ArticleHuman molecular genetics2011
Modifier genes and non-genetic factors reshape anatomical deficits in Zfp423-deficient mice.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Modelling phenotypes, variants and pathomechanisms of syndromic diseases in different systems.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2024Article
- Strain-Dependent Modifier Genes Determine Survival inG3 (Bethesda, Md.) · 2020Article
- Know Your Model: Why mouse inbred strain contribution matters.Lab animal · 2020Article
- TBR2 antagonizes retinoic acid dependent neuronal differentiation by repressing Zfp423 during corticogenesis.Developmental biology · 2018Article
- ZNF423: A New Player in Estrogen Receptor-Positive Breast Cancer.Frontiers in endocrinology · 2018Review
- ZNF424 Induces Apoptosis and Inhibits Proliferation in Lung Carcinoma Cells.Current molecular medicine · 2018Article
- Article
- Zfp423 Regulates Sonic Hedgehog Signaling via Primary Cilium Function.PLoS genetics · 2016Article
- Nmf9 Encodes a Highly Conserved Protein Important to Neurological Function in Mice and Flies.PLoS genetics · 2015Article
- Zfp423 binds autoregulatory sites in p19 cell culture model.PloS one · 2013Article
- Article
- Strain-specific modifier genes governing craniofacial phenotypes.Birth defects research. Part A, Clinical and molecular teratology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
Development of neural circuitry depends on the integration of signaling pathways to coordinate specification, proliferation and differentiation of cell types in the right number, in the right place, at the right time. Zinc finger protein 423 (Zfp423), a 30-zinc finger transcription factor, forms alternate complexes with components of several developmental signaling pathways, suggesting it as a point of signal integration during brain development. We previously showed that mice lacking Zfp423 have reduced proliferation of cerebellar precursor cells, resulting in complete loss of vermis and variable hypoplasia of cerebellar hemispheres. Here, we show that Zfp423(-/-) hemisphere malformations are shaped by both genetic and non-genetic factors, producing distinct phenotype distributions in different inbred genetic backgrounds. In genetic mapping studies, we identify four additive modifier loci (Amzn1-4) and seven synthetically interacting loci (Smzn1.1-3.1) that together explain approximately one-third of the phenotypic variance. Strain-specific sequence polymorphism and expression data provide a reduced list of functional variant candidate genes at each modifier locus. Environmental covariates add only modest explanatory power, suggesting an additional stochastic component. These results provide a comprehensive analysis of sources of phenotype variation in a model of hindbrain malformation.
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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.