Evidence map›Paper›PMID 40667253›Full record

ArticlebioRxiv : the preprint server for biology2025

Loss of Bbs8 leads to cystic kidney disease in mice with reduced acetylation of ciliary alpha-tubulin through HDAC2.

Emilia Kieckhöfer, Julia Günzler, Peter A Matthiessen, Lena K Ebert, Christina Klausen, Dagmar Wachten, Metin Cetiner, Max C Liebau, Thomas Benzing, Helen May-Simera and 1 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Emilia KieckhöferDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.ORCID 0009-0004-7888-9185
Julia Günzler *Department II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.ORCID 0009-0009-2703-6680
Peter A Matthiessen *Faculty of Biology, Ciliary Cell Biology, Institute of Molecular Physiology, Johannes Gutenberg-University, Mainz, Germany.
Lena K EbertDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.ORCID 0009-0000-6583-3220
Christina KlausenInstitute of Innate Immunity, Biophysical Imaging, Medical Faculty, University of Bonn, Bonn, Germany.
Dagmar WachtenInstitute of Innate Immunity, Biophysical Imaging, Medical Faculty, University of Bonn, Bonn, Germany.ORCID 0000-0003-4800-6332
Metin CetinerDepartment of Pediatric Nephrology, Pediatrics II, University of Duisburg-Essen, Essen, Germany.ORCID 0000-0002-0918-9204
Max C LiebauDepartment of Pediatrics and Center for Molecular Medicine Cologne, University Hospital Cologne and Faculty of Medicine, University of Cologne, Cologne, Germany.ORCID 0000-0003-0494-9080
Thomas BenzingDepartment II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.ORCID 0000-0003-0512-1066
Helen May-Simera *Faculty of Biology, Ciliary Cell Biology, Institute of Molecular Physiology, Johannes Gutenberg-University, Mainz, Germany.ORCID 0000-0002-9477-4036
Bernhard Schermer *Department II of Internal Medicine and Center for Molecular Medicine Cologne, University of Cologne, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.ORCID 0000-0002-5194-9000

Funding

ChimeraX -- Next Generation Visualization and Analysis Software for Multiscale ModelingR01GM129325 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FERRIN, THOMAS E · 2018 to 2025
$5.2M
NIGMS NIH HHS R01 GM129325
6 · The paper itself

Abstract

Primary cilia dysfunction underlies a group of severe disorders known as ciliopathies. These include Bardet-Biedl syndrome (BBS), which is caused by mutations in BBS genes encoding for components of ciliary protein complexes essential for the assembly and maintenance of primary cilia. As in most ciliopathies, a hallmark feature of BBS is the development of cystic kidney disease. However, the molecular mechanisms linking ciliary dysfunction to cystogenesis remain incompletely understood. Here, we show that

Indexed as

BBSciliopathiescystsHDAC2kidneyprimary cilium

Identifiers

PMID40667253
PMCPMC12262213

What OpenQuestion holds

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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.