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Notch1 signaling is limited in healthy mature kidneys in vivo
OBJECTIVE: A Delta-Notch signaling component, Notch1, is involved in the normal development and multiple disorders of the kidney. Although the increase in Notch1 signaling is crucial to these pathogeneses, the basal signaling level in ‘healthy’ mature kidneys is still unclear. To address this questi...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10111784/ https://www.ncbi.nlm.nih.gov/pubmed/37069662 http://dx.doi.org/10.1186/s13104-023-06326-x |
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author | Sugiura, Ryosuke Nakayama, Takahiro Nishino, Teppei Sambe, Naoto Radtke, Freddy Yoshihara, Masaharu Takahashi, Satoru |
author_facet | Sugiura, Ryosuke Nakayama, Takahiro Nishino, Teppei Sambe, Naoto Radtke, Freddy Yoshihara, Masaharu Takahashi, Satoru |
author_sort | Sugiura, Ryosuke |
collection | PubMed |
description | OBJECTIVE: A Delta-Notch signaling component, Notch1, is involved in the normal development and multiple disorders of the kidney. Although the increase in Notch1 signaling is crucial to these pathogeneses, the basal signaling level in ‘healthy’ mature kidneys is still unclear. To address this question, we used an artificial Notch1 receptor fused with Gal4/UAS components in addition to the Cre/loxP system and fluorescent proteins in mice. This transgenic reporter mouse system enabled labeling of past and ongoing Notch1 signaling with tdsRed or Cre recombinase, respectively. RESULTS: We confirmed that our transgenic reporter mouse system mimicked the previously reported Notch1 signaling pattern. Using this successful system, we infrequently observed cells with ongoing Notch1 signaling only in Bowman’s capsule and tubules. We consider that Notch1 activation in several lines of disease model mice was pathologically significant itself. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-023-06326-x. |
format | Online Article Text |
id | pubmed-10111784 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-101117842023-04-19 Notch1 signaling is limited in healthy mature kidneys in vivo Sugiura, Ryosuke Nakayama, Takahiro Nishino, Teppei Sambe, Naoto Radtke, Freddy Yoshihara, Masaharu Takahashi, Satoru BMC Res Notes Research Note OBJECTIVE: A Delta-Notch signaling component, Notch1, is involved in the normal development and multiple disorders of the kidney. Although the increase in Notch1 signaling is crucial to these pathogeneses, the basal signaling level in ‘healthy’ mature kidneys is still unclear. To address this question, we used an artificial Notch1 receptor fused with Gal4/UAS components in addition to the Cre/loxP system and fluorescent proteins in mice. This transgenic reporter mouse system enabled labeling of past and ongoing Notch1 signaling with tdsRed or Cre recombinase, respectively. RESULTS: We confirmed that our transgenic reporter mouse system mimicked the previously reported Notch1 signaling pattern. Using this successful system, we infrequently observed cells with ongoing Notch1 signaling only in Bowman’s capsule and tubules. We consider that Notch1 activation in several lines of disease model mice was pathologically significant itself. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13104-023-06326-x. BioMed Central 2023-04-17 /pmc/articles/PMC10111784/ /pubmed/37069662 http://dx.doi.org/10.1186/s13104-023-06326-x Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Note Sugiura, Ryosuke Nakayama, Takahiro Nishino, Teppei Sambe, Naoto Radtke, Freddy Yoshihara, Masaharu Takahashi, Satoru Notch1 signaling is limited in healthy mature kidneys in vivo |
title | Notch1 signaling is limited in healthy mature kidneys in vivo |
title_full | Notch1 signaling is limited in healthy mature kidneys in vivo |
title_fullStr | Notch1 signaling is limited in healthy mature kidneys in vivo |
title_full_unstemmed | Notch1 signaling is limited in healthy mature kidneys in vivo |
title_short | Notch1 signaling is limited in healthy mature kidneys in vivo |
title_sort | notch1 signaling is limited in healthy mature kidneys in vivo |
topic | Research Note |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10111784/ https://www.ncbi.nlm.nih.gov/pubmed/37069662 http://dx.doi.org/10.1186/s13104-023-06326-x |
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