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Institution

Kyoto University

EducationKyoto, Japan
About: Kyoto University is a education organization based out in Kyoto, Japan. It is known for research contribution in the topics: Population & Catalysis. The organization has 85837 authors who have published 217215 publications receiving 6526826 citations. The organization is also known as: Kyōto University & Kyōto daigaku.


Papers
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Journal ArticleDOI
TL;DR: It is shown that mice deficient in Hes1 (encoding Hes-1) display severe pancreatic hypoplasia caused by depletion of pancreatic epithelial precursors due to accelerated differentiation of post-mitotic endocrine cells expressing glucagon, and upregulation of several bHLH components is associated with precocious and excessive differentiation of multiple endocrine cell types in the developing stomach and gut, showing that Hes- 1 operates as a general negative regulator of endodermal endocrine differentiation.
Abstract: Development of endocrine cells in the endoderm involves Atonal and Achaete/Scute-related basic helix-loop-helix (bHLH) proteins. These proteins also serve as neuronal determination and differentiation factors, and are antagonized by the Notch pathway partly acting through Hairy and Enhancer-of-split (HES)-type proteins. Here we show that mice deficient in Hes1 (encoding Hes-1) display severe pancreatic hypoplasia caused by depletion of pancreatic epithelial precursors due to accelerated differentiation of post-mitotic endocrine cells expressing glucagon. Moreover, upregulation of several bHLH components is associated with precocious and excessive differentiation of multiple endocrine cell types in the developing stomach and gut, showing that Hes-1 operates as a general negative regulator of endodermal endocrine differentiation.

1,160 citations

Journal ArticleDOI
TL;DR: It is shown that oligomers of islet amyloid polypeptide (IAPP), a protein that formsAmyloid deposits in the pancreas during type 2 diabetes, triggered the NLRP3 inflammasome and generated mature IL-1β.
Abstract: Interleukin 1β (IL-1β) is an important inflammatory mediator of type 2 diabetes Here we show that oligomers of islet amyloid polypeptide (IAPP), a protein that forms amyloid deposits in the pancreas during type 2 diabetes, triggered the NLRP3 inflammasome and generated mature IL-1β One therapy for type 2 diabetes, glyburide, suppressed IAPP-mediated IL-1β production in vitro Processing of IL-1β initiated by IAPP first required priming, a process that involved glucose metabolism and was facilitated by minimally oxidized low-density lipoprotein Finally, mice transgenic for human IAPP had more IL-1β in pancreatic islets, which localized together with amyloid and macrophages Our findings identify previously unknown mechanisms in the pathogenesis of type 2 diabetes and treatment of pathology caused by IAPP

1,157 citations

Journal ArticleDOI

1,157 citations

Journal ArticleDOI
01 Aug 2008-Science
TL;DR: Genetic lineage tracings suggest that iPS cells are generated by direct reprogramming of lineage-committed somatic cells and that retroviral integration into specific sites is not required.
Abstract: Induced pluripotent stem (iPS) cells have been generated from mouse and human fibroblasts by the retroviral transduction of four transcription factors. However, the cell origins and molecular mechanisms of iPS cell induction remain elusive. This report describes the generation of iPS cells from adult mouse hepatocytes and gastric epithelial cells. These iPS cell clones appear to be equivalent to embryonic stem cells in gene expression and are competent to generate germline chimeras. Genetic lineage tracings show that liver-derived iPS cells are derived from albumin-expressing cells. No common retroviral integration sites are found among multiple clones. These data suggest that iPS cells are generated by direct reprogramming of lineage-committed somatic cells and that retroviral integration into specific sites is not required.

1,154 citations


Authors

Showing all 86225 results

NameH-indexPapersCitations
Kari Alitalo174817114231
Ralph M. Steinman171453121518
Masayuki Yamamoto1711576123028
Karl Deisseroth160556101487
Kenji Kangawa1531117110059
Takashi Taniguchi1522141110658
Ben Zhong Tang1492007116294
Takeo Kanade147799103237
Yuji Matsuzawa143836116711
Tasuku Honjo14171288428
Kenneth M. Yamada13944672136
Y. B. Hsiung138125894278
Shuh Narumiya13759570183
Kevin P. Campbell13752160854
Junji Tojo13587884615
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023234
2022679
20218,533
20208,740
20198,050
20187,932