type
DOI: 10.6084/m9.figshare.6807170
title: USP14 regulates DNA damage repair by targeting RNF168-dependent ubiquitination

description: Recent reports have made important revelations, uncovering direct regulation of DNA damage response (DDR)-associated proteins and chromatin ubiquitination (Ubn) by macroautophagy/autophagy. Here, we report a previously unexplored connection between autophagy and DDR, via a deubiquitnase (DUB), USP14. Loss of autophagy in prostate cancer cells led to unrepaired DNA double-strand breaks (DSBs) as indicated by persistent ionizing radiation (IR)-induced foci (IRIF) formation for γH2AFX, and decreased protein levels and IRIF formation for RNF168, an E3-ubiquitin ligase essential for chromatin Ubn and recruitment of critical DDR effector proteins in response to DSBs, including TP53BP1. Consistently, RNF168-associated Ubn signaling and TP53BP1 IRIF formation were reduced in autophagy-deficient cells. An activity assay identified several DUBs, including USP14, which showed higher activity in autophagy-deficient cells. Importantly, inhibiting USP14 could overcome DDR defects in autophagy-deficient cells. USP14 IRIF formation and protein stability were increased in autophagy-deficient cells. Co-immunoprecipitation and colocalization of USP14 with MAP1LC3B and the UBA-domain of SQSTM1 identified USP14 as a substrate of autophagy and SQSTM1. Additionally, USP14 directly interacted with RNF168, which depended on the MIU1 domain of RNF168. These findings identify USP14 as a novel substrate of autophagy and regulation of RNF168-dependent Ubn and TP53BP1 recruitment by USP14 as a critical link between DDR and autophagy. Given the role of Ubn signaling in non-homologous end joining (NHEJ), the major pathway for repair of IR-induced DNA damage, these findings provide unique insights into the link between autophagy, DDR-associated Ubn signaling and NHEJ DNA repair. <b>Abbreviations:</b> ATG7: autophagy related 7; CQ: chloroquine; DDR: DNA damage response; DUB: deubiquitinase; HR: homologous recombination; IR: ionizing radiation; IRIF: ionizing radiation-induced foci; LAMP2: lysosomal associated membrane protein 2; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MIU1: motif interacting with ubiquitin; NHEJ: non homologous end-joining; PCa: prostate cancer; TP53BP1/53BP1: tumor protein p53 binding protein 1; RNF168: ring finger protein 168; SQSTM1/p62 sequestosome 1; γH2AFX/γH2AX: H2A histone family member X: phosphorylated, UBA: ubiquitin-associated; Ub: ubiquitin; Ubn: ubiquitination; USP14: ubiquitin specific peptidase 14.
DOI: 10.6084/m9.figshare.6807170.v1
title: USP14 regulates DNA damage repair by targeting RNF168-dependent ubiquitination

description: Recent reports have made important revelations, uncovering direct regulation of DNA damage response (DDR)-associated proteins and chromatin ubiquitination (Ubn) by macroautophagy/autophagy. Here, we report a previously unexplored connection between autophagy and DDR, via a deubiquitnase (DUB), USP14. Loss of autophagy in prostate cancer cells led to unrepaired DNA double-strand breaks (DSBs) as indicated by persistent ionizing radiation (IR)-induced foci (IRIF) formation for γH2AFX, and decreased protein levels and IRIF formation for RNF168, an E3-ubiquitin ligase essential for chromatin Ubn and recruitment of critical DDR effector proteins in response to DSBs, including TP53BP1. Consistently, RNF168-associated Ubn signaling and TP53BP1 IRIF formation were reduced in autophagy-deficient cells. An activity assay identified several DUBs, including USP14, which showed higher activity in autophagy-deficient cells. Importantly, inhibiting USP14 could overcome DDR defects in autophagy-deficient cells. USP14 IRIF formation and protein stability were increased in autophagy-deficient cells. Co-immunoprecipitation and colocalization of USP14 with MAP1LC3B and the UBA-domain of SQSTM1 identified USP14 as a substrate of autophagy and SQSTM1. Additionally, USP14 directly interacted with RNF168, which depended on the MIU1 domain of RNF168. These findings identify USP14 as a novel substrate of autophagy and regulation of RNF168-dependent Ubn and TP53BP1 recruitment by USP14 as a critical link between DDR and autophagy. Given the role of Ubn signaling in non-homologous end joining (NHEJ), the major pathway for repair of IR-induced DNA damage, these findings provide unique insights into the link between autophagy, DDR-associated Ubn signaling and NHEJ DNA repair. <b>Abbreviations:</b> ATG7: autophagy related 7; CQ: chloroquine; DDR: DNA damage response; DUB: deubiquitinase; HR: homologous recombination; IR: ionizing radiation; IRIF: ionizing radiation-induced foci; LAMP2: lysosomal associated membrane protein 2; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MIU1: motif interacting with ubiquitin; NHEJ: non homologous end-joining; PCa: prostate cancer; TP53BP1/53BP1: tumor protein p53 binding protein 1; RNF168: ring finger protein 168; SQSTM1/p62 sequestosome 1; γH2AFX/γH2AX: H2A histone family member X: phosphorylated, UBA: ubiquitin-associated; Ub: ubiquitin; Ubn: ubiquitination; USP14: ubiquitin specific peptidase 14.
DOI: 10.5517/ccdc.csd.cc2d9f5b
title: CCDC 2213591: Experimental Crystal Structure Determination

description: Related Article: David Reber, Jonathan R. Thurston, Maximilian Becker, Michael P. Marshak|2023|Cell Reports Physical Science|4|101215|doi:10.1016/j.xcrp.2022.101215
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2frm0v
title: CCDC 2257017: Experimental Crystal Structure Determination

description: Related Article: Mio Matsumura, Ayaka Nakamura, Atsuki Yanagida, Yuki Murata, Shuji Yasuike|2023|Tetrahedron|142|133526|doi:10.1016/j.tet.2023.133526
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5281/zenodo.8172429
title: Replication package for: Strategic Exploration: Preemption and Prioritization

description: Liu, Qingmin, and Yu Fu Wong. "Strategic Exploration: Preemption and Prioritization." (2022), Accepted for Publication by the Review of Economic Studies. The replication package contains LaTex and MATLAB files for figures used in the paper.
DOI: 10.5281/zenodo.7353279
title: Replication package for: Strategic Exploration: Preemption and Prioritization

description: Liu, Qingmin, and Yu Fu Wong. "Strategic Exploration: Preemption and Prioritization." (2022), Accepted for Publication by the Review of Economic Studies. The replication package contains LaTex and MATLAB files for figures used in the paper.
DOI: 10.5281/zenodo.8206104
title: Data and scripts for the analysis of the influence of crop pollinator dependence and growth form on yield decline

description: Marcelo A. Aizen, Gabriela R. Gleiser, Thomas Kitzberger, Ruben Milla. <strong>Being a tree crop increases the odds of experiencing yield declines irrespective of pollinator dependence </strong>(to be submitted to PCI) Data and R scripts to reproduce the analyses and the figures shown in the paper. All analyses were performed using R 4.0.2. <strong>Data</strong> 1. FAOdata_21-12-2021.csv This file includes yearly data (1961-2020, column 8) on yield and cultivated area (columns 6 and 10) at the country, sub-regional, and regional levels (column 2) for each crop (column 4) drawn from the United Nations Food and Agriculture Organization database (data available at http://www.fao.org/faostat/en; accessed July 21-12-2021). [Used in Script 1 to generate the synthesis dataset] 2. countries.csv This file provides information on the region (column 2) to which each country (column 1) belongs. [Used in Script 1 to generate the synthesis dataset] 3. dependence.csv This file provides information on the pollinator dependence category (column 2) of each crop (column 1). 4. traits.csv This file provides information on the traits of each crop other than pollinator dependence, including, besides the crop name (column1), the variables type of harvested organ (column 5) and growth form (column 6). [Used in Script 1 to generate the synthesis dataset] 5. dataset.csv The synthesis dataset generated by Script 1. 6. growth.csv The yield growth dataset generated by Script 1 and used as input by Scripts 2 and 3. 7. phylonames.csv This file lists all the crops (column 1) and their equivalent tip names in the crop phylogeny (column 2). [Used in Script 2 for the phylogenetically-controlled analyses] 8.phylo137.tre File containing the phylogenetic tree. <strong>Scripts</strong> 1. dataset This R script curates and merges all the individual datasets mentioned above into a single dataset, estimating and adding to this single dataset the growth rate for each crop and country, and the (log) cumulative harvested area per crop and country over the period 1961-2020. 2. analyses This R script includes all the analyses described in the article’s main text. 3. figures This R script creates all the main and supplementary figures of this article. 4. lme4_phylo_setup R function written by Li and Bolker (2019) to carry out phylogenetically-controlled generalized linear mixed-effects models as described in the main text of the article. <strong>References</strong> Li, M., and B. Bolker. 2019. wzmli/phyloglmm: First release of phylogenetic comparative analysis in lme4- verse. Zenodo. https://doi.org/10.5281/zenodo.2639887.
description: The R scripts included here are updated versions of those than can be found at https://doi.org/10.5281/zenodo.7863825
DOI: 10.5281/zenodo.7863824
title: Data and scripts for the analysis of the influence of crop pollinator dependence and growth form on yield decline

description: Marcelo A. Aizen, Gabriela R. Gleiser, Thomas Kitzberger, Ruben Milla. <strong>Being a tree crop increases the odds of experiencing yield declines irrespective of pollinator dependence </strong>(to be submitted to PCI) Data and R scripts to reproduce the analyses and the figures shown in the paper. All analyses were performed using R 4.0.2. <strong>Data</strong> 1. FAOdata_21-12-2021.csv This file includes yearly data (1961-2020, column 8) on yield and cultivated area (columns 6 and 10) at the country, sub-regional, and regional levels (column 2) for each crop (column 4) drawn from the United Nations Food and Agriculture Organization database (data available at http://www.fao.org/faostat/en; accessed July 21-12-2021). [Used in Script 1 to generate the synthesis dataset] 2. countries.csv This file provides information on the region (column 2) to which each country (column 1) belongs. [Used in Script 1 to generate the synthesis dataset] 3. dependence.csv This file provides information on the pollinator dependence category (column 2) of each crop (column 1). 4. traits.csv This file provides information on the traits of each crop other than pollinator dependence, including, besides the crop name (column1), the variables type of harvested organ (column 5) and growth form (column 6). [Used in Script 1 to generate the synthesis dataset] 5. dataset.csv The synthesis dataset generated by Script 1. 6. growth.csv The yield growth dataset generated by Script 1 and used as input by Scripts 2 and 3. 7. phylonames.csv This file lists all the crops (column 1) and their equivalent tip names in the crop phylogeny (column 2). [Used in Script 2 for the phylogenetically-controlled analyses] 8.phylo137.tre File containing the phylogenetic tree. <strong>Scripts</strong> 1. dataset This R script curates and merges all the individual datasets mentioned above into a single dataset, estimating and adding to this single dataset the growth rate for each crop and country, and the (log) cumulative harvested area per crop and country over the period 1961-2020. 2. analyses This R script includes all the analyses described in the article’s main text. 3. figures This R script creates all the main and supplementary figures of this article. 4. lme4_phylo_setup R function written by Li and Bolker (2019) to carry out phylogenetically-controlled generalized linear mixed-effects models as described in the main text of the article. <strong>References</strong> Li, M., and B. Bolker. 2019. wzmli/phyloglmm: First release of phylogenetic comparative analysis in lme4- verse. Zenodo. https://doi.org/10.5281/zenodo.2639887.
description: The R scripts included here are updated versions of those than can be found at https://doi.org/10.5281/zenodo.7863825