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Analysis of Claudin 18 deficiency in lung epithelial type 2 cells.

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NIAID Data Ecosystem2026-03-10 收录
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https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE106233
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Constitutive knockdown of Cldn18 in mice showed lung enlargement and increased proliferation of alveolar epithelial type II (AT2) cells. Lung AT2 cells were isolated from wild-type and knockout mice and subjected to microarray analysis. Results provide insight into the role of Cldn18 in controlling organ size and stem progenitor cells. Cldn18-/- mice were obtained by crossing Cldn18 floxed mice with CMV-Cre mice. Deletion of exons 2 and 3 of Cldn18 by Cre/loxP recombination resulted in truncation of both lung- (Cldn18.1) and stomach-specific (Cldn18.2) isoforms in Cldn18-/- mice.
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2018-07-01
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