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Record W4408989438 · doi:10.1101/2025.03.27.25324722

Clinical Validity of Autosomal Dominant <i>ALPK3</i> Loss-of-function Variants as a Cause of Hypertrophic Cardiomyopathy

2025· preprint· en· W4408989438 on OpenAlexaff
Sophie Hespe, Emma S. Singer, Chloe M. Reuter, Brittney Murray, Elizabeth Jordan, Jessica L. Chowns, Stacey Peters, Megan Mayers, Belinda Gray, Ray E Hershberger, Anjali Owens, Christopher Semsarian, Amber Waddell, Babken Asatryan, Emma Owens, Courtney Thaxton, Mhy-Lanie Adduru, Kailyn Anderson, Emily Brown, Lily Hoffman‐Andrews, Fergus Stafford, Richard D. Bagnall, Lucas Bronicki, Bert Callewaert, C. Anwar A. Chahal, Cynthia A. James, Olga Jarinova, Andrew P. Landstrom, Elizabeth M. McNally, Laura Muiño Mosquera, Victoria N. Parikh, Roddy Walsh, Bess Wayburn, James S. Ware, Benjamin L. Parker, Enzo R. Porrello, David A. Elliott, James W. McNamara, Jodie Ingles

Bibliographic record

VenuemedRxiv · 2025
Typepreprint
Languageen
FieldMedicine
TopicCardiomyopathy and Myosin Studies
Canadian institutionsChildren's Hospital of Eastern OntarioUniversity of Ottawa
FundersBritish Heart FoundationNational Institute for Health and Care ResearchNational Health and Medical Research CouncilAmgenPfizerNSW Ministry of HealthImperial College LondonMyoKardiaMedical Research CouncilCytokineticsBristol-Myers Squibb
KeywordsHypertrophic cardiomyopathyInternal medicineCardiologyFunction (biology)CardiomyopathyLoss functionMedicineGeneticsBiologyHeart failurePhenotypeGene

Abstract

fetched live from OpenAlex

Abstract ALPK3 encodes the protein α-kinase 3, an essential cardiac-enriched atypical a-kinase that inserts in the nuclear envelope and the sarcomere M-band of cardiac myocytes, functioning to aid in myosin-mediated force buffering and sarcomere proteostasis. Previously, bi-allelic loss-of-function ALPK3 variants have been reported causative in a severe paediatric phenotype including hypertrophic (HCM) and dilated cardiomyopathy (DCM). Very few heterozygous carries in these cases express any cardiac phenotype. However, recently studies have reported heterozygous loss-of-function ALPK3 variants causative of HCM. In this research letter we present a patient series of 29 cardiac patients (26 probands) with heterozygous putative loss-of-function ALPK3 variants without another causative variant in other definitive HCM genes. As well as, a ClinGen gene curation assessing the clinical validity of the gene-disease association of ALPK3 for autosomal dominant HCM, which was evaluated to be strong. With reduced penetrance compared to other HCM genes and issues with historic genetic reports using a superseded transcript care needs to be taken when interpreting these variants to account for these nuances.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.002
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Observational · Consensus signal: Observational
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.003
Threshold uncertainty score0.011

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.002
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0010.000
Science and technology studies0.0010.001
Scholarly communication0.0010.000
Open science0.0000.000
Research integrity0.0010.000
Insufficient payload (model declined to judge)0.0030.001

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.059
GPT teacher head0.341
Teacher spread0.282 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designObservational
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations2
Published2025
Admission routes1
Has abstractyes

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