cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.30820176
title: ATG9A-PLA2G6 axis reprograms phospholipid metabolism to drive metabolic liver disease and hepatocellular carcinoma

description: The liver orchestrates systemic metabolism, and its dysfunction drives diseases including metabolic dysfunction-associated steatotic liver disease (MASLD) and hepatocellular carcinoma (HCC). ATG9A, an autophagy-related transmembrane protein and lipid scramblase, regulates lipid dynamics, yet its role in hepatic pathogenesis remains unclear. Using multi-model approaches, we demonstrate that liver-specific ATG9A overexpression in mice enhanced autophagic flux but impaired autophagosome degradation. ATG9A disrupted hepatic lipid metabolism, reduced lipid droplet accumulation and exacerbated inflammation and fibrosis. Furthermore, we identified PLA2G6 as an ATG9A binding protein. ATG9A-PLA2G6 interaction accelerated phosphatidylcholine degradation, perturbing fatty acid metabolism and causing mitochondrial dysfunction. Besides, ATG9A promoted tumor growth in vivo, independent of canonical macroautophagy/autophagy. Our findings redefine ATG9A as a dual metabolic effector, driving liver disease progression through lipid remodeling and organelle stress. The ATG9A-PLA2G6 axis presents a therapeutic target for metabolic liver disorders and HCC.
DOI: 10.6084/m9.figshare.30820176.v1
title: ATG9A-PLA2G6 axis reprograms phospholipid metabolism to drive metabolic liver disease and hepatocellular carcinoma

description: The liver orchestrates systemic metabolism, and its dysfunction drives diseases including metabolic dysfunction-associated steatotic liver disease (MASLD) and hepatocellular carcinoma (HCC). ATG9A, an autophagy-related transmembrane protein and lipid scramblase, regulates lipid dynamics, yet its role in hepatic pathogenesis remains unclear. Using multi-model approaches, we demonstrate that liver-specific ATG9A overexpression in mice enhanced autophagic flux but impaired autophagosome degradation. ATG9A disrupted hepatic lipid metabolism, reduced lipid droplet accumulation and exacerbated inflammation and fibrosis. Furthermore, we identified PLA2G6 as an ATG9A binding protein. ATG9A-PLA2G6 interaction accelerated phosphatidylcholine degradation, perturbing fatty acid metabolism and causing mitochondrial dysfunction. Besides, ATG9A promoted tumor growth in vivo, independent of canonical macroautophagy/autophagy. Our findings redefine ATG9A as a dual metabolic effector, driving liver disease progression through lipid remodeling and organelle stress. The ATG9A-PLA2G6 axis presents a therapeutic target for metabolic liver disorders and HCC.
DOI: 10.6084/m9.figshare.30656508
title: SH3P2-mediated autophagosomal targeting of the CCZ1-MON1-RABG3e module regulates autophagosome-vacuole fusion in <i>Arabidopsis</i>

description: Macroautophagy/autophagy is a highly conserved pathway responsible for the bulk degradation of cytoplasmic material through the formation of a double-membrane structure known as the autophagosome. However, the precise mechanisms governing the transport of autophagosomes to the vacuole for degradation in plants remain largely elusive. There exists an ongoing debate about whether RAB7, a key regulatory protein, is involved in the plant autophagy pathway. In this study, we demonstrate that upon autophagy induction by BTH treatment, RABG3e, a member of the RAB7 family, exhibits a partial localization with late-stage autophagosomes in <i>Arabidopsis</i> root cells, and its dysfunction leads to the accumulation of enlarged multilayered autophagosomes and a significant reduction in autophagic flux. We also showed that RABG3e is recruited to autophagosomes by its guanine nucleotide exchange factor (GEF) complex, MON1-CCZ1, which is targeted through the interaction between CCZ1 and SH3P2 (SH3 DOMAIN-CONTAINING PROTEIN 2), a plant-specific autophagy regulator. Subsequently, RABG3e recruits downstream effectors such as VPS39, which in turn promotes the recruitment of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) proteins, including SYP21, VTI12, SYP51, and VAMP711, that are essential for the fusion process. <i>Arabidopsis</i> mutants with dysfunction in the autophagosome-vacuole fusion process exhibit accelerated senescence and increased sensitivity to nitrogen starvation. Collectively, our findings provide new insights into the regulation of autophagosome-vacuole fusion in <i>Arabidopsis</i>, highlighting the essential roles of SH3P2-dependent targeting of the CCZ1-MON1-RABG3e module to late-stage autophagosomes as well as RABG3e effectors and a unique SNARE complex.
DOI: 10.6084/m9.figshare.30656508.v2
title: SH3P2-mediated autophagosomal targeting of the CCZ1-MON1-RABG3e module regulates autophagosome-vacuole fusion in <i>Arabidopsis</i>

description: Macroautophagy/autophagy is a highly conserved pathway responsible for the bulk degradation of cytoplasmic material through the formation of a double-membrane structure known as the autophagosome. However, the precise mechanisms governing the transport of autophagosomes to the vacuole for degradation in plants remain largely elusive. There exists an ongoing debate about whether RAB7, a key regulatory protein, is involved in the plant autophagy pathway. In this study, we demonstrate that upon autophagy induction by BTH treatment, RABG3e, a member of the RAB7 family, exhibits a partial localization with late-stage autophagosomes in <i>Arabidopsis</i> root cells, and its dysfunction leads to the accumulation of enlarged multilayered autophagosomes and a significant reduction in autophagic flux. We also showed that RABG3e is recruited to autophagosomes by its guanine nucleotide exchange factor (GEF) complex, MON1-CCZ1, which is targeted through the interaction between CCZ1 and SH3P2 (SH3 DOMAIN-CONTAINING PROTEIN 2), a plant-specific autophagy regulator. Subsequently, RABG3e recruits downstream effectors such as VPS39, which in turn promotes the recruitment of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) proteins, including SYP21, VTI12, SYP51, and VAMP711, that are essential for the fusion process. <i>Arabidopsis</i> mutants with dysfunction in the autophagosome-vacuole fusion process exhibit accelerated senescence and increased sensitivity to nitrogen starvation. Collectively, our findings provide new insights into the regulation of autophagosome-vacuole fusion in <i>Arabidopsis</i>, highlighting the essential roles of SH3P2-dependent targeting of the CCZ1-MON1-RABG3e module to late-stage autophagosomes as well as RABG3e effectors and a unique SNARE complex.
DOI: 10.6084/m9.figshare.30867589
title: Chronic enteritis triggered by diet westernization is driven by epithelial ATG16L1-mediated autophagy

description: Macroautophagy/autophagy exerts multilayered protective functions in intestinal epithelial cells (IECs) while a loss-of-function genetic variant in ATG16L1 (autophagy related 16 like 1) is associated with risk for developing Crohn disease (CD). Westernization of diet, partly characterized by excess of long-chain fatty acids, contributes to CD, and a metabolic control of intestinal inflammation is emerging. Here, we report an unexpected inflammatory function for ATG16L1-mediated autophagy in Crohn-like metabolic enteritis of mice induced by polyunsaturated fatty acid (PUFA) excess in a western diet. Dietary PUFAs induce ATG16L1-mediated conventional autophagy in IECs, which is required for PUFA-induced chemokine production and metabolic enteritis. By transcriptomic and lipidomic profiling of IECs, we demonstrate that ATG16L1 is required for PUFA-induced inflammatory stress signaling specifically mediated by TLR2 (toll-like receptor 2) and the production of arachidonic acid metabolites. Our study identifies ATG16L1-mediated autophagy in IECs as an inflammatory hub driving metabolic enteritis, which challenges the perception of protective autophagy in the context of diet westernization. <b>Abbreviations</b>: AA: arachidonic acid; ATG16L1: autophagy related 16 like 1; CD: Crohn disease; CXCL1: C-X-C motif chemokine ligand 1; ER: endoplasmic reticulum; GFP: green fluorescent protein; GPX4: glutathione peroxidase 4; IBD: inflammatory bowel disease; IECs: intestinal epithelial cells; PTGS2/COX2: prostaglandin-endoperoxide synthase 2; PUFA: polyunsaturated fatty acid; SDA: stearidonic acid; TLR2: toll-like receptor 2; WT: wild-type
DOI: 10.6084/m9.figshare.30867589.v1
title: Chronic enteritis triggered by diet westernization is driven by epithelial ATG16L1-mediated autophagy

description: Macroautophagy/autophagy exerts multilayered protective functions in intestinal epithelial cells (IECs) while a loss-of-function genetic variant in ATG16L1 (autophagy related 16 like 1) is associated with risk for developing Crohn disease (CD). Westernization of diet, partly characterized by excess of long-chain fatty acids, contributes to CD, and a metabolic control of intestinal inflammation is emerging. Here, we report an unexpected inflammatory function for ATG16L1-mediated autophagy in Crohn-like metabolic enteritis of mice induced by polyunsaturated fatty acid (PUFA) excess in a western diet. Dietary PUFAs induce ATG16L1-mediated conventional autophagy in IECs, which is required for PUFA-induced chemokine production and metabolic enteritis. By transcriptomic and lipidomic profiling of IECs, we demonstrate that ATG16L1 is required for PUFA-induced inflammatory stress signaling specifically mediated by TLR2 (toll-like receptor 2) and the production of arachidonic acid metabolites. Our study identifies ATG16L1-mediated autophagy in IECs as an inflammatory hub driving metabolic enteritis, which challenges the perception of protective autophagy in the context of diet westernization. <b>Abbreviations</b>: AA: arachidonic acid; ATG16L1: autophagy related 16 like 1; CD: Crohn disease; CXCL1: C-X-C motif chemokine ligand 1; ER: endoplasmic reticulum; GFP: green fluorescent protein; GPX4: glutathione peroxidase 4; IBD: inflammatory bowel disease; IECs: intestinal epithelial cells; PTGS2/COX2: prostaglandin-endoperoxide synthase 2; PUFA: polyunsaturated fatty acid; SDA: stearidonic acid; TLR2: toll-like receptor 2; WT: wild-type
DOI: 10.6084/m9.figshare.30610493
title: Autophagy regulates the maternal-to-zygotic transition through MAP1LC3B-mediated maternal mRNA decay

description: During the maternal-to-zygotic transition (MZT), the programmed decay of maternal mRNAs is critical for successful embryonic development. Although autophagy is known to participate in early embryonic development, its specific role in maternal mRNA clearance remains unclear. MAP1LC3B/LC3B, a key autophagy-related protein, has recently been identified as an RNA-binding protein; however, whether it contributes to maternal mRNA degradation has not been established. Through integrative analyses combining RIP-seq, RNA-seq, and CUT&Tag in early embryos, we identified LC3B as a maternal mRNA-binding protein essential for mRNA degradation. LC3B-mediated mRNA decay exhibited faster kinetics than the classical BTG4-CCR4-NOT pathway. Knockdown of LC3B or inhibition of autophagy significantly delayed maternal mRNA clearance, resulting in impaired zygotic genome activation (ZGA) and developmental arrest. Further analysis revealed the maternal <i>Suv39h2</i> as a key LC3B-target gene, whose abnormal persistence correlates with developmental failure. Our findings revealed an autophagy-dependent mRNA clearance pathway mediated by LC3B, providing novel mechanistic insights into maternal mRNA decay and developmental regulation during mammalian MZT. <b>Abbreviations</b>: BTG4: BTG anti-proliferation factor 4; E2C: early 2-cell; GV: germinal vesicle; H3K9me3: histone H3 lysine 9 trimethylation; L2C: late 2-cell; MII: metaphase II; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MD: maternal mRNAs decay; MERVL: murine endogenous retrovirus-L; MZT: maternal-to-zygotic transition; PN5: pronuclear stage 5; <i>Suv39h2</i>: suppressor of variegation 3–9 2; TUT7: terminal uridylyl transferase 7; TUT4: terminal uridylyl transferase 4; ZGA: zygotic genome activation.
DOI: 10.6084/m9.figshare.30610493.v1
title: Autophagy regulates the maternal-to-zygotic transition through MAP1LC3B-mediated maternal mRNA decay

description: During the maternal-to-zygotic transition (MZT), the programmed decay of maternal mRNAs is critical for successful embryonic development. Although autophagy is known to participate in early embryonic development, its specific role in maternal mRNA clearance remains unclear. MAP1LC3B/LC3B, a key autophagy-related protein, has recently been identified as an RNA-binding protein; however, whether it contributes to maternal mRNA degradation has not been established. Through integrative analyses combining RIP-seq, RNA-seq, and CUT&Tag in early embryos, we identified LC3B as a maternal mRNA-binding protein essential for mRNA degradation. LC3B-mediated mRNA decay exhibited faster kinetics than the classical BTG4-CCR4-NOT pathway. Knockdown of LC3B or inhibition of autophagy significantly delayed maternal mRNA clearance, resulting in impaired zygotic genome activation (ZGA) and developmental arrest. Further analysis revealed the maternal <i>Suv39h2</i> as a key LC3B-target gene, whose abnormal persistence correlates with developmental failure. Our findings revealed an autophagy-dependent mRNA clearance pathway mediated by LC3B, providing novel mechanistic insights into maternal mRNA decay and developmental regulation during mammalian MZT. <b>Abbreviations</b>: BTG4: BTG anti-proliferation factor 4; E2C: early 2-cell; GV: germinal vesicle; H3K9me3: histone H3 lysine 9 trimethylation; L2C: late 2-cell; MII: metaphase II; MAP1LC3B/LC3B: microtubule-associated protein 1 light chain 3 beta; MD: maternal mRNAs decay; MERVL: murine endogenous retrovirus-L; MZT: maternal-to-zygotic transition; PN5: pronuclear stage 5; <i>Suv39h2</i>: suppressor of variegation 3–9 2; TUT7: terminal uridylyl transferase 7; TUT4: terminal uridylyl transferase 4; ZGA: zygotic genome activation.
DOI: 10.6084/m9.figshare.30656508.v1
title: SH3P2-mediated autophagosomal targeting of the CCZ1-MON1-RABG3e module regulates autophagosome-vacuole fusion in Arabidopsis

description: Macroautophagy/autophagy is a highly conserved pathway responsible for the bulk degradation of cytoplasmic material through the formation of a double-membrane structure known as the autophagosome. However, the precise mechanisms governing the transport of autophagosomes to the vacuole for degradation in plants remain largely elusive. There exists an ongoing debate about whether RAB7, a key regulatory protein, is involved in the plant autophagy pathway. In this study, we demonstrate that upon autophagy induction by BTH treatment, RABG3e, a member of the RAB7 family, exhibits a partial localization with late-stage autophagosomes in <i>Arabidopsis</i> root cells, and its dysfunction leads to the accumulation of enlarged multilayered autophagosomes and a significant reduction in autophagic flux. We also showed that RABG3e is recruited to autophagosomes by its guanine nucleotide exchange factor (GEF) complex, MON1-CCZ1, which is targeted through the interaction between CCZ1 and SH3P2 (SH3 DOMAIN-CONTAINING PROTEIN 2), a plant-specific autophagy regulator. Subsequently, RABG3e recruits downstream effectors such as VPS39, which in turn promotes the recruitment of soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNARE) proteins, including SYP21, VTI12, SYP51, and VAMP711, that are essential for the fusion process. <i>Arabidopsis</i> mutants with dysfunction in the autophagosome-vacuole fusion process exhibit accelerated senescence and increased sensitivity to nitrogen starvation. Collectively, our findings provide new insights into the regulation of autophagosome-vacuole fusion in <i>Arabidopsis</i>, highlighting the essential roles of SH3P2-dependent targeting of the CCZ1-MON1-RABG3e module to late-stage autophagosomes as well as RABG3e effectors and a unique SNARE complex.
DOI: 10.6084/m9.figshare.30814932
title: Autophagy regulates PVALB (parvalbumin) interneuron excitability and memory

description: Macroautophagy/autophagy was previously shown to play a critical role in the hippocampus for memory formation, with age-related autophagy deficits being further linked to cognitive decline. However, the neuronal subtypes where autophagy is required to form new memories remain unknown. Given the well-established role of PVALB (parvalbumin) interneurons in hippocampus-dependent memory formation and consolidation, we examined whether autophagy in these cells is required for such complex behaviors. We show that contrary to other neuronal subtypes, the vast majority of PVALB neurons, with the exception of cerebellar Purkinje cells, survive and are maintained long-term independently of autophagy. However, autophagy controls the homeostasis of mitochondria, endoplasmic reticulum, and synaptic proteins within PVALB interneurons, ultimately regulating their synaptic excitation, neuronal excitability and excitation-inhibition balance in the hippocampus. Consequently, mice with conditional impairment of autophagy in PVALB-expressing neurons exhibit impaired inhibitory neurotransmission and deficits in hippocampus-dependent memory. Taken together, these findings identify PVALB interneurons as key cellular substrates of autophagy in the context of learning and memory. <b>Abbreviation</b>: ATG5: autophagy related 5; BNIP3: BCL2/adenovirus E1B interacting protein 3; BNIP3L: BCL2/adenovirus E1B interacting protein 3-like; CA1: cornu ammonis 1; CALCOCO1: calcium binding and coiled coil domain 1; ER: endoplasmic reticulum; GABA: gamma-aminobutyric acid; GRIA/AMPAR: glutamate receptor, ionotropic, AMPA; GRIN2A/NR2A/GluN2A: glutamate receptor, ionotropic, NMDA2A (epsilon 1); PRKN: parkin RBR E3 ubiquitin protein ligase; PC: pyramidal cells; PJ: Purkinje; PVALB: parvalbumin; RTN3: reticulon 3; SQSTM1/p62: sequestosome 1.
DOI: 10.6084/m9.figshare.30814932.v1
title: Autophagy regulates PVALB (parvalbumin) interneuron excitability and memory

description: Macroautophagy/autophagy was previously shown to play a critical role in the hippocampus for memory formation, with age-related autophagy deficits being further linked to cognitive decline. However, the neuronal subtypes where autophagy is required to form new memories remain unknown. Given the well-established role of PVALB (parvalbumin) interneurons in hippocampus-dependent memory formation and consolidation, we examined whether autophagy in these cells is required for such complex behaviors. We show that contrary to other neuronal subtypes, the vast majority of PVALB neurons, with the exception of cerebellar Purkinje cells, survive and are maintained long-term independently of autophagy. However, autophagy controls the homeostasis of mitochondria, endoplasmic reticulum, and synaptic proteins within PVALB interneurons, ultimately regulating their synaptic excitation, neuronal excitability and excitation-inhibition balance in the hippocampus. Consequently, mice with conditional impairment of autophagy in PVALB-expressing neurons exhibit impaired inhibitory neurotransmission and deficits in hippocampus-dependent memory. Taken together, these findings identify PVALB interneurons as key cellular substrates of autophagy in the context of learning and memory. <b>Abbreviation</b>: ATG5: autophagy related 5; BNIP3: BCL2/adenovirus E1B interacting protein 3; BNIP3L: BCL2/adenovirus E1B interacting protein 3-like; CA1: cornu ammonis 1; CALCOCO1: calcium binding and coiled coil domain 1; ER: endoplasmic reticulum; GABA: gamma-aminobutyric acid; GRIA/AMPAR: glutamate receptor, ionotropic, AMPA; GRIN2A/NR2A/GluN2A: glutamate receptor, ionotropic, NMDA2A (epsilon 1); PRKN: parkin RBR E3 ubiquitin protein ligase; PC: pyramidal cells; PJ: Purkinje; PVALB: parvalbumin; RTN3: reticulon 3; SQSTM1/p62: sequestosome 1.
DOI: 10.5281/zenodo.15089490
title: Textline Detection Dataset

description: In document layout analysis (DLA), the detection and classification of multiple classes of layout elements such as headings, images, tables etc. is required in order to extract and process them in subsequent steps. This proves to be a challenging task in digitised cultural heritage items such as books, newspapers and archival records. In order to train a convolutional neural network capable of recognising text lines, a dataset was created. The machine learning task for which this dataset was collected falls into the domain of image segmentation and, more generally, of computer vision. The dataset was compiled by Vahid Rezanezhad within the research project “Mensch.Maschine.Kultur – Künstliche Intelligenz für das Digitale Kulturelle Erbe” at the Staatsbibliothek zu Berlin – Berlin State Library (SBB). The research project was funded by the Federal Government Commissioner for Culture and the Media (BKM), project grant no. 2522DIG002. The Minister of State for Culture and the Media is part of the German Federal Government.
DOI: 10.5281/zenodo.15089491
title: Textline Detection Dataset

description: In document layout analysis (DLA), the detection and classification of multiple classes of layout elements such as headings, images, tables etc. is required in order to extract and process them in subsequent steps. This proves to be a challenging task in digitised cultural heritage items such as books, newspapers and archival records. In order to train a convolutional neural network capable of recognising text lines, a dataset was created. The machine learning task for which this dataset was collected falls into the domain of image segmentation and, more generally, of computer vision. The dataset was compiled by Vahid Rezanezhad within the research project “Mensch.Maschine.Kultur – Künstliche Intelligenz für das Digitale Kulturelle Erbe” at the Staatsbibliothek zu Berlin – Berlin State Library (SBB). The research project was funded by the Federal Government Commissioner for Culture and the Media (BKM), project grant no. 2522DIG002. The Minister of State for Culture and the Media is part of the German Federal Government.
DOI: 10.21950/u8j697
title: Federico-Tena World Population Historical Database : Malawi

description: Project developed by Giovanni Federico (New York University Abu Dhabi) and Antonio Tena Junguito (Universidad Carlos III de Madrid). Dataset: Malawi
description: Microsoft Excel
description: Web site: <strong>https://www.uc3m.es/investigacion/federico-tena-population</strong>



<strong>SEE MAP</strong>
DOI: 10.5281/zenodo.10086789
title: Dataset DT22

description: The database is a collection of the emotional states of 112 participants involved in the experiment named “Sperimentazione DT22”.

The database was gathered with contributions from Prof. Beatrice Lazzerini and Prof. Cosimo Antonio Prete of the University of Pisa. 

The database was presented in part and cited in the following article and book:



Di Tecco, A., Foglia, P., & Prete, C. A. (2024). Video Quality Prediction: An Exploratory Study with Valence and Arousal Signals. IEEE Access. DOI: 0.1109/ACCESS.2024.3374056.

Di Tecco, A. (2024). Intelligent Systems for Human Health and Well-Being. ISBN: 979-12-210-5664-8. DOI: 10.979.12210/56648.

Di Tecco, A. (2025).  From Facial Expressions to User Experience (UX): How User Emotions Define the Design of Intelligent Systems. IEEE Access. DOI: 10.1109/ACCESS.2025.3644691.
description: This license covers only public files. Antonio Di Tecco can be contacted at www.ditecco.it/contacts to request the database.