Evidence map›Paper›PMID 25355493›Full record

ArticleScientific reports2014

Loss of α-catenin elicits a cholestatic response and impairs liver regeneration.

Keira Joann Herr, Ying-hung Nicole Tsang, Joanne Wei En Ong, Qiushi Li, Lai Lai Yap, Weimiao Yu, Hao Yin, Roman L Bogorad, James E Dahlman, Yee Gek Chan and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026
    Article
  2. Article
  3. A modular analysis of bile canalicular function and its implications for cholestasis.American journal of physiology. Gastrointestinal and liver physiology · 2023
    Review
  4. Article
  5. Hippo signalling in the liver: role in development, regeneration and disease.Nature reviews. Gastroenterology & hepatology · 2022
    Review
  6. Bile Duct-on-a-Chip.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  7. A Bile Duct-on-a-Chip With Organ-Level Functions.Hepatology (Baltimore, Md.) · 2020
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Peribiliary Glands as the Cellular Origin of Biliary Tract Cancer.International journal of molecular sciences · 2018
    Review
  13. Cell Junctions in Hippo Signaling.Cold Spring Harbor perspectives in biology · 2018
    Review
  14. Article
  15. Barcoded nanoparticles for high throughput in vivo discovery of targeted therapeutics.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Review
  17. Article
  18. Yes-associated protein impacts adherens junction assembly through regulating actin cytoskeleton organization.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Article
  19. Article
  20. 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

16 authors at 4 institutions in 2 countries.

Keira Joann HerrInstitute of Molecular and Cell Biology, A*STAR (Agency for Science, Technology and Research), Singapore, Singapore.
Ying-hung Nicole TsangInstitute of Molecular and Cell Biology, A*STAR (Agency for Science, Technology and Research), Singapore, Singapore.
Joanne Wei En OngInstitute of Molecular and Cell Biology, A*STAR (Agency for Science, Technology and Research), Singapore, Singapore.
Qiushi LiMechanobiology Institute, National University of Singapore, Singapore.
Lai Lai YapInstitute of Molecular and Cell Biology, A*STAR (Agency for Science, Technology and Research), Singapore, Singapore.
Weimiao YuInstitute of Molecular and Cell Biology, A*STAR (Agency for Science, Technology and Research), Singapore, Singapore.
Hao YinKoch Institute for Integrative Cancer Research, MIT, Massachusetts, U.S.A.
Roman L BogoradKoch Institute for Integrative Cancer Research, MIT, Massachusetts, U.S.A.
James E Dahlman1] Koch Institute for Integrative Cancer Research, MIT, Massachusetts, U.S.A [2] Department of Biology, MIT, Massachusetts, U.S.A [3] Institute for Medical Engineering and Science, MIT, Massachusetts, U.S.A.
Yee Gek ChanDepartment of Anatomy, National University of Singapore, Singapore.
Boon Huat BayDepartment of Anatomy, National University of Singapore, Singapore.
Roshni SingarajaTranslational Laboratory in Genetic Medicine, A*STAR, Singapore, Singapore.
Daniel G Anderson1] Koch Institute for Integrative Cancer Research, MIT, Massachusetts, U.S.A [2] Institute for Medical Engineering and Science, MIT, Massachusetts, U.S.A [3] Department of Chemical Engineering, MIT, Massachusetts, U.S.A [4] Department of Anaesthesiology, Children's Hospital Boston, Harvard Medical School, Massachusetts, U.S.A.
Victor KotelianskySkolkovo Institute of Science and Technology ul, Skolkovo, Russian Federation.
Virgile ViasnoffMechanobiology Institute, National University of Singapore, Singapore.
Jean Paul Thiery1] Institute of Molecular and Cell Biology, A*STAR (Agency for Science, Technology and Research), Singapore, Singapore [2] Department of Biochemistry School of Medicine National University of Singapore, Singapore [3] Cancer Science Institute National University of Singapore, Singapore.
National University of Singapore · SGAgency for Science, Technology and Research · SGInstitute of Molecular and Cell Biology · SGSkolkovo Institute of Science and Technology · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver is unique in its capacity to regenerate after injury, during which hepatocytes actively divide and establish cell-cell contacts through cell adhesion complexes. Here, we demonstrate that the loss of α-catenin, a well-established adhesion component, dramatically disrupts liver regeneration. Using a partial hepatectomy model, we show that regenerated livers from α-catenin knockdown mice are grossly larger than control regenerated livers, with an increase in cell size and proliferation. This increased proliferation correlated with increased YAP activation, implicating α-catenin in the Hippo/YAP pathway. Additionally, α-catenin knockdown mice exhibited a phenotype reminiscent of clinical cholestasis, with drastically altered bile canaliculi, elevated levels of bile components and signs of jaundice and inflammation. The disrupted regenerative capacity is a result of actin cytoskeletal disorganisation, leading to a loss of apical microvilli, dilated lumens in the bile canaliculi, and leaky tight junctions. This study illuminates a novel, essential role for α-catenin in liver regeneration.

Indexed as

ActinsAdaptor Proteins, Signal Transducingalpha CateninAnimalsBile CanaliculiCell Cycle ProteinsCell ProliferationCholestasisFemaleHepatocytesLiver RegenerationMiceMice, KnockoutMicrovilliModels, AnimalPhosphoproteinsActinsAdaptor Proteins, Signal Transducingalpha CateninCell Cycle ProteinsPhosphoproteinsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID25355493
PMCPMC4213774
OpenAlexW2141926729

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.