Evidence map›Paper›PMID 34067858›Full record

ArticleCells2021

Pathological Role of Pin1 in the Development of DSS-Induced Colitis.

Yasuka Matsunaga, Shun Hasei, Takeshi Yamamotoya, Hiroaki Honda, Akifumi Kushiyama, Hideyuki Sakoda, Midori Fujishiro, Hiraku Ono, Hisanaka Ito, Takayoshi Okabe and 2 more

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

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Advances in pharmacological and pharmaceutical sciences · 2024
    Article
  5. Article
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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

12 authors at 7 institutions in 1 country.

Yasuka MatsunagaDepartment of Medical Chemistry, Division of Molecular Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
Shun HaseiDepartment of Medical Chemistry, Division of Molecular Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
Takeshi YamamotoyaDepartment of Medical Chemistry, Division of Molecular Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
Hiroaki HondaDepartment of Disease Model, Research Institute of Radiation Biology and Medicine, Hiroshima University, Hiroshima 734-8553, Japan.
Akifumi KushiyamaDepartment of Pharmacotherapy, Meiji Pharmaceutical University, Kiyose City, Tokyo 204-8588, Japan.ORCID 0000-0003-1385-7487
Hideyuki SakodaDivision of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Miyazaki 889-1692, Japan.
Midori FujishiroDivision of Diabetes and Metabolic Diseases, Department of Internal Medicine, Nihon University School of Medicine, Tokyo 173-8610, Japan.
Hiraku OnoDepartment of Endocrinology, Hematology and Gerontorogy, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Hisanaka ItoSchool of Life Sciences, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.
Takayoshi OkabeDrug Discovery Initiative, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Tomoichiro AsanoDepartment of Medical Chemistry, Division of Molecular Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
Yusuke NakatsuDepartment of Medical Chemistry, Division of Molecular Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan.
Hiroshima University · JPChiba University · JPMeiji Pharmaceutical University · JPNihon University · JPThe University of Tokyo · JPTokyo University of Pharmacy and Life Sciences · JPUniversity of Miyazaki · JP

Funding

Japan Society for the Promotion of Science 16J09463Japan Society for the Promotion of Science 16K15431Uehara Memorial Foundation None
6 · The paper itself

Abstract

Inflammatory bowel diseases (IBDs) are serious disorders of which the etiologies are not, as yet, fully understood. In this study, Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) protein was shown to be dramatically upregulated in the colons of dextran sodium sulfate (DSS)-induced ulcerative colitis model mice. Interestingly,

Indexed as

AnimalsAnti-Inflammatory AgentsColitisColonCytokinesDextran SulfateDisease Models, AnimalEnzyme InhibitorsInflammation MediatorsIntestinal MucosaMacrophagesMiceMice, Inbred C57BLMice, KnockoutNaphthoquinonesNIMA-Interacting Peptidylprolyl IsomeraseAnti-Inflammatory AgentsCytokinesDextran SulfateEnzyme InhibitorsInflammation MediatorsjugloneNaphthoquinonesNIMA-Interacting Peptidylprolyl IsomerasePin1 protein, mousedextran sodium sulfateknockout micePin1Pin1 inhibitorulcerative colitis

Identifiers

PMID34067858
PMCPMC8155908
OpenAlexW3162844834

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.