ArticleThe Journal of biological chemistry2017
Ankyrin repeat and zinc-finger domain-containing 1 mutations are associated with infantile-onset inflammatory bowel disease.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Role of Mitochondria in Inflammatory Bowel Diseases: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- ANKZF1 helps to eliminate stress-damaged mitochondria by LC3-mediated mitophagy.Cell death discovery · 2025Article
- Overexpression of ZNF169 promotes the growth and proliferation of colorectal cancer cells via the upregulation of ANKZF1.Oncology reports · 2024Article
- Human ESC-derived vascular cells promote vascular regeneration in a HIF-1α dependent manner.Protein & cell · 2024Article
- Transglutaminases are oncogenic biomarkers in human cancers and therapeutic targeting of TGM2 blocks chemoresistance and macrophage infiltration in pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- The regulatory role of alternative splicing in inflammatory bowel disease.Frontiers in immunology · 2023Review
- EVC-EVC2 complex stability and ciliary targeting are regulated by modification with ubiquitin and SUMO.Frontiers in cell and developmental biology · 2023Article
- Inverse and Concordant Mucosal Pathway Gene Expressions in Inflamed and Non-Inflamed Ulcerative Colitis Patients: Potential Relevance to Aetiology and Pathogenesis.International journal of molecular sciences · 2022Article
- Aplysia Neurons as a Model of Alzheimer's Disease: Shared Genes and Differential Expression.Journal of molecular neuroscience : MN · 2022Article
- Cytosolic Quality Control of Mitochondrial Protein Precursors-The Early Stages of the Organelle Biogenesis.International journal of molecular sciences · 2021Review
- Identification of a Hypoxia-Related Gene Model for Predicting the Prognosis and Formulating the Treatment Strategies in Kidney Renal Clear Cell Carcinoma.Frontiers in oncology · 2021Article
- The E3 ubiquitin ligase UBR5 interacts with TTC7A and may be associated with very early onset inflammatory bowel disease.Scientific reports · 2020Article
- Mechanisms Linking Mitochondrial Dysfunction and Proteostasis Failure.Trends in cell biology · 2020Review
- T-cell mitochondrial dysfunction and lymphopenia in DOCK2-deficient patients.The Journal of allergy and clinical immunology · 2019Article
- Early-onset inflammatory bowel disease as a model disease to identify key regulators of immune homeostasis mechanisms.Immunological reviews · 2019Review
- Very early-onset inflammatory bowel disease: an integrated approach.Current opinion in allergy and clinical immunology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infantile-onset inflammatory bowel disease (IO IBD) is an invalidating illness with an onset before 2 years of age and has a complex pathophysiology in which genetic factors are important. Homozygosity mapping and whole-exome sequencing in an IO IBD patient and subsequent sequencing of the candidate gene in 12 additional IO IBD patients revealed two patients with two mutated ankyrin repeat and zinc-finger domain-containing 1 (
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What OpenQuestion holds
Registered trials
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.