ArticleGenetics2007
A genetic screen for modifiers of the delta1-dependent notch signaling function in the mouse.
Article in Genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 23 citations in OpenAlex.
- Current strategies for mutation detection in phenotype-driven screens utilising next generation sequencing.Mammalian genome : official journal of the International Mammalian Genome Society · 2015Review
- The intracellular domains of Notch1 and Notch2 are functionally equivalent during development and carcinogenesis.Development (Cambridge, England) · 2015Article
- New insights into behaviour using mouse ENU mutagenesis.Human molecular genetics · 2012Review
- New mouse models for metabolic bone diseases generated by genome-wide ENU mutagenesis.Mammalian genome : official journal of the International Mammalian Genome Society · 2012Article
- Sensitized phenotypic screening identifies gene dosage sensitive region on chromosome 11 that predisposes to disease in mice.EMBO molecular medicine · 2011Article
- Loss of Par-1a/MARK3/C-TAK1 kinase leads to reduced adiposity, resistance to hepatic steatosis, and defective gluconeogenesis.Molecular and cellular biology · 2010Article
- Mouse mutagenesis with the chemical supermutagen ENU.Methods in enzymology · 2010Article
- Dll1 haploinsufficiency in adult mice leads to a complex phenotype affecting metabolic and immunological processes.PloS one · 2009Article
- Towards better mouse models: enhanced genotypes, systemic phenotyping and envirotype modelling.Nature reviews. Genetics · 2009Review
- Genome-wide search for genes that modulate inflammatory arthritis caused by Ali18 mutation in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2009Article
- Animal models of exfoliation syndrome, now and future.Journal of glaucomaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Notch signaling pathway is an evolutionarily conserved transduction pathway involved in embryonic patterning and regulation of cell fates during development. Recent studies have demonstrated that this pathway is integral to a complex system of interactions, which are also involved in distinct human diseases. Delta1 is one of the known ligands of the Notch receptors. Mice homozygous for a loss-of-function allele of the Delta1 gene Dll1(lacZ/lacZ) die during embryonic development. Here, we present the results of two phenotype-driven modifier screens. Heterozygous Dll1(lacZ) knockout animals were crossed with ENU-mutagenized mice and screened for dysmorphological, clinical chemical, and immunological variants that are dependent on the Delta1 loss-of-function allele. First, we show that mutagenized heterozygous Dll1(lacZ) offspring have reduced body weight and altered specific clinical chemical parameters, including changes in metabolites and electrolytes relevant for kidney function. In our mutagenesis screen we have successfully generated 35 new mutant lines. Of major interest are 7 mutant lines that exhibit a Dll1(lacZ/+)-dependent phenotype. These mutant mouse lines provide excellent in vivo tools for studying the role of Notch signaling in kidney and liver function, cholesterol and iron metabolism, cell-fate decisions, and during maturation of T cells in the immune system.
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.