ArticleGenetics1996
Complementation mapping of skeletal and central nervous system abnormalities in mice of the piebald deletion complex.
Article in Genetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- MicroRNA-124-3p suppresses mouse lip mesenchymal cell proliferation through the regulation of genes associated with cleft lip in the mouse.BMC genomics · 2019Article
- Spry2 regulates signalling dynamics and terminal bud branching behaviour during lung development.Genetics research · 2015Article
- Nemo-like kinase regulates postnatal skeletal homeostasis.Journal of cellular physiology · 2014Article
- Nephroblastoma overexpressed (Nov) inactivation sensitizes osteoblasts to bone morphogenetic protein-2, but nov is dispensable for skeletal homeostasis.Endocrinology · 2010Article
- Shaping skeletal growth by modular regulatory elements in the Bmp5 gene.PLoS genetics · 2008Article
- X-ray-induced deletion complexes in embryonic stem cells on mouse chromosome 15.Mammalian genome : official journal of the International Mammalian Genome Society · 2005Article
- Evidence for a conserved function in synapse formation reveals Phr1 as a candidate gene for respiratory failure in newborn mice.Molecular and cellular biology · 2004Article
- Molecular and functional mapping of the piebald deletion complex on mouse chromosome 14.Genetics · 2001Article
- Expression and functional analysis of Uch-L3 during mouse development.Molecular and cellular biology · 2000Article
- Deletion mapping of the head tilt (het) gene in mice: a vestibular mutation causing specific absence of otoliths.Genetics · 1998Article
- Differential response of mouse male germ-cell stages to radiation-induced specific-locus and dominant mutations.Genetics · 1998Article
- Defects in limb, craniofacial, and thymic development in Jagged2 mutant mice.Genes & development · 1998Article
- Molecular characterization of four induced alleles at the Ednrb locus.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Genetic and physical mapping of the mouse Ulnaless locus.Genetics · 1996Article
- Spontaneous mutations recovered as mosaics in the mouse specific-locus test.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The s15DttMb, s36Pub, s1Acrg and s24Pub piebald deletion alleles belong to a set of overlapping deficiencies on the distal portion of chromosome 14. Molecular analysis was used to define the extent of the deletions. Mice homozygous for the smallest deletion, s15DttMb, die shortly after delivery and display alterations in the central nervous system, including hydrocephalus and a dorsally restricted malformation of the spinal cord. These mice also display homeotic transformations of vertebrae in the midthoracic and lumbar regions. Homozygous s27Pub mice contain a point mutation in the piebald gene, survive to weaning, and display no central nervous system or skeletal defects, arguing that the s15DttMb phenotype results from the loss of genes in addition to piebald. A larger deletion, s36Pub, exhibits additional cartilage malformations and defects in the anterior axial and cranial skeleton. The skeletal defects in both s15DttMb and s36Pub mice resemble transformations associated with the targeted disruption of Hox genes and genes encoding the retinoic acid receptors, which play a role in the specification of segmental identity along the anteroposterior axis. Complementation analysis of the s15DttMb and s36Pub phenotypes, using two additional deletions, localized the gene(s) associated with each phenotype to a defined chromosomal region.
Indexed as
Identifiers
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.