Bottom-up proteomics (mouse)

This project serves as a centralized repository for omics datasets published by research groups within the SyNergy Cluster. It encompasses investigations such as proteomics and transcriptomics, which are further divided into individual studies led by SyNergy members. Each study is linked to relevant publications, assays and data files (with links to external repositories).

To explore investigations and their associated studies in more detail, please visit the 'Related items' tab on the Project ...

Loss-of-function mutations in CLN3 cause juvenile Batten disease, featuring neurodegeneration and early-stage neuroinflammation. How loss of CLN3 function leads to early neuroinflammation is not yet understood. Here, we have comprehensively studied microglia from Cln3∆ex7/8 mice, a genetically accurate disease model. Loss of CLN3 function in microglia leads to lysosomal storage material accumulation and abnormal morphology of subcellular organelles. Moreover, pathological proteomic signatures are ...

The microglial proteome of homozygous Cln3Δex7/8/Δex7/8 was compared with those of littermate control heterozygous (Cln3Δex7/8/+) or wildtype (Cln3+/+) mice at 3 (Cln3Δex7/8/Δex7/8 n=5 vs controls n=7) and 12 months (Cln3Δex7/8/Δex7/8 n=4 vs controls n=5) of age. Microglia were acutely isolated using MACS with CD11b microbeads (Miltenyi Biotec) as previously described in Colombo et al. 36 Sample preparation and mass spectrometric measurements using data independent acquisition were performed as ...