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Relevance
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The TAM−/− mouse model (triple homozygous deletions of the Mer, Axl, and Tyro3 receptor tyrosine kinases) has delayed apoptotic cell clearance which causes the production of autoantibodies and autoimmune disease in these mice. The FUS/TLS monoclonal antibody is produced from a spontaneous splenic B cell hybridoma generated from the TAM−/− mouse. FUS/TLS binds DNA, RNA, and ribonucleoprotein in the nucleus and the cytoplasm of live and apoptotic cells. FUS/TLS is involved gene expression, genomic integrity and mRNA processing including pre-mRNA splicing and the export of mRNA to the cytoplasm. Mutations in this gene results in amyotrophic lateral sclerosis type 6 and liposarcoma.
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