ArticlePLoS genetics2008
Positional cloning of "Lisch-Like", a candidate modifier of susceptibility to type 2 diabetes in mice.
Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 63 citations in OpenAlex.
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- Retinoic acid receptor signaling is required to maintain glucose-stimulated insulin secretion and β-cell mass.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Use of Drosophila as an evaluation method reveals imp as a candidate gene for type 2 diabetes in rat locus Niddm22.Journal of diabetes research · 2015Article
- The genetic basis of obesity-associated type 2 diabetes (diabesity) in polygenic mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Review
- Insights into obesity and diabetes at the intersection of mouse and human genetics.Trends in endocrinology and metabolism: TEM · 2014Review
- Leptin- and leptin receptor-deficient rodent models: relevance for human type 2 diabetes.Current diabetes reviews · 2014Review
- Molecular organization of tricellular tight junctions.Tissue barriers · 2014Review
- Article
- Genetic and epigenetic control of metabolic health.Molecular metabolism · 2013Review
- Molecular basis for the regulation of islet beta cell mass in mice: the role of E-cadherin.Diabetologia · 2013Article
- Genetic control of obesity and gut microbiota composition in response to high-fat, high-sucrose diet in mice.Cell metabolism · 2013Article
- The apoptosis inhibitor ARC alleviates the ER stress response to promote β-cell survival.Diabetes · 2013Article
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
Abstract
In 404 Lep(ob/ob) F2 progeny of a C57BL/6J (B6) x DBA/2J (DBA) intercross, we mapped a DBA-related quantitative trait locus (QTL) to distal Chr1 at 169.6 Mb, centered about D1Mit110, for diabetes-related phenotypes that included blood glucose, HbA1c, and pancreatic islet histology. The interval was refined to 1.8 Mb in a series of B6.DBA congenic/subcongenic lines also segregating for Lep(ob). The phenotypes of B6.DBA congenic mice include reduced beta-cell replication rates accompanied by reduced beta-cell mass, reduced insulin/glucose ratio in blood, reduced glucose tolerance, and persistent mild hypoinsulinemic hyperglycemia. Nucleotide sequence and expression analysis of 14 genes in this interval identified a predicted gene that we have designated "Lisch-like" (Ll) as the most likely candidate. The gene spans 62.7 kb on Chr1qH2.3, encoding a 10-exon, 646-amino acid polypeptide, homologous to Lsr on Chr7qB1 and to Ildr1 on Chr16qB3. The largest isoform of Ll is predicted to be a transmembrane molecule with an immunoglobulin-like extracellular domain and a serine/threonine-rich intracellular domain that contains a 14-3-3 binding domain. Morpholino knockdown of the zebrafish paralog of Ll resulted in a generalized delay in endodermal development in the gut region and dispersion of insulin-positive cells. Mice segregating for an ENU-induced null allele of Ll have phenotypes comparable to the B.D congenic lines. The human ortholog, C1orf32, is in the middle of a 30-Mb region of Chr1q23-25 that has been repeatedly associated with type 2 diabetes.
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