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Generation of an obese diabetic mouse model upon conditional Atrx disruption

2023-06-01Journal article Open access
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dc.contributor.authorGaspar, Tiago Bordeira
dc.contributor.authorJesus, Tito Teles
dc.contributor.authorAzevedo, Maria Teresa
dc.contributor.authorMacedo, Sofia
dc.contributor.authorSoares, Mariana Alves
dc.contributor.authorMartins, Rui Sousa
dc.contributor.authorLeite, Rúben
dc.contributor.authorRodrigues, Lia
dc.contributor.authorRodrigues, Daniela Ferreira
dc.contributor.authorCardoso, Luís
dc.contributor.authorBorges, Inês
dc.contributor.authorCanberk, Sule
dc.contributor.authorGärtner, Fátima
dc.contributor.authorMiranda-Alves, Leandro
dc.contributor.authorLopes, José Manuel
dc.contributor.authorSoares, Paula
dc.contributor.authorVinagre, João
dc.date.accessioned2024-05-20T13:23:24Z
dc.date.available2024-05-20T13:23:24Z
dc.date.issued2023-06-01
dc.description.abstractATRX mutations occur in up to 17% of human pancreatic neuroendocrine tumours (PanNETs), and recent evidence points towards its inability to drive PanNET formation in mouse pancreas while predisposing individuals to inflammageing. Aiming to explore the additional non-tumourigenic consequences of Atrx deletion, we characterised an aged series of Atrx conditional disruption in β cells using the Pdx1 promoter. Homozygous mice (P.AtrxHOM) exhibited obesity, diabetes, glucose intolerance, and pancreatic adiposity at a higher extent than age- and sex-matched controls (P.AtrxWT).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationGaspar, T. B., Jesus, T. T., Azevedo, M. T., Macedo, S., Soares, M. A., Martins, R. S., Leite, R., Rodrigues, L., Rodrigues, D. F., Cardoso, L., Borges, I., Canberk, S., Gärtner, F., Miranda-Alves, L., Lopes, J. M., Soares, P., & Vinagre, J. (2023). Generation of an obese diabetic mouse model upon conditional Atrx Disruption. Cancers, 15(11), Artigo 11. https://doi.org/10.3390/cancers15113018pt_PT
dc.identifier.doi10.3390/cancers15113018pt_PT
dc.identifier.eissn2072-6694
dc.identifier.urihttp://hdl.handle.net/10400.22/25532
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherMDPIpt_PT
dc.relationFCT—Fundação para a Ciência e Tecnologia, I.P. - SFRH/BD/129431/2017, CEECIND/00201/2017 e 2022.00276.CEECIND, PTDC/MED-ONC/0531/2021—CTRL+ALT+CEL; “Institute for Research and Innovation in Health Sciences” (UID/BIM/04293/2019); “Cancer Research on Therapy Resistance: From Basic Mechanisms to Novel Targets”-NORTE-01-0145-FEDER-000051 (NORTE 2020); NORTE-01-0145-FEDER-072678-Consórcio PORTO.CCC–Porto.Comprehensive Cancer Center Raquel Seruca. SFRH/BD/137802/2018; Coordenação de Aperfeiçoamento de Pessoal de Nível Superior-Brazil (CAPES)—88881.361674/2019-01; and L.M.-A. by CNE-FAPERJ E-26/200.798/2021 e o Programa de Redes de Pesquisa em Saúde do Estado do Rio de Janeiro—2019 E-26/010.002429/2019).pt_PT
dc.relation.publisherversionhttps://www.mdpi.com/2072-6694/15/11/3018pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectAtrxpt_PT
dc.subjectConditional mouse modelpt_PT
dc.subjectEndocrine dysfunctionpt_PT
dc.subjectFatty pancreaspt_PT
dc.subjectPancreatic fatty replacementpt_PT
dc.subjectHyperglycaemiapt_PT
dc.subjectHepatic stetosispt_PT
dc.subjectInflammageingpt_PT
dc.subjectObesitypt_PT
dc.subjectPdx1-Crept_PT
dc.titleGeneration of an obese diabetic mouse model upon conditional Atrx disruptionpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage19pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titleCancerspt_PT
oaire.citation.volume15(11)pt_PT
person.familyNameRodrigues
person.givenNameLia
person.identifier2587034
person.identifier.ciencia-idE413-028E-86EB
person.identifier.orcid0000-0002-3718-1111
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication842411e6-9342-46d6-974a-740eb3dff276
relation.isAuthorOfPublication.latestForDiscovery842411e6-9342-46d6-974a-740eb3dff276

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