ArticleJournal of developmental biology2022
The Core Splicing Factors EFTUD2, SNRPB and TXNL4A Are Essential for Neural Crest and Craniofacial Development.
Article in Journal of developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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.
Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Signalling Pathways and Mechanical Forces Interact in Craniofacial Development and Homeostasis.International dental journal · 2026Review
- Article
- Splicing as an integrative layer linking cell cycle regulation, epigenetic dynamics, and environmental responses in plants.Frontiers in plant science · 2026Review
- Human stem cell model of neural crest cell differentiation reveals a requirement of SF3B4 in survival, maintenance, and differentiation.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
- Splicing Defects and Cell Death CauseJournal of dental research · 2025Article
- SNRPB/CCNB1 axis promotes hepatocellular carcinoma progression and cisplatin resistance through enhancing lipid metabolism reprogramming.Journal of experimental & clinical cancer research : CR · 2025Article
- Article
- Tri-snRNP activity modulates tauopathy phenotypes.NAR molecular medicine · 2025Article
- Spliceosome protein EFTUD2: A potential pathogenetic factor in tumorigenesis and some developmental defects (Review).Molecular medicine reports · 2025Review
- Deletion of sf3b4 causes splicing defects and gene dysregulation that disrupt craniofacial development and survival.Disease models & mechanisms · 2025Article
- Addressing the tissue specificity of U5 snRNP spliceosomopathies.Frontiers in cell and developmental biology · 2025Article
- Modeling craniofacial spliceosomopathies: a pathway toward deciphering disease mechanisms.Frontiers in cell and developmental biology · 2025Review
- Human stem cell model of neural crest cell differentiation reveals a requirement of SF3B4 in survival, maintenance, and differentiation.bioRxiv : the preprint server for biology · 2024Article
- Article
- A common cellular response to broad splicing perturbations is characterized by metabolic transcript downregulation driven by the Mdm2-p53 axis.Disease models & mechanisms · 2024Article
- Small molecule-mediated reprogramming of Xenopus blastula stem cells to a neural crest state.Developmental biology · 2024Article
- Clinical report and genetic analysis of a Chinese neonate with craniofacial microsomia caused by a splicing variant of the splicing factor 3b subunit 2 gene.Molecular genetics & genomic medicine · 2023Article
- The emerging significance of splicing in vertebrate development.Development (Cambridge, England) · 2022Review
- Function of chromatin modifier Hmgn1 during neural crest and craniofacial development.Genesis (New York, N.Y. : 2000) · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mandibulofacial dysostosis (MFD) is a human congenital disorder characterized by hypoplastic neural-crest-derived craniofacial bones often associated with outer and middle ear defects. There is growing evidence that mutations in components of the spliceosome are a major cause for MFD. Genetic variants affecting the function of several core splicing factors, namely
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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.