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dc.contributor.authorBarbarani, Gloria
dc.contributor.authorRonchi, Antonella
dc.contributor.authorRuoppolo, Margherita
dc.contributor.authorSantorelli, Lucia
dc.contributor.authorSteinfelder, Robert
dc.contributor.authorElangovan, Sudharshan
dc.contributor.authorFugazza, Cristina
dc.contributor.authorCaterino, Marianna
dc.date.accessioned2017-10-30T07:55:31Z
dc.date.available2017-10-30T07:55:31Z
dc.date.issued2017-10-26
dc.identifier.citationBarbarani G, Ronchi A, Ruoppolo M, Santorelli L, Steinfelder R, et al. (2017) Unravelling pathways downstream Sox6 induction in K562 erythroid cells by proteomic analysis. Scientific Reports 7. Available: http://dx.doi.org/10.1038/s41598-017-14336-6.
dc.identifier.issn2045-2322
dc.identifier.pmid29074889
dc.identifier.doi10.1038/s41598-017-14336-6
dc.identifier.urihttp://hdl.handle.net/10754/625979
dc.description.abstractThe Sox6 transcription factor is crucial for terminal maturation of definitive red blood cells. Sox6-null mouse fetuses present misshapen and nucleated erythrocytes, due to impaired actin assembly and cytoskeleton stability. These defects are accompanied with a reduced survival of Sox6-/- red blood cells, resulting in a compensated anemia. Sox6-overexpression in K562 cells and in human primary ex vivo erythroid cultures enhances erythroid differentiation and leads to hemoglobinization, the hallmark of erythroid maturation. To obtain an overview on processes downstream to Sox6 expression, we performed a differential proteomic analysis on human erythroid K562 cells overexpressing Sox6. Sox6-overexpression induces dysregulation of 64 proteins, involved in cytoskeleton remodeling and in protein synthesis, folding and trafficking, key processes for erythroid maturation. Moreover, 43 out of 64 genes encoding for differentially expressed proteins contain within their proximal regulatory regions sites that are bound by SOX6 according to ENCODE ChIP-seq datasets and are possible direct SOX6 targets. SAR1B, one of the most induced proteins upon Sox6 overexpression, shares a conserved regulatory module, composed by a double SOX6 binding site and a GATA1 consensus, with the adjacent SEC24 A gene. Since both genes encode for COPII components, this element could concur to the coordinated expression of these proteins during erythropoiesis.
dc.description.sponsorshipThis work was supported by Fondazione Cariplo grant no 2012.0517 to A.R. and by the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework Programme FP7/2007-2013/under REA grant agreement no 289611 (HEM_ID Project).
dc.publisherSpringer Nature
dc.relation.urlhttps://www.nature.com/articles/s41598-017-14336-6
dc.rightsThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.titleUnravelling pathways downstream Sox6 induction in K562 erythroid cells by proteomic analysis
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.identifier.journalScientific Reports
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionDipartimento di Biotecnologie e Bioscienze, Università degli studi di Milano-Bicocca, Milan, Italy.
dc.contributor.institutionCEINGE Biotecnologie Avanzate, Naples, Italy.
dc.contributor.institutionDipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli,
dc.contributor.institutionFred Hutchinson Cancer Research Center, Seattle, USA.
dc.contributor.institutionDipartimento di Biotecnologie e Bioscienze, Università degli studi di Milano-Bicocca, Milan, Italy. cristina.fugazza@unimib.it.
kaust.personElangovan, Sudharshan
refterms.dateFOA2018-06-14T03:37:17Z
dc.date.published-online2017-10-26
dc.date.published-print2017-12


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This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Except where otherwise noted, this item's license is described as This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.