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The FGF4–integrin β1 axis restores directed collective migration to accelerate diabetic wound regeneration [ChIP-Seq].

GSE318682 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 3 samples Submitted 2026/05/01 Platform GPL34284
Summary
This dataset was generated to investigate the mechanism by which Fibroblast Growth Factor 4 (FGF4) regulates the binding of C-FOS to the ITGB1 promoter. ChIP sequencing was performed on high glucose-induced HacaT cells, which were divided into low glucose, high glucose, and high glucose plus FGF4 treatment groups.
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Direct links to NCBI, no account and no request form: the whole study as GSE318682_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 3 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1419768 and SRA study SRP675214. Searching any of these in the dataset finder brings you back here.

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