Evidence map›Paper›PMID 34523780›Full record

ArticleAmerican journal of medical genetics. Part A2022

Genetic and phenotypic heterogeneity in KIAA0753-related ciliopathies.

Katherine A Inskeep, Yuri A Zarate, Danielle Monteil, Jurgen Spranger, Dan Doherty, Rolf W Stottmann, K Nicole Weaver

Open access · greenAbstract readCase Reports
In one paragraph

Article in American journal of medical genetics. Part A, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. UFMylation Modulates OFIP Stability and Centrosomal Localization.Journal of clinical laboratory analysis · 2025
    Article
  2. Article
  3. KIAA0753 enhances osteoblast differentiation suppressed by diabetes.Journal of cellular and molecular medicine · 2024
    Article
  4. Genotype-phenotype correlates in Joubert syndrome: A review.American journal of medical genetics. Part C, Seminars in medical genetics · 2022
    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

7 authors at 5 institutions in 2 countries.

Katherine A InskeepDivision of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
Yuri A ZarateSection of Genetics and Metabolism, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.ORCID 0000-0001-8235-6200
Danielle MonteilDepartment of Pediatrics, Naval Medical Center Portsmouth, Portsmouth, Virginia, USA.
Jurgen SprangerChildren's Hospital, University of Mainz, Mainz, Germany.
Dan DohertyDepartment of Pediatrics, Center on Human Development and Disability, University of Washington, Seattle, Washington, USA.ORCID 0000-0001-9377-028X
Rolf W StottmannDivision of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.
K Nicole WeaverDivision of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA.ORCID 0000-0002-3991-135X
Cincinnati Children's Hospital Medical Center · USNaval Medical Center Portsmouth · USUniversity of Applied Sciences Mainz · DEUniversity of Arkansas for Medical Sciences · USUniversity of Washington · US

Funding

Identifying the missing heritability in recessive disorders using Joubert syndrome as a modelR01HD100730 · NICHD · UNIVERSITY OF WASHINGTON · PI DOHERTY, DANIEL · 2020 to 2023
$2.0M
Molecular Analysis of primary cilia proteins in human development and diseaseR35GM131875 · NIGMS · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI STOTTMANN, ROLF W · 2019 to 2023
$2.0M
NICHD NIH HHS R01 HD100730NIGMS NIH HHS R35GM121875NIGMS NIH HHS R35 GM131875
6 · The paper itself

Abstract

Primary ciliopathies are heterogenous disorders resulting from perturbations in primary cilia form and/or function. Primary cilia are cellular organelles which mediate key signaling pathways during development, such as the sonic hedgehog (SHH) pathway which is required for neuroepithelium and central nervous system development. Joubert syndrome is a primary ciliopathy characterized by cerebellar/brain stem malformation, hypotonia, and developmental delays. At least 35 genes are associated with Joubert syndrome, including the gene KIAA0753, which is part of a complex required for primary ciliogenesis. The phenotypic spectrum associated with biallelic pathogenic variants in KIAA0753 is broad and not well-characterized. We describe four individuals with biallelic pathogenic KIAA0753 variants, including five novel variants. We report in vitro results assessing the function of each variant indicating that mutant proteins are not fully competent to promote primary ciliogenesis. Ablation of KIAA0753 in vitro blocks primary ciliogenesis and SHH pathway activity. Correspondingly, KIAA0753 patient fibroblasts have a deficit in primary ciliation and improper SHH and WNT signaling, with a particularly blunted response to SHH pathway stimulation. Our work expands the phenotypic spectrum of KIAA0753 ciliopathies and demonstrates the utility of patient-focused functional assays for proving causality of genetic variants.

Indexed as

Abnormalities, MultipleCiliopathiesEye AbnormalitiesKidney Diseases, CysticCerebellumCiliaHedgehog ProteinsHumansMicrotubule-Associated ProteinsRetinaHedgehog ProteinsKIAA0753 protein, humanMicrotubule-Associated ProteinsciliopathiesJoubert syndromeKIAA0753

Identifiers

PMID34523780
PMCPMC9274454
OpenAlexW3200061393

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.