ArticleThe Journal of cell biology1996
Human multidrug resistance 3-P-glycoprotein expression in transgenic mice induces lens membrane alterations leading to cataract.
Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 34 citations in OpenAlex.
- Upregulations of Clcn3 and P-Gp Provoked by Lens Osmotic Expansion in Rat Galactosemic Cataract.Journal of diabetes research · 2017Article
- Mitomycin C induces multidrug resistance in glaucoma surgery.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2008Article
- Function and pathophysiological importance of ABCB4 (MDR3 P-glycoprotein).Pflugers Archiv : European journal of physiology · 2007Review
- P-glycoprotein structure and evolutionary homologies.Cytotechnology · 1998Article
- The genetics of cataract: our vision becomes clearer.American journal of human genetics · 1998Article
- Peripheral neuropathy in mice transgenic for a human MDR3 P-glycoprotein mini-gene.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1996Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have generated mice transgenic for a human multidrug resistance (MDR)3 mini-gene driven by a hamster vimentin promoter. The MDR3 gene encodes a P-Glycoprotein that resembles the mouse multidrug resistance 2 P-Glycoprotein shown to be involved in the translocation of the phospholipid phosphatidylcholine through the hepatocyte canalicular membrane (Smit et al., 1993. Cell. 75:451-462). The vimentin promoter drives expression of the MDR3 transgene in mesenchymal tissues and in the eye lens. We show here that the presence of human multidrug resistance 3 P-Glycoprotein in the lens results in a severe lenticular pathology. Lens structural abnormalities initiate at a late embryonic stage and increase during postnatal lens development. Differentiation of the primary fibers is affected, and the terminal differentiation of the lens epithelium into secondary fibers is also perturbed. The ultrastructural alterations, particularly of the lens plasma membranes, resemble those identified in congenital mouse osmotic cataract.
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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.