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Record W3133607649 · doi:10.1093/jcag/gwab002.165

A167 UNDERSTANDING THE IMPACT OF DOWNSTREAM OF KINASE 4 (DOK4) DAMAGING GENETIC VARIANTS IN THE PATHOGENESIS OF PEDIATRIC INFLAMMATORY BOWEL DISEASE (IBD).

2021· article· en· W3133607649 on OpenAlexaff
Vritika Batura, Amanda Ricciuto, Neil Warner, Changlong Guo, Daniel Kotlarz, Christoph Klein, A Muise

Bibliographic record

VenueJournal of the Canadian Association of Gastroenterology · 2021
Typearticle
Languageen
FieldMedicine
TopicHelicobacter pylori-related gastroenterology studies
Canadian institutionsHospital for Sick ChildrenUniversity of Toronto
Fundersnot available
KeywordsInflammatory bowel diseasePathogenesisImmune systemImmune dysregulationImmunologyBiologyDiseasePI3K/AKT/mTOR pathwaySignal transductionCancer researchMedicineGeneticsPathology

Abstract

fetched live from OpenAlex

Abstract Background IBD is a chronic inflammatory disorder of the gastrointestinal (GI) tract whose precise pathological mechanisms remain elusive. It is thought that in pediatric IBD, pathogenic exposure does not appear sufficient to cause disease, thus genetic variations are critical to disease pathogenesis. The Muise Lab uses genetic sequencing of patients with IBD from all over the world to identify crucial genetic variations that are critical to IBD development. We report two patients with IBD from unrelated families with mutations in DOK4. Both patients had profound extra-intestinal disease complicating their IBD. Downstream of kinase (DOK) proteins are a family of adaptor molecules that are important in regulating cell signaling, especially in immune cells. They are known to suppress MAPK and PI3K/AKT pathways, whose dysregulation result in cancer. DOK4 has not been extensively studied, but research suggests that this gene produces two isoforms. It is known to have negative regulatory effects on immune cell activation but is also expressed across various other tissues, where its function is yet to be determined. Aims We hypothesize that these variations in DOK4 lead to immune cell dysregulation, which manifests in both gastrointestinal and systemic chronic inflammatory disease. Through this study, we aim to elucidate the mechanism of novel genetic defects in DOK4. Methods It will be critical to understand how variants within both patients are contributing to the onset of IBD through in vitro studies. Therefore, we will characterize and quantify how changes in expression of DOK4 alters essential cell signaling pathways. We have established immortalized cell lines from patients bearing these mutations to specifically characterize potential immune defects. We will also be using knock out cell models to understand the effect of loss of function of DOK4 in different cell types. Results Preliminary data shows variation in expression of the protein within patient peripheral blood mononuclear cells (PBMCs) compared to a healthy donor. Overexpression in HEK293T cells shows changes in MAPK and NFkB signaling. Conclusions With this study, we hope to identify new therapeutic targets for patients with DOK4 mutations. Funding Agencies CIHRThe Leona M. and Harry B. Helmsley Charitable Trust

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)0.001
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: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.001
Threshold uncertainty score0.005

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.001
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0010.000
Science and technology studies0.0000.000
Scholarly communication0.0010.001
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0010.000

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 head0.246
Teacher spread0.231 · 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

Citations0
Published2021
Admission routes1
Has abstractyes

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