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dc.creatorTesone, Amelia J.-
dc.creatorRutkowski, Melanie R.-
dc.creatorBrencicova, Eva-
dc.creatorSvoronos, Nikolaos-
dc.creatorPerales Puchal, Alfredo-
dc.creatorStephen, Tom L.-
dc.creatorAllegrezza, Michael J.-
dc.creatorPayne, Kyle K.-
dc.creatorNguyen, Jenny M.-
dc.creatorWickramasinghe, Jayamanna-
dc.creatorTchou, Julia-
dc.creatorBorowsky, Mark E.-
dc.creatorRabinovich, Gabriel Adrián-
dc.creatorKossenkov, Andrew V.-
dc.creatorConejo Garcia, José R.-
dc.date2017-08-24T20:43:49Z-
dc.date2017-08-24T20:43:49Z-
dc.date2016-02-11-
dc.date2017-08-09T16:56:52Z-
dc.date.accessioned2019-04-29T15:52:04Z-
dc.date.available2019-04-29T15:52:04Z-
dc.date.issued2016-02-11-
dc.identifierTesone, Amelia J.; Rutkowski, Melanie R.; Brencicova, Eva; Svoronos, Nikolaos; Perales Puchal, Alfredo; et al.; Satb1 overexpression drives tumor-promoting activities in cancer-associated dendritic cells; Cell Press; Cell reports; 14; 7; 11-2-2016; 1774-1786-
dc.identifier2211-1247-
dc.identifierhttp://hdl.handle.net/11336/22980-
dc.identifier2211-1247-
dc.identifierCONICET Digital-
dc.identifierCONICET-
dc.identifier.urihttp://rodna.bn.gov.ar:8080/jspui/handle/bnmm/304124-
dc.descriptionSpecial AT-rich sequence-binding protein 1 (Satb1) governs genome-wide transcriptional programs. Using a conditional knockout mouse, we find that Satb1 is required for normal differentiation of conventional dendritic cells (DCs). Furthermore, Satb1 governs the differentiation of inflammatory DCs by regulating major histocompatibility complex class II (MHC II) expression through Notch1 signaling. Mechanistically, Satb1 binds to the Notch1 promoter, activating Notch expression and driving RBPJ occupancy of the H2-Ab1 promoter, which activates MHC II transcription. However, tumor-driven, unremitting expression of Satb1 in activated Zbtb46(+) inflammatory DCs that infiltrate ovarian tumors results in an immunosuppressive phenotype characterized by increased secretion of tumor-promoting Galectin-1 and IL-6. In vivo silencing of Satb1 in tumor-associated DCs reverses their tumorigenic activity and boosts protective immunity. Therefore, dynamic fluctuations in Satb1 expression govern the generation and immunostimulatory activity of steady-state and inflammatory DCs, but continuous Satb1 overexpression in differentiated DCs converts them into tolerogenic/pro-inflammatory cells that contribute to malignant progression.-
dc.descriptionFil: Tesone, Amelia J.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Rutkowski, Melanie R.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Brencicova, Eva. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Svoronos, Nikolaos. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Perales Puchal, Alfredo. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Stephen, Tom L.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Allegrezza, Michael J.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Payne, Kyle K.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Nguyen, Jenny M.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.descriptionFil: Wickramasinghe, Jayamanna. The Wistar Institute. Center for Systems and Computational Biology; Estados Unidos-
dc.descriptionFil: Tchou, Julia. University of Pennsylvania; Estados Unidos-
dc.descriptionFil: Borowsky, Mark E.. Christiana Care Health System. Helen F. Graham Cancer Center; Estados Unidos-
dc.descriptionFil: Rabinovich, Gabriel Adrián. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentina-
dc.descriptionFil: Kossenkov, Andrew V.. The Wistar Institute. Center for Systems and Computational Biology; Estados Unidos-
dc.descriptionFil: Conejo Garcia, José R.. The Wistar Institute. Tumor Microenvironment and Metastasis Program; Estados Unidos-
dc.formatapplication/pdf-
dc.formatapplication/pdf-
dc.languageeng-
dc.publisherCell Press-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S2211124716300341-
dc.relationinfo:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1016/j.celrep.2016.01.056-
dc.relationinfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4767618/-
dc.rightsinfo:eu-repo/semantics/openAccess-
dc.rightshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/-
dc.sourcereponame:CONICET Digital (CONICET)-
dc.sourceinstname:Consejo Nacional de Investigaciones Científicas y Técnicas-
dc.sourceinstacron:CONICET-
dc.subjectSATB1-
dc.subjectTRANSCRIPTION FACTOR-
dc.subjectDENDRITIC CELLS-
dc.subjectINFLAMMATION-
dc.subjectIMMUNE TOLERANCE-
dc.subjectBioquímica y Biología Molecular-
dc.subjectCiencias Biológicas-
dc.subjectCIENCIAS NATURALES Y EXACTAS-
dc.titleSatb1 overexpression drives tumor-promoting activities in cancer-associated dendritic cells-
dc.typeinfo:eu-repo/semantics/article-
dc.typeinfo:eu-repo/semantics/publishedVersion-
dc.typeinfo:ar-repo/semantics/articulo-
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