Evidence map›Paper›PMID 27786288›Full record

ArticleScientific reports2016

An inhibitor of fibroblast growth factor receptor-1 (FGFR1) promotes late-stage terminal differentiation from NGN3+ pancreatic endocrine progenitors.

Yzumi Yamashita-Sugahara, Masahito Matsumoto, Manami Ohtaka, Ken Nishimura, Mahito Nakanishi, Kohnosuke Mitani, Yasushi Okazaki

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Stem Cell-Derived Islets for Type 2 Diabetes.International journal of molecular sciences · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Beta-cell replacement strategies for diabetes.Journal of diabetes investigation · 2017
    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 3 institutions in 1 country.

Yzumi Yamashita-SugaharaDivision of Functional Genomics and Systems Medicine, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.
Masahito MatsumotoDivision of Functional Genomics and Systems Medicine, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.
Manami OhtakaBiotechnology Research Institute for Drug Discovery, National Institute of Advanced Industrial Science and Technology (AIST), Ibaraki, Japan.
Ken NishimuraLaboratory of Gene Regulation, Faculty of Medicine, University of Tsukuba, Ibaraki, Japan.
Mahito NakanishiBiotechnology Research Institute for Drug Discovery, National Institute of Advanced Industrial Science and Technology (AIST), Ibaraki, Japan.
Kohnosuke MitaniDivision of Gene Therapy, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.
Yasushi OkazakiDivision of Functional Genomics and Systems Medicine, Research Center for Genomic Medicine, Saitama Medical University, Saitama, Japan.
Saitama Medical University · JPNational Institute of Advanced Industrial Science and Technology · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human induced pluripotent stem cells (hiPSCs) provide a potential resource for regenerative medicine. To identify the signalling pathway(s) contributing to the development of functional β cells, we established a tracing model consisting of dual knock-in hiPSCs (INS-Venus/NGN3-mCherry) (hIveNry) expressing the fluorescent proteins Venus and mCherry under the control of intrinsic insulin (INS) and neurogenin 3 (NGN3) promoters, respectively. hIveNry iPSCs differentiated into NGN3- and mCherry-positive endocrine progenitors and then into Venus-positive β cells expressing INS, PDX1, NKX6.1, and glucokinase (GCK). Using these cells, we conducted high-throughput screening of chemicals and identified a specific kinase inhibitor of fibroblast growth factor receptor 1 (FGFR1) that acted in a stage-dependent manner to promote the terminal differentiation of pancreatic endocrine cells, including β cells, from the intermediate stage of pancreatic endocrine progenitors while blocking the early development of pancreatic progenitors. This FGFR1 inhibitor augmented the expression of functional β cell markers (SLC30A8 and ABCC8) and improved glucose-stimulated INS secretion. Our findings indicate that the hIveNry model could provide further insights into the mechanisms of hiPS-derived β cell differentiation controlled by FGFR1-mediated regulatory pathways in a temporal-dependent fashion.

Indexed as

Bacterial ProteinsBasic Helix-Loop-Helix ProteinsCell DifferentiationCell LineCell LineageGene Knock-In TechniquesGene TargetingHumansInduced Pluripotent Stem CellsInsulinInsulin SecretionIslets of LangerhansLuminescent ProteinsModels, BiologicalNerve Tissue ProteinsPromoter Regions, GeneticBacterial ProteinsBasic Helix-Loop-Helix ProteinsFGFR1 protein, humanInsulinLuminescent ProteinsNerve Tissue ProteinsNEUROG3 protein, humanReceptor, Fibroblast Growth Factor, Type 1Red Fluorescent Proteinyellow fluorescent protein, Bacteria

Identifiers

PMID27786288
PMCPMC5081516
OpenAlexW2545599580

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.