Evidence map›Paper›PMID 28931408›Full record

ArticleNeural development2017

Cell type-specific effects of p27

Mariko Ogawa, Fuminori Saitoh, Norihiro Sudou, Fumi Sato, Hiroki Fujieda

Open access · goldAbstract read
In one paragraph

Article in Neural development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. The Hippo pathway and p27Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Review
  4. Mouse Retinal Organoid Growth and Maintenance in Longer-Term Culture.Frontiers in cell and developmental biology · 2021
    Article
  5. Article
  6. Review
  7. Article
  8. Article
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

5 authors at 2 institutions in 1 country.

Mariko OgawaDepartment of Anatomy, School of Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.
Fuminori SaitohDepartment of Anatomy, School of Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.
Norihiro SudouDepartment of Anatomy, School of Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan.
Fumi SatoDepartment of Anatomy, School of Medicine, Toho University, 5-21-16 Omorinishi, Ota-ku, Tokyo, 143-8540, Japan.
Hiroki FujiedaDepartment of Anatomy, School of Medicine, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo, 162-8666, Japan. hfujieda@twmu.ac.jp.ORCID http://orcid.org/0000-0002-4021-8982
Tokyo Women's Medical University · JPToho University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCyclin-dependent kinase (CDK) inhibitors play an important role in regulating cell cycle progression, cell cycle exit and cell differentiation. p27

methodsExpression of p27 in the developing and mature mouse retina was analyzed by immunohistochemistry using antibodies against p27 and cell type-specific markers. Cell proliferation and differentiation were examined in the wild-type and p27-deficient retinas by immunohistochemistry using various cell cycle and differentiation markers.

resultsAll postmitotic retinal cell types expressed p27 in the mouse retinas. p27 loss caused extension of the period of proliferation in the developing retinas. This extra proliferation was mainly due to ectopic cell cycle reentry of differentiating cells including bipolar cells, Müller glial cells and cones, rather than persistent division of progenitors as previously suggested. Aberrant cell cycle activity of cones was followed by cone death resulting in a significant reduction in cone number in the mature p27-deficient retinas.

conclusionsAlthough expressed in all retinal cell types, p27 is required to maintain the quiescence of specific cell types including bipolar cells, Müller glia, and cones while it is dispensable for preventing cell cycle reentry in other cell types.

Indexed as

AnimalsCell DifferentiationCell ProliferationCyclin-Dependent Kinase Inhibitor p27MiceMice, KnockoutNeurogenesisRetinaCdkn1b protein, mouseCyclin-Dependent Kinase Inhibitor p27Cone deathCyclin-dependent kinase inhibitorEctopic cell cycle reentryp27KIP1Retinal development

Identifiers

PMID28931408
PMCPMC5607500
OpenAlexW2755798598

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.