Evidence map›Paper›PMID 37069662›Full record

ArticleBMC research notes2023

Notch1 signaling is limited in healthy mature kidneys in vivo.

Ryosuke Sugiura, Takahiro Nakayama, Teppei Nishino, Naoto Sambe, Freddy Radtke, Masaharu Yoshihara, Satoru Takahashi

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC research notes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 43% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Recent advances inFrontiers in cell and developmental biology · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

Ryosuke Sugiura *College of Medicine, School of Medicine and Health Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.ORCID http://orcid.org/0000-0003-4175-4987
Takahiro Nakayama *College of Medicine, School of Medicine and Health Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.ORCID http://orcid.org/0000-0002-4023-4560
Teppei NishinoDepartment of Anatomy and Embryology, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.ORCID http://orcid.org/0000-0003-2544-4639
Naoto SambeCollege of Medicine, School of Medicine and Health Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.ORCID http://orcid.org/0000-0002-8319-8301
Freddy RadtkeSchool of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), Swiss Institute for Experimental Cancer Research (ISREC), SV 2534 (Bâtiment SV) Station 19, Lausanne, CH-1015, Switzerland.ORCID http://orcid.org/0000-0003-4315-4045
Masaharu YoshiharaPhD Program in Humanics, School of Integrative and Global Majors, University of Tsukuba, 1- 1-1 Tennodai, Tsukuba, Ibaraki, 305-8577, Japan. yoshihara.masahar.ly@alumni.tsukuba.ac.jp.ORCID http://orcid.org/0000-0002-0212-0909
Satoru TakahashiDepartment of Anatomy and Embryology, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki, 305-8575, Japan.ORCID http://orcid.org/0000-0002-8540-7760
University of Tsukuba · JPÉcole Polytechnique Fédérale de Lausanne · CH

Funding

Japan Society for the Promotion of Science 22K20734YOKOYAMA Foundation for Clinical Pharmacology YRY-2207
6 · The paper itself

Abstract

objectiveA 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.

resultsWe 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.

Indexed as

HealthKidneyReceptor, Notch1Signal TransductionAnimalsAttachment Sites, MicrobiologicalBowman CapsuleEpithelial CellsGenes, ReporterIntegrasesKidney Tubules, ProximalLigandsMiceCre recombinaseIntegrasesLigandsNotch1 protein, mouseReceptor, Notch1Cre/loxP systemDelta-Notch signaling pathwayDisease modelGal4/UAS systemTransgenic mouse

Identifiers

PMID37069662
PMCPMC10111784
OpenAlexW4366170920

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.