Papantonis, Argyris

[["dc.bibliographiccitation.firstpage","jcs228684"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Cell Science"],["dc.bibliographiccitation.volume","132"],["dc.contributor.author","Lalioti, Maria-Eleni"],["dc.contributor.author","Arbi, Marina"],["dc.contributor.author","Loukas, Ioannis"],["dc.contributor.author","Kaplani, Konstantina"],["dc.contributor.author","Kalogeropoulou, Argyro"],["dc.contributor.author","Lokka, Georgia"],["dc.contributor.author","Kyrousi, Christina"],["dc.contributor.author","Mizi, Athanasia"],["dc.contributor.author","Georgomanolis, Theodore"],["dc.contributor.author","Josipovic, Natasa"],["dc.contributor.author","Gkikas, Dimitrios"],["dc.contributor.author","Benes, Vladimir"],["dc.contributor.author","Politis, Panagiotis K."],["dc.contributor.author","Papantonis, Argyris"],["dc.contributor.author","Lygerou, Zoi"],["dc.contributor.author","Taraviras, Stavros"],["dc.date.accessioned","2020-12-10T18:41:53Z"],["dc.date.available","2020-12-10T18:41:53Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1242/jcs.228684"],["dc.identifier.eissn","1477-9137"],["dc.identifier.issn","0021-9533"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77716"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","GemC1 governs multiciliogenesis through direct interaction with and transcriptional regulation of p73"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular & Cellular Oncology"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Zampetidis, Christos P."],["dc.contributor.author","Papantonis, Argyris"],["dc.contributor.author","Gorgoulis, Vassilis G."],["dc.date.accessioned","2022-04-01T10:01:49Z"],["dc.date.available","2022-04-01T10:01:49Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1080/23723556.2022.2030158"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105755"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","2372-3556"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Escape from senescence: revisiting cancer therapeutic strategies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","3014"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Kargapolova, Yulia"],["dc.contributor.author","Rehimi, Rizwan"],["dc.contributor.author","Kayserili, Hülya"],["dc.contributor.author","Brühl, Joanna"],["dc.contributor.author","Sofiadis, Konstantinos"],["dc.contributor.author","Zirkel, Anne"],["dc.contributor.author","Palikyras, Spiros"],["dc.contributor.author","Mizi, Athanasia"],["dc.contributor.author","Li, Yun"],["dc.contributor.author","Papantonis, Argyris"],["dc.date.accessioned","2021-06-01T10:50:39Z"],["dc.date.available","2021-06-01T10:50:39Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Members of the chromodomain-helicase-DNA binding (CHD) protein family are chromatin remodelers implicated in human pathologies, with CHD6 being one of its least studied members. We discovered a de novo CHD6 missense mutation in a patient clinically presenting the rare Hallermann-Streiff syndrome (HSS). We used genome editing to generate isogenic iPSC lines and model HSS in relevant cell types. By combining genomics with functional in vivo and in vitro assays, we show that CHD6 binds a cohort of autophagy and stress response genes across cell types. The HSS mutation affects CHD6 protein folding and impairs its ability to recruit co-remodelers in response to DNA damage or autophagy stimulation. This leads to accumulation of DNA damage burden and senescence-like phenotypes. We therefore uncovered a molecular mechanism explaining HSS onset via chromatin control of autophagic flux and genotoxic stress surveillance."],["dc.description.sponsorship","Open-Access-Finanzierung durch die Universitätsmedizin Göttingen 2021"],["dc.identifier.doi","10.1038/s41467-021-23327-1"],["dc.identifier.pmid","34021162"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86739"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/278"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","2041-1723"],["dc.relation.workinggroup","RG Wollnik"],["dc.rights","CC BY 4.0"],["dc.title","Overarching control of autophagy and DNA damage response by CHD6 revealed by modeling a rare human pathology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Nature Reviews. Molecular Cell Biology"],["dc.contributor.author","Rippe, Karsten"],["dc.contributor.author","Papantonis, Argyris"],["dc.date.accessioned","2021-08-12T07:44:59Z"],["dc.date.available","2021-08-12T07:44:59Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1038/s41580-021-00401-6"],["dc.identifier.pii","401"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88343"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.relation.eissn","1471-0080"],["dc.relation.issn","1471-0072"],["dc.title","RNA polymerase II transcription compartments: from multivalent chromatin binding to liquid droplet formation?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","33"],["dc.bibliographiccitation.journal","Methods"],["dc.bibliographiccitation.lastpage","37"],["dc.bibliographiccitation.volume","170"],["dc.contributor.author","Mizi, Athanasia"],["dc.contributor.author","Gade Gusmao, Eduardo"],["dc.contributor.author","Papantonis, Argyris"],["dc.date.accessioned","2020-12-10T15:21:49Z"],["dc.date.available","2020-12-10T15:21:49Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/j.ymeth.2019.07.003"],["dc.identifier.issn","1046-2023"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73176"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","iHi-C 2.0: A simple approach for mapping native spatial chromatin organisation from low cell numbers"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","EMBO reports"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Ahuja, Gaurav"],["dc.contributor.author","Bartsch, Deniz"],["dc.contributor.author","Yao, Wenjie"],["dc.contributor.author","Geissen, Simon"],["dc.contributor.author","Frank, Stefan"],["dc.contributor.author","Aguirre, Aitor"],["dc.contributor.author","Russ, Nicole"],["dc.contributor.author","Messling, Jan‐Erik"],["dc.contributor.author","Dodzian, Joanna"],["dc.contributor.author","Lagerborg, Kim A"],["dc.contributor.author","Vargas, Natalia Emilse"],["dc.contributor.author","Muck, Joscha Sergej"],["dc.contributor.author","Brodesser, Susanne"],["dc.contributor.author","Baldus, Stephan"],["dc.contributor.author","Sachinidis, Agapios"],["dc.contributor.author","Hescheler, Juergen"],["dc.contributor.author","Dieterich, Christoph"],["dc.contributor.author","Trifunovic, Aleksandra"],["dc.contributor.author","Papantonis, Argyris"],["dc.contributor.author","Petrascheck, Michael"],["dc.contributor.author","Klinke, Anna"],["dc.contributor.author","Jain, Mohit"],["dc.contributor.author","Valenzano, Dario Riccardo"],["dc.contributor.author","Kurian, Leo"],["dc.date.accessioned","2020-12-10T18:42:39Z"],["dc.date.available","2020-12-10T18:42:39Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.15252/embr.201847407"],["dc.identifier.eissn","1469-3178"],["dc.identifier.issn","1469-221X"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78033"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Loss of genomic integrity induced by lysosphingolipid imbalance drives ageing in the heart"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Journal of Extracellular Vesicles"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Wallis, Ryan"],["dc.contributor.author","Josipovic, Natasa"],["dc.contributor.author","Mizen, Hannah"],["dc.contributor.author","Robles‐Tenorio, Arturo"],["dc.contributor.author","Tyler, Eleanor J."],["dc.contributor.author","Papantonis, Argyris"],["dc.contributor.author","Bishop, Cleo L."],["dc.date.accessioned","2021-04-14T08:29:24Z"],["dc.date.available","2021-04-14T08:29:24Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1002/jev2.12041"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82892"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2001-3078"],["dc.relation.issn","2001-3078"],["dc.title","Isolation methodology is essential to the evaluation of the extracellular vesicle component of the senescence‐associated secretory phenotype"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","5756"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Brackley, C. A."],["dc.contributor.author","Gilbert, N."],["dc.contributor.author","Michieletto, D."],["dc.contributor.author","Papantonis, A."],["dc.contributor.author","Pereira, M. C. F."],["dc.contributor.author","Cook, P. R."],["dc.contributor.author","Marenduzzo, D."],["dc.date.accessioned","2021-12-01T09:23:44Z"],["dc.date.available","2021-12-01T09:23:44Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract The discovery that overexpressing one or a few critical transcription factors can switch cell state suggests that gene regulatory networks are relatively simple. In contrast, genome-wide association studies (GWAS) point to complex phenotypes being determined by hundreds of loci that rarely encode transcription factors and which individually have small effects. Here, we use computer simulations and a simple fitting-free polymer model of chromosomes to show that spatial correlations arising from 3D genome organisation naturally lead to stochastic and bursty transcription as well as complex small-world regulatory networks (where the transcriptional activity of each genomic region subtly affects almost all others). These effects require factors to be present at sub-saturating levels; increasing levels dramatically simplifies networks as more transcription units are pressed into use. Consequently, results from GWAS can be reconciled with those involving overexpression. We apply this pan-genomic model to predict patterns of transcriptional activity in whole human chromosomes, and, as an example, the effects of the deletion causing the diGeorge syndrome."],["dc.description.abstract","Abstract The discovery that overexpressing one or a few critical transcription factors can switch cell state suggests that gene regulatory networks are relatively simple. In contrast, genome-wide association studies (GWAS) point to complex phenotypes being determined by hundreds of loci that rarely encode transcription factors and which individually have small effects. Here, we use computer simulations and a simple fitting-free polymer model of chromosomes to show that spatial correlations arising from 3D genome organisation naturally lead to stochastic and bursty transcription as well as complex small-world regulatory networks (where the transcriptional activity of each genomic region subtly affects almost all others). These effects require factors to be present at sub-saturating levels; increasing levels dramatically simplifies networks as more transcription units are pressed into use. Consequently, results from GWAS can be reconciled with those involving overexpression. We apply this pan-genomic model to predict patterns of transcriptional activity in whole human chromosomes, and, as an example, the effects of the deletion causing the diGeorge syndrome."],["dc.identifier.doi","10.1038/s41467-021-25875-y"],["dc.identifier.pii","25875"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94741"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","2041-1723"],["dc.title","Complex small-world regulatory networks emerge from the 3D organisation of the human genome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5351"],["dc.bibliographiccitation.issue","21"],["dc.bibliographiccitation.journal","Cancers"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Meier-Soelch, Johanna"],["dc.contributor.author","Mayr-Buro, Christin"],["dc.contributor.author","Juli, Jana"],["dc.contributor.author","Leib, Lisa"],["dc.contributor.author","Linne, Uwe"],["dc.contributor.author","Dreute, Jan"],["dc.contributor.author","Papantonis, Argyris"],["dc.contributor.author","Schmitz, M. Lienhard"],["dc.contributor.author","Kracht, Michael"],["dc.contributor.editor","Kolettas, Evangelos"],["dc.contributor.editor","Marcu, Kenneth B."],["dc.contributor.editor","Schmid, Johannes A."],["dc.date.accessioned","2021-12-01T09:22:47Z"],["dc.date.available","2021-12-01T09:22:47Z"],["dc.date.issued","2021"],["dc.description.abstract","The NF-κB signaling system plays an important regulatory role in the control of many biological processes. The activities of NF-κB signaling networks and the expression of their target genes are frequently elevated in pathophysiological situations including inflammation, infection, and cancer. In these conditions, the outcome of NF-κB activity can vary according to (i) differential activation states, (ii) the pattern of genomic recruitment of the NF-κB subunits, and (iii) cellular heterogeneity. Additionally, the cytosolic NF-κB activation steps leading to the liberation of DNA-binding dimers need to be distinguished from the less understood nuclear pathways that are ultimately responsible for NF-κB target gene specificity. This raises the need to more precisely determine the NF-κB activation status not only for the purpose of basic research, but also in (future) clinical applications. Here we review a compendium of different methods that have been developed to assess the NF-κB activation status in vitro and in vivo. We also discuss recent advances that allow the assessment of several NF-κB features simultaneously at the single cell level."],["dc.description.abstract","The NF-κB signaling system plays an important regulatory role in the control of many biological processes. The activities of NF-κB signaling networks and the expression of their target genes are frequently elevated in pathophysiological situations including inflammation, infection, and cancer. In these conditions, the outcome of NF-κB activity can vary according to (i) differential activation states, (ii) the pattern of genomic recruitment of the NF-κB subunits, and (iii) cellular heterogeneity. Additionally, the cytosolic NF-κB activation steps leading to the liberation of DNA-binding dimers need to be distinguished from the less understood nuclear pathways that are ultimately responsible for NF-κB target gene specificity. This raises the need to more precisely determine the NF-κB activation status not only for the purpose of basic research, but also in (future) clinical applications. Here we review a compendium of different methods that have been developed to assess the NF-κB activation status in vitro and in vivo. We also discuss recent advances that allow the assessment of several NF-κB features simultaneously at the single cell level."],["dc.identifier.doi","10.3390/cancers13215351"],["dc.identifier.pii","cancers13215351"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94482"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.publisher","MDPI"],["dc.relation.eissn","2072-6694"],["dc.rights","Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/)."],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Monitoring the Levels of Cellular NF-κB Activation States"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical Epigenetics"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Sen, Madhobi"],["dc.contributor.author","Wang, Xin"],["dc.contributor.author","Hamdan, Feda H."],["dc.contributor.author","Rapp, Jacobe"],["dc.contributor.author","Eggert, Jessica"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Kutschat, Ana Patricia"],["dc.contributor.author","Younesi, Fereshteh S."],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Papantonis, Argyris"],["dc.contributor.author","Strӧbel, Philipp"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2020-12-10T18:39:06Z"],["dc.date.available","2020-12-10T18:39:06Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s13148-019-0690-5"],["dc.identifier.eissn","1868-7083"],["dc.identifier.issn","1868-7075"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77543"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","ARID1A facilitates KRAS signaling-regulated enhancer activity in an AP1-dependent manner in colorectal cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]