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Bulk RNA-seq of alveolar type II epithelial cells from wild-type and Cry1/2 double-knockout mice with or without Nobiletin treatment.

GSE313683 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/07/30 Platform GPL24247
Summary
Chronic obstructive pulmonary disease (COPD) is a progressive inflammatory lung disease characterized by alveolar destruction and impaired tissue repair. While circadian disruption has been linked to COPD pathogenesis, the specific molecular mechanisms remain unclear. Here, we isolated primary alveolar epithelial transcriptional profiles in WT, Cry1/2-deficient epithelial cells, as well as in epithelial cells from Cry1/2-deficient mice fed Nobiletin chow. These studies will help identify key mediators of CRY1/2 as critical circadian regulators that maintain lung structure.
Published in
Cryptochrome Loss Drives COPD-like Lung Pathology through Disrupted Alveolar Epithelial Proliferation and Immune Homeostasis
Mills TW, Han C, Lim JY et al. · bioRxiv : the preprint server for biology 2026 · PMID 42239331 · doi:10.64898/2026.05.19.726266
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Direct links to NCBI, no account and no request form: the whole study as GSE313683_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1381336 and SRA study SRP655133. Searching any of these in the dataset finder brings you back here.

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