cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.17198570
title: ATG12 deficiency results in intracellular glutamine depletion, abrogation of tumor hypoxia and a favorable prognosis in cancer

description: Hypoxia is a common feature of solid tumors and is associated with increased tumor progression, resistance to therapy and increased metastasis. Hence, tumor hypoxia is a prognostic factor independent of treatment modality. To survive hypoxia, cells activate macroautophagy/autophagy. Paradoxically, in several cancer types, mutations or loss of essential autophagy genes have been reported that are associated with earlier onset of tumor growth. However, to our knowledge, the phenotypic and therapeutic consequences of autophagy deficiency have remained unexplored. In this study, we determined autophagy-defects in head and neck squamous cell carcinoma (HNSCC) and observed that expression of ATG12 (autophagy related 12) was lost in 25%-40% of HNSCC. In line, ATG12 loss is associated with absence of hypoxia, as determined by pimonidazole immunohistochemistry. Hence, ATG12 loss is associated with improved prognosis after therapy in two independent HNSCC cohorts and 7 additional cancer types. In <i>vivo</i>, ATG12 targeting resulted in decreased hypoxia tolerance, increased necrosis and sensitivity of the tumor to therapy, but <i>in vitro</i> ATG12-deficient cells displayed enhanced survival in nutrient-rich culture medium. Besides oxygen, delivery of glucose was hampered in hypoxic regions <i>in vivo</i>, which increases the reliance of cells on other carbon sources (e.g., L-glutamine). We observed decreased intracellular L-glutamine levels in ATG12-deficient cells during hypoxia and increased cell killing after L-glutamine depletion, indicating a central role for ATG12 in maintaining L-glutamine homeostasis. Our results demonstrate that ATG12<sup>low</sup> tumors represent a phenotypically different subtype that, due to the lowered hypoxia tolerance, display a favorable outcome after therapy. <b>Abbreviations:</b> ARCON:accelerated radiotherapy with carbogen and nicotinamide; ATG: autophagy related; BrdUrd: bromodeoxyuridine; CA9/CAIX: carbonic anhydrase 9; HIF1A/HIF1α: hypoxia inducible factor 1 subunit alpha; HNSCC: head and neck squamous cell carcinoma; HPV: human papilloma virus; HR: hazard ratio; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MEF: mouse embryonic fibroblast; mRNA: messenger ribonucleic acid; PCR: polymerase chain reaction; SLC2A1/GLUT1: solute carrier family 2 member 1; TCGA: the Cancer Genome Atlas; TME: tumor microenvironment; UTR: untranslated region; VEGF: vascular endothelial growth factor
DOI: 10.6084/m9.figshare.17054824
title: AMBRA1 regulates mitophagy by interacting with ATAD3A and promoting PINK1 stability

description: PINK1 accumulation at the outer mitochondrial membrane (OMM) is a key event required to signal depolarized mitochondria to the autophagy machinery. How this early step is, in turn, modulated by autophagy proteins remains less characterized. Here, we show that, upon mitochondrial depolarization, the proautophagic protein AMBRA1 is recruited to the OMM and interacts with PINK1 and ATAD3A, a transmembrane protein that mediates mitochondrial import and degradation of PINK1. Downregulation of AMBRA1 expression results in reduced levels of PINK1 due to its enhanced degradation by the mitochondrial protease LONP1, which leads to a decrease in PINK1-mediated ubiquitin phosphorylation and mitochondrial PRKN/PARKIN recruitment. Notably, ATAD3A silencing rescues defective PINK1 accumulation in AMBRA1-deficient cells upon mitochondrial damage. Overall, our findings underline an upstream contribution of AMBRA1 in the control of PINK1-PRKN mitophagy by interacting with ATAD3A and promoting PINK1 stability. This novel regulatory element may account for changes of PINK1 levels in neuropathological conditions. <b>Abbreviations:</b> ACTB/β-actin: actin beta; AMBRA1: autophagy and beclin 1 regulator 1; ATAD3A: ATPase family AAA domain containing 3A; BCL2L1/BCL-xL: BCL2 like 1; CCCP: carbonyl cyanide m-chlorophenyl hydrazone; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; OMA1: OMA1 zinc metallopeptidase; OMM: outer mitochondrial membrane; PARL: presenilin associated rhomboid like; PARP: poly(ADP-ribose) polymerase; PD: Parkinson disease; PINK1: PTEN induced kinase 1; PRKN/PARKIN: parkin RBR E3 ubiquitin protein ligase; SDHA: succinate dehydrogenase complex flavoprotein subunit A; TOMM70: translocase of outer mitochondrial membrane 70.
DOI: 10.6084/m9.figshare.17054824.v1
title: AMBRA1 regulates mitophagy by interacting with ATAD3A and promoting PINK1 stability

description: PINK1 accumulation at the outer mitochondrial membrane (OMM) is a key event required to signal depolarized mitochondria to the autophagy machinery. How this early step is, in turn, modulated by autophagy proteins remains less characterized. Here, we show that, upon mitochondrial depolarization, the proautophagic protein AMBRA1 is recruited to the OMM and interacts with PINK1 and ATAD3A, a transmembrane protein that mediates mitochondrial import and degradation of PINK1. Downregulation of AMBRA1 expression results in reduced levels of PINK1 due to its enhanced degradation by the mitochondrial protease LONP1, which leads to a decrease in PINK1-mediated ubiquitin phosphorylation and mitochondrial PRKN/PARKIN recruitment. Notably, ATAD3A silencing rescues defective PINK1 accumulation in AMBRA1-deficient cells upon mitochondrial damage. Overall, our findings underline an upstream contribution of AMBRA1 in the control of PINK1-PRKN mitophagy by interacting with ATAD3A and promoting PINK1 stability. This novel regulatory element may account for changes of PINK1 levels in neuropathological conditions. <b>Abbreviations:</b> ACTB/β-actin: actin beta; AMBRA1: autophagy and beclin 1 regulator 1; ATAD3A: ATPase family AAA domain containing 3A; BCL2L1/BCL-xL: BCL2 like 1; CCCP: carbonyl cyanide m-chlorophenyl hydrazone; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; OMA1: OMA1 zinc metallopeptidase; OMM: outer mitochondrial membrane; PARL: presenilin associated rhomboid like; PARP: poly(ADP-ribose) polymerase; PD: Parkinson disease; PINK1: PTEN induced kinase 1; PRKN/PARKIN: parkin RBR E3 ubiquitin protein ligase; SDHA: succinate dehydrogenase complex flavoprotein subunit A; TOMM70: translocase of outer mitochondrial membrane 70.
DOI: 10.6084/m9.figshare.17293896
title: Autophagy modulates cell fate decisions during lineage commitment

description: Early events during development leading to exit from a pluripotent state and commitment toward a specific germ layer still need in-depth understanding. Autophagy has been shown to play a crucial role in both development and differentiation. This study employs human embryonic and induced pluripotent stem cells to understand the early events of lineage commitment with respect to the role of autophagy in this process. Our data indicate that a dip in autophagy facilitates exit from pluripotency. Upon exit, we demonstrate that the modulation of autophagy affects SOX2 levels and lineage commitment, with induction of autophagy promoting SOX2 degradation and mesendoderm formation, whereas inhibition of autophagy causes SOX2 accumulation and neuroectoderm formation. Thus, our results indicate that autophagy-mediated SOX2 turnover is a determining factor for lineage commitment. These findings will deepen our understanding of development and lead to improved methods to derive different lineages and cell types. <b>Abbreviations:</b> ACTB: Actin, beta; ATG: Autophagy-related; BafA1: Bafilomycin A<sub>1</sub>; CAS9: CRISPR-associated protein 9; CQ: Chloroquine; DE: Definitive endoderm; hESCs: Human Embryonic Stem Cells; hiPSCs: Human Induced Pluripotent Stem Cells; LAMP1: Lysosomal Associated Membrane Protein 1; MAP1LC3: Microtubule-Associated Protein 1 Light Chain 3; MTOR: Mechanistic Target Of Rapamycin Kinase; NANOG: Nanog Homeobox; PAX6: Paired Box 6; PE: Phosphatidylethanolamine; POU5F1: POU class 5 Homeobox 1; PRKAA2: Protein Kinase AMP-Activated Catalytic Subunit Alpha 2; SOX2: SRY-box Transcription Factor 2; SQSTM1: Sequestosome 1; ULK1: unc-51 like Autophagy Activating Kinase 1; WDFY3: WD Repeat and FYVE Domain Containing 3.
DOI: 10.6084/m9.figshare.17198570.v1
title: ATG12 deficiency results in intracellular glutamine depletion, abrogation of tumor hypoxia and a favorable prognosis in cancer

description: Hypoxia is a common feature of solid tumors and is associated with increased tumor progression, resistance to therapy and increased metastasis. Hence, tumor hypoxia is a prognostic factor independent of treatment modality. To survive hypoxia, cells activate macroautophagy/autophagy. Paradoxically, in several cancer types, mutations or loss of essential autophagy genes have been reported that are associated with earlier onset of tumor growth. However, to our knowledge, the phenotypic and therapeutic consequences of autophagy deficiency have remained unexplored. In this study, we determined autophagy-defects in head and neck squamous cell carcinoma (HNSCC) and observed that expression of ATG12 (autophagy related 12) was lost in 25%-40% of HNSCC. In line, ATG12 loss is associated with absence of hypoxia, as determined by pimonidazole immunohistochemistry. Hence, ATG12 loss is associated with improved prognosis after therapy in two independent HNSCC cohorts and 7 additional cancer types. In <i>vivo</i>, ATG12 targeting resulted in decreased hypoxia tolerance, increased necrosis and sensitivity of the tumor to therapy, but <i>in vitro</i> ATG12-deficient cells displayed enhanced survival in nutrient-rich culture medium. Besides oxygen, delivery of glucose was hampered in hypoxic regions <i>in vivo</i>, which increases the reliance of cells on other carbon sources (e.g., L-glutamine). We observed decreased intracellular L-glutamine levels in ATG12-deficient cells during hypoxia and increased cell killing after L-glutamine depletion, indicating a central role for ATG12 in maintaining L-glutamine homeostasis. Our results demonstrate that ATG12<sup>low</sup> tumors represent a phenotypically different subtype that, due to the lowered hypoxia tolerance, display a favorable outcome after therapy. <b>Abbreviations:</b> ARCON:accelerated radiotherapy with carbogen and nicotinamide; ATG: autophagy related; BrdUrd: bromodeoxyuridine; CA9/CAIX: carbonic anhydrase 9; HIF1A/HIF1α: hypoxia inducible factor 1 subunit alpha; HNSCC: head and neck squamous cell carcinoma; HPV: human papilloma virus; HR: hazard ratio; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MEF: mouse embryonic fibroblast; mRNA: messenger ribonucleic acid; PCR: polymerase chain reaction; SLC2A1/GLUT1: solute carrier family 2 member 1; TCGA: the Cancer Genome Atlas; TME: tumor microenvironment; UTR: untranslated region; VEGF: vascular endothelial growth factor
DOI: 10.6084/m9.figshare.17293896.v2
title: Autophagy modulates cell fate decisions during lineage commitment

description: Early events during development leading to exit from a pluripotent state and commitment toward a specific germ layer still need in-depth understanding. Autophagy has been shown to play a crucial role in both development and differentiation. This study employs human embryonic and induced pluripotent stem cells to understand the early events of lineage commitment with respect to the role of autophagy in this process. Our data indicate that a dip in autophagy facilitates exit from pluripotency. Upon exit, we demonstrate that the modulation of autophagy affects SOX2 levels and lineage commitment, with induction of autophagy promoting SOX2 degradation and mesendoderm formation, whereas inhibition of autophagy causes SOX2 accumulation and neuroectoderm formation. Thus, our results indicate that autophagy-mediated SOX2 turnover is a determining factor for lineage commitment. These findings will deepen our understanding of development and lead to improved methods to derive different lineages and cell types. <b>Abbreviations:</b> ACTB: Actin, beta; ATG: Autophagy-related; BafA1: Bafilomycin A<sub>1</sub>; CAS9: CRISPR-associated protein 9; CQ: Chloroquine; DE: Definitive endoderm; hESCs: Human Embryonic Stem Cells; hiPSCs: Human Induced Pluripotent Stem Cells; LAMP1: Lysosomal Associated Membrane Protein 1; MAP1LC3: Microtubule-Associated Protein 1 Light Chain 3; MTOR: Mechanistic Target Of Rapamycin Kinase; NANOG: Nanog Homeobox; PAX6: Paired Box 6; PE: Phosphatidylethanolamine; POU5F1: POU class 5 Homeobox 1; PRKAA2: Protein Kinase AMP-Activated Catalytic Subunit Alpha 2; SOX2: SRY-box Transcription Factor 2; SQSTM1: Sequestosome 1; ULK1: unc-51 like Autophagy Activating Kinase 1; WDFY3: WD Repeat and FYVE Domain Containing 3.
DOI: 10.6084/m9.figshare.17021871
title: Dysregulated endolysosomal trafficking in cells arrested in the G<sub>1</sub> phase of the host cell cycle impairs <i>Salmonella</i> vacuolar replication

description: Modulation of the host cell cycle has emerged as a common theme among the pathways regulated by bacterial pathogens, arguably to promote host cell colonization. However, in most cases the exact benefit ensuing from such interference to the infection process remains unclear. Previously, we have shown that <i>Salmonella</i> actively induces G<sub>2</sub>/M arrest of host cells, and that infection is severely inhibited in cells arrested in G<sub>1</sub>. In this study, we demonstrate that <i>Salmonella</i> vacuolar replication is inhibited in host cells blocked in G<sub>1</sub>, whereas the cytosolic replication of the closely related pathogen <i>Shigella</i> is not affected. Mechanistically, we show that cells arrested in G<sub>1</sub>, but not cells arrested in G<sub>2</sub>, present dysregulated endolysosomal trafficking, displaying an abnormal accumulation of vesicles positive for late endosomal and lysosomal markers. In addition, the macroautophagic/autophagic flux and degradative lysosomal function are strongly impaired. This endolysosomal trafficking dysregulation results in sustained activation of the SPI-1 type III secretion system and lack of vacuole repair by the autophagy pathway, ultimately compromising the maturation and integrity of the <i>Salmonella-</i>containing vacuole. As such, <i>Salmonella</i> is released in the host cytosol. Collectively, our findings demonstrate that the modulation of the host cell cycle occurring during <i>Salmonella</i> infection is related to a disparity in the permissivity of cells arrested in G<sub>1</sub> and G<sub>2</sub>/M, due to their intrinsic characteristics. <b>Abbreviations:</b> CDK4: cyclin dependent kinase 4; CDK6: cyclin dependent kinase 6; CDK4-CDK6i: CDK4-CDK6 inhibitor IV; cfu: colony-forming units; CHQ: chloroquine; DMSO: dimethyl sulfoxide; EEA1: early endosome antigen 1; FITC: fluorescein isothiocyanate; GFP: green fluorescent protein; hpi: hours post-infection; LAMP1: lysosomal associated membrane protein 1; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MOI: multiplicity of infection; RAB7: RAB7, member RAS oncogene family; SCV: <i>Salmonella-</i>containing vacuole; SPI-1: <i>Salmonella</i> pathogenicity island-1; SPI-2: <i>Salmonella</i> pathogenicity island-2; TFEB: transcription factor EB; T3SS: type III secretion system
DOI: 10.6084/m9.figshare.17021871.v1
title: Dysregulated endolysosomal trafficking in cells arrested in the G<sub>1</sub> phase of the host cell cycle impairs <i>Salmonella</i> vacuolar replication

description: Modulation of the host cell cycle has emerged as a common theme among the pathways regulated by bacterial pathogens, arguably to promote host cell colonization. However, in most cases the exact benefit ensuing from such interference to the infection process remains unclear. Previously, we have shown that <i>Salmonella</i> actively induces G<sub>2</sub>/M arrest of host cells, and that infection is severely inhibited in cells arrested in G<sub>1</sub>. In this study, we demonstrate that <i>Salmonella</i> vacuolar replication is inhibited in host cells blocked in G<sub>1</sub>, whereas the cytosolic replication of the closely related pathogen <i>Shigella</i> is not affected. Mechanistically, we show that cells arrested in G<sub>1</sub>, but not cells arrested in G<sub>2</sub>, present dysregulated endolysosomal trafficking, displaying an abnormal accumulation of vesicles positive for late endosomal and lysosomal markers. In addition, the macroautophagic/autophagic flux and degradative lysosomal function are strongly impaired. This endolysosomal trafficking dysregulation results in sustained activation of the SPI-1 type III secretion system and lack of vacuole repair by the autophagy pathway, ultimately compromising the maturation and integrity of the <i>Salmonella-</i>containing vacuole. As such, <i>Salmonella</i> is released in the host cytosol. Collectively, our findings demonstrate that the modulation of the host cell cycle occurring during <i>Salmonella</i> infection is related to a disparity in the permissivity of cells arrested in G<sub>1</sub> and G<sub>2</sub>/M, due to their intrinsic characteristics. <b>Abbreviations:</b> CDK4: cyclin dependent kinase 4; CDK6: cyclin dependent kinase 6; CDK4-CDK6i: CDK4-CDK6 inhibitor IV; cfu: colony-forming units; CHQ: chloroquine; DMSO: dimethyl sulfoxide; EEA1: early endosome antigen 1; FITC: fluorescein isothiocyanate; GFP: green fluorescent protein; hpi: hours post-infection; LAMP1: lysosomal associated membrane protein 1; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MOI: multiplicity of infection; RAB7: RAB7, member RAS oncogene family; SCV: <i>Salmonella-</i>containing vacuole; SPI-1: <i>Salmonella</i> pathogenicity island-1; SPI-2: <i>Salmonella</i> pathogenicity island-2; TFEB: transcription factor EB; T3SS: type III secretion system
DOI: 10.6084/m9.figshare.17293896.v1
title: Autophagy modulates cell fate decisions during lineage commitment

description: Early events during development leading to exit from a pluripotent state and commitment toward a specific germ layer still need in depth understanding. Autophagy has been shown to play a crucial role in both development and differentiation. This study employs human embryonic and induced pluripotent stem cells to understand the early events of lineage commitment with respect to the role of autophagy in this process. Our data indicate that a dip in autophagy facilitates exit from pluripotency. Upon exit, we demonstrate that the modulation of autophagy affects SOX2 levels and lineage commitment, with induction of autophagy promoting SOX2 degradation and mesendoderm formation, whereas inhibition of autophagy causes SOX2 accumulation and neuroectoderm formation. Thus, our results indicate that autophagy-mediated SOX2 turnover is a determining factor for lineage commitment. These findings will deepen our understanding of development and lead to improved methods to derive different lineages and cell types. <b>Abbreviations:</b> ACTB: Actin, beta; ATG: Autophagy-related; BafA1: Bafilomycin A<sub>1</sub>; CAS9: CRISPR associated protein 9; CQ: Chloroquine; DE: Definitive endoderm; hESCs: Human Embryonic Stem Cells; hiPSCs: Human Induced Pluripotent Stem Cells; LAMP1: Lysosomal Associated Membrane Protein 1; MAP1LC3: Microtubule-Associated Protein 1 Light Chain 3; MTOR: Mechanistic Target Of Rapamycin Kinase; NANOG: Nanog Homeobox; PAX6: Paired Box 6; PE: Phosphatidylethanolamine; POU5F1: POU class 5 Homeobox 1; PRKAA2: Protein Kinase AMP-Activated Catalytic Subunit Alpha 2; SOX2: SRY-box Transcription Factor 2; SQSTM1: Sequestosome 1; ULK1: unc-51 like Autophagy Activating Kinase 1; WDFY3: WD Repeat and FYVE Domain Containing 3.
DOI: 10.5519/qd.n44zthix
title: Query on the Natural History Museum Data Portal (data.nhm.ac.uk) (1 records)
DOI: 10.17638/datacat.liverpool.ac.uk/1587
title: Drosophila suzukii

description: A photography collection (lateral, ventral, and dorsal images) of Drosophila suzukii. Part of a collection of photographs at Drosophoto.com
DOI: 10.5281/zenodo.6949011
title: Optical motion capturing of change of direction motions reconstructed with inverse kinematics and dynamics and optimal control simulation

description: This is the data belonging to the publication "Change the direction: 3D optimal control simulation by directly tracking marker and ground reaction force data". This study investigated the feasibility and accuracy of reconstructing, especially change of direction motions with a 3D full-body musculoskeletal model by tracking marker and ground reaction force (GRF) data in optimal control simulations. We recorded in total 30 trials with optical motion capture. Using this data, we compared inverse methods (inverse kinematics and dynamics) to coordinate tracking simulations and marker tracking simulations. Please see the README and the publication for further details.
DOI: 10.22023/mdx.20411343
title: Exploration of Social Sharing Interview Transcript C.pdf

description: The Museum of Domestic Design and Architecture ran a student project in spring 2022, funded by the Art Fund. Eight students were employed to improve the museum's instagram presence using an experimental model based on Culture 24's Let's Get Real.
DOI: 10.57745/aq0opt/6swjd6
title: 8.explo_APC-paid_frenchCA_trusted.tab

description: Valeurs du graphique 5 du rapport
DOI: 10.57745/aq0opt/xugnda
title: 17.explo_french-CA_discipline_trusted.tab

description: Valeurs du graphique 6 du rapport
DOI: 10.57745/aq0opt/mqoz6k
title: 18.explo_french-CA_tier_trusted.tab

description: Valeurs du graphique 8 du rapport
DOI: 10.57745/aq0opt/fzuo5i
title: 19.explo_french-CA_OAcolor_trusted.tab

description: Valeurs du graphique 7 du rapport
DOI: 10.57745/aq0opt/sgsrbq
title: 21_22.models_frenchCA_sum.tab

description: Valeurs du graphique 12 du rapport
DOI: 10.57745/aq0opt/ncpoaa
title: 23.original_APC_cost.tab

description: Valeurs du graphique 9 du rapport
DOI: 10.57745/aq0opt/tlfdrs
title: 24.reconstructed_APC_cost.tab

description: Valeurs du graphique 10 du rapport
DOI: 10.57745/aq0opt/qb3ulh
title: 25-30.prev_S1.tab

description: Valeurs des graphiques 13, 14 et 15 du rapport
DOI: 10.57745/aq0opt/lz6kmz
title: 37-39.prev_S1.tab

description: Valeurs du graphique 18 du rapport
DOI: 10.57745/aq0opt/pbvsxj
title: 34-36.prev_S1.tab

description: Valeurs du graphique 17 du rapport
DOI: 10.57745/aq0opt/aiwyqm
title: 31-33.prev_S1.tab

description: Valeurs du graphique 16 du rapport
DOI: 10.57745/aq0opt/egalw9
title: 43-45.prev_S2A_1.25.tab

description: Valeurs du graphique 20 du rapport
DOI: 10.57745/aq0opt/akbaxw
title: 52-54.prev_S2B_0.9.tab

description: Valeurs du graphique 21 du rapport
DOI: 10.57745/aq0opt/t3ceud
title: 66.prev_resume_facet.tab

description: Valeurs du graphique 23 du rapport
DOI: 10.57745/aq0opt/mf2zls
title: 64.prev_subscriptions.tab

description: Valeurs du graphique 11 du rapport
DOI: 10.57745/aq0opt/nmeprw
title: 71.redo_tier.tab

description: Valeurs du graphique 3 du rapport
DOI: 10.57745/aq0opt/vnvrmd
title: 65_67.prev_resume.tab

description: Valeurs du graphique 22 du rapport
DOI: 10.57745/aq0opt/loji53
title: 69.redo_color.tab

description: Valeurs du graphique 2 du rapport
DOI: 10.57745/aq0opt/6vskqu
title: 61-63.prev_S3.tab

description: Valeurs du graphique 19 du rapport
DOI: 10.57745/aq0opt/xplisk
title: 70.2.discipline_repartition.tab

description: Valeurs du graphique 1 du rapport
DOI: 10.57745/aq0opt/eba2nk
title: 70_70.1.redo_discipline.tab

description: Valeurs du graphique 4 du rapport
DOI: 10.57745/aq0opt/hvbp8k
title: BSO_final_reconstructed.csv

description: Données du BSO enrichies et complétées
DOI: 10.6084/m9.figshare.20411526
title: Activated platelets - FCS files

description: FCS files - activated platelets
DOI: 10.22023/mdx.20411340
title: Exploration of Social Sharing Interview Transcript B.pdf

description: The Museum of Domestic Design and Architecture ran a student project in spring 2022, funded by the Art Fund. Eight students were employed to improve the museum's instagram presence using an experimental model based on Culture 24's Let's Get Real.
DOI: 10.6084/m9.figshare.20411625
title: Erythrocyte ghosts - FCS files

description: FCS files