Abstract:
:Rheumatoid arthritis (RA) is a destructive polyarthritis in which synovial-like fibroblasts (SFs) invade and erode cartilage by expressing membrane-anchored type 1 matrix metalloproteinase (MT1-MMP). The mitogen activated protein kinase (MAPK) pathway is activated in RA SFs, but the mechanism of activation is unknown. Here we identify aberrant BRAF splice variants with deletions in both the kinase domain and RAS-binding domain (RBD) in SFs from the majority of RA patients and show that these BRAF splice variants constitutively activate MAPK through CRAF, increase expression of MT1-MMP, and enhance fibroblast invasion of collagen.
journal_name
Mol Immunoljournal_title
Molecular immunologyauthors
Weisbart RH,Chan G,Li E,Farmani N,Heinze E,Rubell A,Nishimura RN,Colburn Kdoi
10.1016/j.molimm.2013.02.001subject
Has Abstractpub_date
2013-10-01 00:00:00pages
247-52issue
3-4eissn
0161-5890issn
1872-9142pii
S0161-5890(13)00039-4journal_volume
55pub_type
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