Papantonis, Argyris

[["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.artnumber","e101533"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The EMBO Journal"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Weiterer, Sinah‐Sophia"],["dc.contributor.author","Meier‐Soelch, Johanna"],["dc.contributor.author","Georgomanolis, Theodore"],["dc.contributor.author","Mizi, Athanasia"],["dc.contributor.author","Beyerlein, Anna"],["dc.contributor.author","Weiser, Hendrik"],["dc.contributor.author","Brant, Lilija"],["dc.contributor.author","Mayr‐Buro, Christin"],["dc.contributor.author","Jurida, Liane"],["dc.contributor.author","Beuerlein, Knut"],["dc.contributor.author","Müller, Helmut"],["dc.contributor.author","Weber, Axel"],["dc.contributor.author","Tenekeci, Ulas"],["dc.contributor.author","Dittrich‐Breiholz, Oliver"],["dc.contributor.author","Bartkuhn, Marek"],["dc.contributor.author","Nist, Andrea"],["dc.contributor.author","Stiewe, Thorsten"],["dc.contributor.author","IJcken, Wilfred FJ"],["dc.contributor.author","Riedlinger, Tabea"],["dc.contributor.author","Schmitz, M Lienhard"],["dc.contributor.author","Papantonis, Argyris"],["dc.contributor.author","Kracht, Michael"],["dc.date.accessioned","2019-12-05T15:22:53Z"],["dc.date.accessioned","2021-10-27T13:21:48Z"],["dc.date.available","2019-12-05T15:22:53Z"],["dc.date.available","2021-10-27T13:21:48Z"],["dc.date.issued","2019"],["dc.description.abstract","How cytokine-driven changes in chromatin topology are converted into gene regulatory circuits during inflammation still remains unclear. Here, we show that interleukin (IL)-1α induces acute and widespread changes in chromatin accessibility via the TAK1 kinase and NF-κB at regions that are highly enriched for inflammatory disease-relevant SNPs. Two enhancers in the extended chemokine locus on human chromosome 4 regulate the IL-1α-inducible IL8 and CXCL1-3 genes. Both enhancers engage in dynamic spatial interactions with gene promoters in an IL-1α/TAK1-inducible manner. Microdeletions of p65-binding sites in either of the two enhancers impair NF-κB recruitment, suppress activation and biallelic transcription of the IL8/CXCL2 genes, and reshuffle higher-order chromatin interactions as judged by i4C interactome profiles. Notably, these findings support a dominant role of the IL8 \"master\" enhancer in the regulation of sustained IL-1α signaling, as well as for IL-8 and IL-6 secretion. CRISPR-guided transactivation of the IL8 locus or cross-TAD regulation by TNFα-responsive enhancers in a different model locus supports the existence of complex enhancer hierarchies in response to cytokine stimulation that prime and orchestrate proinflammatory chromatin responses downstream of NF-κB."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaſt (DFG) http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship","Deutsche Krebshilfe http://dx.doi.org/10.13039/501100005972"],["dc.description.sponsorship","Max‐Planck Society http://dx.doi.org/10.13039/501100004189"],["dc.description.sponsorship","Excellence Cluster Cardio‐Pulmonary System and Cardio‐Pulmonary Institute (EXC 147: Kardiopulmonales System)"],["dc.description.sponsorship","Cardio‐Pulmonary Institute (CPI)"],["dc.description.sponsorship","DZL/UGMLC Program"],["dc.description.sponsorship","Center for Molecular Medicine Cologne (ZMMK)"],["dc.identifier.doi","10.15252/embj.2019101533"],["dc.identifier.isbn","31701553"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16860"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92046"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1460-2075"],["dc.relation.issn","1460-2075"],["dc.relation.issn","0261-4189"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Distinct IL‐1α‐responsive enhancers promote acute and coordinated changes in chromatin topology in a hierarchical manner"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]