ArticleProceedings of the National Academy of Sciences of the United States of America1997
Substantial narrowing of the Niemann-Pick C candidate interval by yeast artificial chromosome complementation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 28 citations in OpenAlex.
- Nystatin Regulates Axonal Extension and Regeneration by Modifying the Levels of Nitric Oxide.Frontiers in molecular neuroscience · 2020Article
- Caveola-dependent endocytic entry of amphotropic murine leukemia virus.Journal of virology · 2005Article
- Amphotropic murine leukaemia virus envelope protein is associated with cholesterol-rich microdomains.Virology journal · 2005Article
- Localization of Niemann-Pick C1 protein in astrocytes: implications for neuronal degeneration in Niemann- Pick type C disease.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Niemann-Pick C1 protein: obligatory roles for N-terminal domains and lysosomal targeting in cholesterol mobilization.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Isolation of human transcripts expressed in hamster cells from YACs by cDNA representational difference analysis.Genome research · 1999Article
- Localization of tumor suppressor activity important in nonsmall cell lung carcinoma on chromosome 11q.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Recent advances in elucidating Niemann-Pick C disease.Brain pathology (Zurich, Switzerland) · 1998Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Niemann-Pick disease type C (NP-C) is an autosomal recessive lipidosis linked to chromosome 18q11-12, characterized by lysosomal accumulation of unesterified cholesterol and delayed induction of cholesterol-mediated homeostatic responses. This cellular phenotype is identifiable cytologically by filipin staining and biochemically by measurement of low-density lipoprotein-derived cholesterol esterification. The mutant Chinese hamster ovary cell line (CT60), which displays the NP-C cellular phenotype, was used as the recipient for a complementation assay after somatic cell fusions with normal and NP-C murine cells suggested that this Chinese hamster ovary cell line carries an alteration(s) in the hamster homolog(s) of NP-C. To narrow rapidly the candidate interval for NP-C, three overlapping yeast artificial chromosomes (YACs) spanning the 1 centimorgan human NP-C interval were introduced stably into CT60 cells and analyzed for correction of the cellular phenotype. Only YAC 911D5 complemented the NP-C phenotype, as evidenced by cytological and biochemical analyses, whereas no complementation was obtained from the other two YACs within the interval or from a YAC derived from chromosome 7. Fluorescent in situ hybridization indicated that YAC 911D5 was integrated at a single site per CT60 genome. These data substantially narrow the NP-C critical interval and should greatly simplify the identification of the gene responsible in mouse and man. This is the first demonstration of YAC complementation as a valuable adjunct strategy for positional cloning of a human gene.
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