{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360004237587056512.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1371/journal.pone.0150010"}},{"identifier":{"@type":"URI","@value":"http://dx.plos.org/10.1371/journal.pone.0150010"}},{"identifier":{"@type":"DOI","@value":"10.60692/j5nw4-sh852"}},{"identifier":{"@type":"DOI","@value":"10.60692/j3wqe-d9554"}},{"identifier":{"@type":"PMID","@value":"26901059"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"β-Cell-Specific Mafk Overexpression Impairs Pancreatic Endocrine Cell Development"}],"description":[{"notation":[{"@value":"Les facteurs de transcription de la famille MAF sont des homologues de v-Maf, la composante oncogène du rétrovirus aviaire AS42. Ils sont subdivisés en 2 groupes, les petites et les grandes protéines MAF, en fonction de leur structure, de leur fonction et de leur taille moléculaire. Le MAFK est un membre de la petite famille des MAF et agit comme une forme négative dominante des grands MAF. Dans des recherches antérieures, nous avons généré des souris transgéniques qui surexpriment MAFK afin de supprimer la fonction des grandes protéines MAF dans les cellules β pancréatiques. Ces souris ont développé une hyperglycémie à l'âge adulte en raison d'une altération de la sécrétion d'insuline stimulée par le glucose. L'objectif de la présente étude est d'examiner les effets de la surexpression de Mafk spécifique des cellules β dans le développement des cellules endocriniennes. Les îlots en développement des embryons transgéniques de Mafk semblaient être désorganisés avec une inversion du nombre total de cellules insuline+ et glucagon+ due à une réduction de la prolifération des cellules β. L'analyse de l'expression génique par RT-PCR quantitative a révélé une diminution des niveaux de gènes liés aux cellules β dont l'expression est connue pour être contrôlée par de grandes protéines MAF. De plus, ces changements s'accompagnaient d'une augmentation significative des facteurs clés de transcription des cellules β probablement due à des mécanismes compensatoires qui auraient pu être activés en réponse à la perte des cellules β. Enfin, la comparaison des profils d'expression génique entre les pancréas de type sauvage et transgéniques a révélé une altération de certains gènes non caractérisés, notamment Pcbd1, Fam132a, Cryba2 et Npy, qui pourraient jouer un rôle important au cours du développement endocrinien pancréatique. Pris ensemble, ces résultats suggèrent que la surexpression de Mafk entrave le développement endocrinien par une régulation de nombreux gènes liés aux cellules β. L'analyse des microréseaux a fourni un ensemble de données unique de gènes exprimés de manière différentielle qui pourrait contribuer à une meilleure compréhension de la base moléculaire qui régit le développement et la fonction du pancréas endocrinien."}]},{"notation":[{"@value":"Los factores de transcripción de la familia MAF son homólogos de v-Maf, el componente oncogénico del retrovirus aviar AS42. Se subdividen en 2 grupos, proteínas MAF pequeñas y grandes, según su estructura, función y tamaño molecular. El MAFK es un miembro de la familia de los MAF pequeños y actúa como una forma negativa dominante de los MAF grandes. En investigaciones anteriores, generamos ratones transgénicos que sobreexpresan MAFK para suprimir la función de las proteínas MAF grandes en las células β pancreáticas. Estos ratones desarrollaron hiperglucemia en la edad adulta debido al deterioro de la secreción de insulina estimulada por glucosa. El objetivo del presente estudio es examinar los efectos de la sobreexpresión de Mafk específica de células β en el desarrollo de células endocrinas. Los islotes en desarrollo de embriones transgénicos de Mafk parecían estar desorganizados con una inversión del número total de células insulina+ y glucagón+ debido a la reducción de la proliferación de células β. El análisis de la expresión génica mediante RT-PCR cuantitativa reveló niveles reducidos de genes relacionados con células β cuyas expresiones se sabe que están controladas por proteínas MAF grandes. Además, estos cambios se acompañaron de un aumento significativo en los factores clave de transcripción de células β, probablemente debido a los mecanismos compensatorios que podrían haberse activado en respuesta a la pérdida de células β. Finalmente, la comparación de micromatrices de perfiles de expresión génica entre páncreas de tipo salvaje y transgénicos reveló la alteración de algunos genes no caracterizados, incluidos Pcbd1, Fam132a, Cryba2 y Npy, que podrían desempeñar papeles importantes durante el desarrollo endocrino pancreático. En conjunto, estos resultados sugieren que la sobreexpresión de Mafk perjudica el desarrollo endocrino a través de una regulación de numerosos genes relacionados con las células β. El análisis de micromatrices proporcionó un conjunto de datos único de genes expresados diferencialmente que podrían contribuir a una mejor comprensión de la base molecular que rige el desarrollo y la función del páncreas endocrino."}]},{"notation":[{"@value":"The MAF family transcription factors are homologs of v-Maf, the oncogenic component of the avian retrovirus AS42. They are subdivided into 2 groups, small and large MAF proteins, according to their structure, function, and molecular size. MAFK is a member of the small MAF family and acts as a dominant negative form of large MAFs. In previous research we generated transgenic mice that overexpress MAFK in order to suppress the function of large MAF proteins in pancreatic β-cells. These mice developed hyperglycemia in adulthood due to impairment of glucose-stimulated insulin secretion. The aim of the current study is to examine the effects of β-cell-specific Mafk overexpression in endocrine cell development. The developing islets of Mafk-transgenic embryos appeared to be disorganized with an inversion of total numbers of insulin+ and glucagon+ cells due to reduced β-cell proliferation. Gene expression analysis by quantitative RT-PCR revealed decreased levels of β-cell-related genes whose expressions are known to be controlled by large MAF proteins. Additionally, these changes were accompanied with a significant increase in key β-cell transcription factors likely due to compensatory mechanisms that might have been activated in response to the β-cell loss. Finally, microarray comparison of gene expression profiles between wild-type and transgenic pancreata revealed alteration of some uncharacterized genes including Pcbd1, Fam132a, Cryba2, and Npy, which might play important roles during pancreatic endocrine development. Taken together, these results suggest that Mafk overexpression impairs endocrine development through a regulation of numerous β-cell-related genes. The microarray analysis provided a unique data set of differentially expressed genes that might contribute to a better understanding of the molecular basis that governs the development and function of endocrine pancreas."}]},{"notation":[{"@value":"عوامل نسخ عائلة MAF هي متجانسات v - Maf، المكون الورمي للفيروس الرجعي للطيور AS42. وتنقسم إلى مجموعتين، بروتينات MAF الصغيرة والكبيرة، وفقًا لهيكلها ووظيفتها وحجمها الجزيئي. MAFK هو عضو في عائلة MAF الصغيرة ويعمل كشكل سلبي مهيمن من MAFs الكبيرة. في الأبحاث السابقة، أنتجنا فئرانًا معدلة وراثيًا تفرط في التعبير عن MAFK من أجل قمع وظيفة بروتينات MAF الكبيرة في خلايا بيتا في البنكرياس. طورت هذه الفئران ارتفاع السكر في الدم في مرحلة البلوغ بسبب ضعف إفراز الأنسولين المحفّز بالجلوكوز. الهدف من الدراسة الحالية هو دراسة آثار التعبير المفرط لمافك الخاص بخلية بيتا في تطور خلايا الغدد الصماء. يبدو أن الجزر النامية للأجنة المعدلة وراثيًا Mafk غير منظمة مع انعكاس الأعداد الإجمالية لخلايا الأنسولين+ والجلوكاجون+ بسبب انخفاض تكاثر الخلايا β. كشف تحليل التعبير الجيني بواسطة RT - PCR الكمي عن انخفاض مستويات الجينات المرتبطة بخلايا بيتا التي من المعروف أن تعبيراتها تتحكم فيها بروتينات MAF الكبيرة. بالإضافة إلى ذلك، ترافقت هذه التغييرات مع زيادة كبيرة في عوامل النسخ الرئيسية لخلايا بيتا على الأرجح بسبب الآليات التعويضية التي ربما تم تنشيطها استجابة لفقدان خلايا بيتا. أخيرًا، كشفت مقارنة المصفوفة الدقيقة لملفات التعبير الجيني بين البنكرياس من النوع البري والبنكرياس المعدل وراثيًا عن تغيير بعض الجينات غير المميزة بما في ذلك Pcbd1 و Fam132a و Cryba2 و Npy، والتي قد تلعب أدوارًا مهمة أثناء نمو الغدد الصماء في البنكرياس. تشير هذه النتائج مجتمعة إلى أن التعبير المفرط لمافك يضعف نمو الغدد الصماء من خلال تنظيم العديد من الجينات المرتبطة بالخلايا بيتا. قدم تحليل المصفوفة الدقيقة مجموعة بيانات فريدة من الجينات المعبر عنها بشكل مختلف والتي قد تسهم في فهم أفضل للأساس الجزيئي الذي يحكم تطور ووظيفة بنكرياس الغدد الصماء."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380004237587056007","@type":"Researcher","foaf:name":[{"@value":"Ahmed M. 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El-Morsy"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004237587056514","@type":"Researcher","foaf:name":[{"@value":"Mesbah A. El-Sayed"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004237587056139","@type":"Researcher","foaf:name":[{"@value":"Mahmoud B. 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