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RNA-seq for iPSC-derived macrophages with/without Lipopolysaccharide (LPS) stimulation.

GSE237489 Homo sapiens Expression profiling by high throughput sequencing 8 samples Submitted 2026/08/08 Platform GPL24676
Summary
Wiskott-Aldrich syndrome (WAS) is an immunodeficiency disorder caused by the dysfunction of the Wiskott-Aldrich syndrome protein (WASP). Although the effect of WASP on actin -polymerization is well studied, less is known about its role in other intracellular systems. Here we show that WASP interacts with the nucleolus in macrophages. Using induced pluripotent stem cells and the CRISPR-Cas system, we show that knocking out WASP results in reduced nucleolar size, loss of roundness, decreased sub-nucleolar structure percentage, and impaired ribosomal RNA transcription. Furthermore, we identified interactions between WASP and two nucleolar proteins, including nucleophosmin 1 (NPM1) and fibrillarin (FBL). Previous research has demonstrated that a loss of NPM1 results in heightened cytokine expression following lipopolysaccharide (LPS) stimulation. We found that WASP-deficient cells presented less NPM1 and more cytokine expression in response to LPS stimulation, providing new insights on the role of the nucleolus in immune functions. Together, our study provides new information on WASP in nucleolar function and its control of inflammatory cytokine expression in response to inflammatory stimuli.
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Direct links to NCBI, no account and no request form: the whole study as GSE237489_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 8 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA995504 and SRA study SRP449835. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, each sampled once — no replicated groups

Read from 8 sample titles: 8 distinct titles with little repetition. Check it against the sample list below before relying on it.

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