ReviewCurrent opinion in immunology2012
Creating diseases to understand what prevents them: genetic analysis of inflammation in the gastrointestinal tract.
Review in Current opinion in immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Trans-Golgi protein TVP23B regulates host-microbe interactions via Paneth cell homeostasis and Goblet cell glycosylation.Nature communications · 2023Article
- The class I myosin MYO1D binds to lipid and protects against colitis.Disease models & mechanisms · 2018Article
- Creatine maintains intestinal homeostasis and protects against colitis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- The Collaborative Cross as a resource for modeling human disease: CC011/Unc, a new mouse model for spontaneous colitis.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Article
- R-spondin 2 signalling mediates susceptibility to fatal infectious diarrhoea.Nature communications · 2013Article
- Linking membrane trafficking and intestinal homeostasis.Tissue barriers · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Inflammatory bowel diseases (IBD), including both ulcerative colitis and Crohn's disease, are extremely variable in severity and have strong genetic components. In mice, several mutations are known to favor or inhibit intestinal inflammation. But a comprehensive picture of the pathogenesis of IBD cannot be assembled based on the limited information so far available from mouse genetic analyses, nor can human IBD be stringently ascribed to mutations known to be influential in mice. This review highlights recent progress made using mouse models created through a forward genetic approach towards the understanding of genes that normally prevent intestinal inflammation.
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.