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Record W2012967220 · doi:10.1016/j.ajhg.2013.07.016

Mutations in FBXL4, Encoding a Mitochondrial Protein, Cause Early-Onset Mitochondrial Encephalomyopathy

2013· article· en· W2012967220 on OpenAlex
Xiaowu Gai, Daniele Ghezzi, Mark Johnson, Caroline Biagosch, Hanan E. Shamseldin, Tobias B. Haack, Aurelio Reyes, Mai Tsukikawa, Claire A. Sheldon, Satish Srinivasan, Matteo Gorza, Laura S. Kremer, Thomas Wieland, Tim M. Strom, Erzsébet Polyák, Emily Place, Mark Consugar, Julian Ostrovsky, Sara Vidoni, Alan J. Robinson, Lee-Jun Wong, Neal Sondheimer, Mustafa A. Salih, Emtethal Al-Jishi, Christopher Raab, Charles Bean, Francesca Furlan, Rossella Parini, Costanza Lamperti, Johannes A. Mayr, Vassiliki Konstantopoulou, Martina Huemer, Eric A. Pierce, Thomas Meitinger, Peter Freisinger, Wolfgang Sperl, Holger Prokisch, Fowzan S. Alkuraya, Marni J. Falk, Massimo Zeviani

Why this work is in the frame

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

fundA Canadian funder is recorded on the work.
no affNo Canadian affiliation: this work is invisible to an affiliation-only frame.
No Canadian affiliation. An affiliation-only frame, the usual design, would never have seen this work. It is one of the works that make the case for inverting the frame.

Bibliographic record

VenueThe American Journal of Human Genetics · 2013
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicMitochondrial Function and Pathology
Canadian institutionsnot available
FundersNational Center for Research ResourcesNational Eye InstituteDeanship of Scientific Research, King Saud UniversityMedical Research CouncilCanadian Institutes of Health ResearchMinistero della SaluteNational Institutes of HealthFondazione CariploChildren's Hospital of PhiladelphiaNational Institute of Diabetes and Digestive and Kidney DiseasesAustrian Science FundBundesministerium für Bildung und ForschungFondazione TelethonEuropean Research CouncilLoyola University Chicago Stritch School of MedicineFondazione Pierfranco e Luisa Mariani
KeywordsMitochondrial encephalomyopathyMitochondrial DNAGeneticsBiologyMutationGene

Abstract

fetched live from OpenAlex

Whole-exome sequencing and autozygosity mapping studies, independently performed in subjects with defective combined mitochondrial OXPHOS-enzyme deficiencies, identified a total of nine disease-segregating FBXL4 mutations in seven unrelated mitochondrial disease families, composed of six singletons and three siblings. All subjects manifested early-onset lactic acidemia, hypotonia, and developmental delay caused by severe encephalomyopathy consistently associated with progressive cerebral atrophy and variable involvement of the white matter, deep gray nuclei, and brainstem structures. A wide range of other multisystem features were variably seen, including dysmorphism, skeletal abnormalities, poor growth, gastrointestinal dysmotility, renal tubular acidosis, seizures, and episodic metabolic failure. Mitochondrial respiratory chain deficiency was present in muscle or fibroblasts of all tested individuals, together with markedly reduced oxygen consumption rate and hyperfragmentation of the mitochondrial network in cultured cells. In muscle and fibroblasts from several subjects, substantially decreased mtDNA content was observed. FBXL4 is a member of the F-box family of proteins, some of which are involved in phosphorylation-dependent ubiquitination and/or G protein receptor coupling. We also demonstrate that FBXL4 is targeted to mitochondria and localizes in the intermembrane space, where it participates in an approximately 400 kDa protein complex. These data strongly support a role for FBXL4 in controlling bioenergetic homeostasis and mtDNA maintenance. FBXL4 mutations are a recurrent cause of mitochondrial encephalomyopathy onset in early infancy.

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.

Full frame distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.253
Threshold uncertainty score0.696

Codex and Gemma teacher scores by category

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

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 head0.015
GPT teacher head0.267
Teacher spread0.252 · 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