Project description:Introduction: HGFL-Ron signaling is augmented in human breast cancer and is associated with poor overall prognosis. Here, we investigate the role of HGFL-Ron signaling in RON-modulated murine macrophages through RNA-sequencing of bone marrow-derived macrophages from FVB WT or FVB RON tyrosine kinase -/- mice. BMDM of each genotype M2-polarized via 72 hour treatment with IL-4 were submitted for transcriptomic characterization on the Illumina HiSeq 2500. High quality reads were aligned to the mm10 genome and quantified to generate RPKM
Project description:Hybridisation of reference strains to the VirEp Staphylococcus aureus microarray, and characterisation of different S. aureus isolates from different locations and associated with different diseases.
Project description:A20 is a negative regulator of NF-κB signaling, crucial to control inflammatory responses and ensure tissue homeostasis. A20 is thought to restrict NF-κB activation both by its ubiquitin-editing activity as by non-enzymatic activities. Besides its role in NF-κB signaling, A20 also acts as a protective factor inhibiting apoptosis and necroptosis. Because of the ability of A20 to both ubiquitinate and deubiquitinate substrates and its involvement in many cellular processes, we hypothesized that deletion of A20 might generally impact on protein levels, thereby disrupting cellular processes. We performed a differential proteomics study of bone marrow derived macrophages (BMDMs) from control and myeloid-specific A20 knockout mice, both in untreated conditions and after LPS and TNF treatment, and demonstrate proteome-wide changes in protein expression upon A20 deletion. Several inflammatory proteins are up-regulated in the absence of A20, even without an inflammatory stimulus. Depending on the treatment and the time, more proteins are regulated. Together these changes may affect multiple signaling pathways disturbing tissue homeostasis and inducing (autoimmune) inflammation, as suggested by genetic studies in patients.