ReviewMolecular and cellular biochemistry1998
Gene disruption in mice: models of development and disease.
Review in Molecular and cellular biochemistry, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 38 citations in OpenAlex.
- Neuronal networks in mental diseases and neuropathic pain: Beyond brain derived neurotrophic factor and collapsin response mediator proteins.World journal of psychiatry · 2016Review
- Comparative genetic analysis: the utility of mouse genetic systems for studying human monogenic disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2007Review
- Male-male competition magnifies inbreeding depression in wild house mice.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Transgenic animals as models for human disease.Transgenic research · 2000Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gene targeting technology in mice by homologous recombination has become an important method to generate loss-of-function of genes in a predetermined locus. Although the inactivation is limited to irreversible alteration of chromosomal DNA and a surprising variety of genes have given unexpected and disappointing results, modification of the basic technology now provides additional choices for a more specific and variety of manipulations of the mouse genome. This includes conditional cell-type specific gene targeting, knockin technique and the induction of the specific balanced chromosomal translocations. In the past decade this technique not only generated a wealth of knowledge concerning the roles of growth factors, oncogenes, hormone receptors and Hox genes but also helped to produce animal models for several human genetic disorders. In the future it may provide more powerful and necessary tools to dissect the psychiatric disorders, understanding the complex central nervous system and to correct the inherited disorders.
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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.