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Menin orchestrates macrophage reprogramming to maintain the pulmonary immune homeostasis [RNA-seq]

GSE265805 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2024/08/31 Platform GPL23479
Summary
Menin is a scaffold protein encoded by the Men1 gene, and it interacts with a variety of chromatin regulators to activate or repress cellular processes. The potential importance of menin in immune regulation remains unclear. Here, we report that myeloid deletion of Men1 results in the development of spontaneous pulmonary alveolar proteinosis (PAP). This is strongly correlated with impaired development of alveolar macrophages (AM) and epigenetic inactivation of the GM-CSF pathway caused by Men1 deficiency. Mechanistically, menin directly interacts with SETD2 through the NTD and Palm domains to maintain protein stability and chromatin recruitment. SETD2 and menin collectively maintain GM-CSF expression through H3K36me3, which orchestrates AM reprogramming and pulmonary immune homeostasis.
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Also filed as BioProject PRJNA1104231 and SRA study SRP503845. Searching any of these in the dataset finder brings you back here.

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