Evidence map›Paper›PMID 30414501›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2019

Atmin modulates Pkhd1 expression and may mediate Autosomal Recessive Polycystic Kidney Disease (ARPKD) through altered non-canonical Wnt/Planar Cell Polarity (PCP) signalling.

Taylor Richards, Kavindiya Modarage, Charlotte Dean, Aidan McCarthy-Boxer, Helen Hilton, Chris Esapa, Jill Norman, Patricia Wilson, Paraskevi Goggolidou

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

Article in Biochimica et biophysica acta. Molecular basis of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Broadening horizons: Pathogenesis and therapeutics of renal ciliopathies.Journal of cell communication and signaling · 2026
    Review
  2. Review
  3. Article
  4. Targeting WNT5A noncanonical signaling attenuates renal fibrosis progression in acute kidney injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. 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

9 authors at 5 institutions in 1 country.

Taylor RichardsSchool of Biomedical Science and Physiology, Faculty of Science and Engineering, University of Wolverhampton, Wulfruna Street, Wolverhampton WV1 1LY, UK.
Kavindiya ModarageSchool of Biomedical Science and Physiology, Faculty of Science and Engineering, University of Wolverhampton, Wulfruna Street, Wolverhampton WV1 1LY, UK.
Charlotte DeanNational Heart and Lung Institute, Imperial College, South Kensington Campus, London SW7 2AZ, UK; MRC Harwell Institute, Mammalian Genetics Unit, Harwell Campus, Oxfordshire OX11 0RD, UK.
Aidan McCarthy-BoxerCentre for Nephrology, UCL Medical School, Royal Free Campus, Rowland Hill, London NW3 2PF, UK.
Helen HiltonMRC Harwell Institute, Mammalian Genetics Unit, Harwell Campus, Oxfordshire OX11 0RD, UK.
Chris EsapaMRC Harwell Institute, Mammalian Genetics Unit, Harwell Campus, Oxfordshire OX11 0RD, UK.
Jill NormanCentre for Nephrology, UCL Medical School, Royal Free Campus, Rowland Hill, London NW3 2PF, UK.
Patricia WilsonCentre for Nephrology, UCL Medical School, Royal Free Campus, Rowland Hill, London NW3 2PF, UK.
Paraskevi GoggolidouSchool of Biomedical Science and Physiology, Faculty of Science and Engineering, University of Wolverhampton, Wulfruna Street, Wolverhampton WV1 1LY, UK; MRC Harwell Institute, Mammalian Genetics Unit, Harwell Campus, Oxfordshire OX11 0RD, UK; Centre for Nephrology, UCL Medical School, Royal Free Campus, Rowland Hill, London NW3 2PF, UK. Electronic address: p.goggolidou@wlv.ac.uk.
Mary Lyon Centre at MRC Harwell · GBUniversity College London · GBUniversity of Wolverhampton · GBImperial College London · GBThe Royal Free Hospital · GB

Funding

Medical Research Council MC_U142684172
6 · The paper itself

Abstract

Autosomal Recessive Polycystic Kidney Disease (ARPKD) is a genetic disorder with an incidence of ~1:20,000 that manifests in a wide range of renal and liver disease severity in human patients and can lead to perinatal mortality. ARPKD is caused by mutations in PKHD1, which encodes the large membrane protein, Fibrocystin, required for normal branching morphogenesis of the ureteric bud during embryonic renal development. The variation in ARPKD phenotype suggests that in addition to PKHD1 mutations, other genes may play a role, acting as modifiers of disease severity. One such pathway involves non-canonical Wnt/Planar Cell Polarity (PCP) signalling that has been associated with other cystic kidney diseases, but has not been investigated in ARPKD. Analysis of the Atmin

Indexed as

Cell PolarityWnt Signaling PathwayAdolescentApoptosisbeta CateninCadherinsCell AdhesionCell LineCell ProliferationChildChild, PreschoolCytoskeletonEmbryo, MammalianHumansInfantInfant, NewbornATMIN protein, humanATMIN protein, mousebeta CateninCadherinsPKHD1 protein, humanPkhd1 protein, mouseReceptors, Cell SurfaceRNA, MessengerTranscription FactorsARPKDATMINPKHD1Wnt signalling

Identifiers

PMID30414501
PMCPMC6335440
OpenAlexW2900041620

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.