c-Fos is a member of the AP-1 transcription factor family under the Fos protein family umbrella, alongside Fra-1, Fra-2 and Fos-B. Also in the AP-1 transcription family are the Jun proteins, c-Jun, Jun-B and Jun-D. Each member of the AP-1 transcription family is a phosphonuclear protein composed of a carboxy-terminal leucine zipper domain, a basic domain and an amino terminal transactivation domain. Together the Fos and Jun families compose a dimeric complex that binds to response elements on DNA in order to regulate gene expression, cell proliferation, cell differentiation, tumorigenesis and more. Their induction can be catalyzed by a number of signals, including cytokines and growth factors, stress and viral infection. Interestingly, c-Fos was first characterized as part of a DNA binding protein complex in the simian virus gene (SV40). The JC virus (JCV) is a human polyomavirus that is a pre-cursor for the demyelinating disease progressive multifocal leukoencephalopathy (PML). Using a c-Fos antibody in PML and JCV research helps researchers to better understand the role of AP-1 transcription factors in their pathogenesis.
c-Fos Antibody [NBP1-89065] - Staining of human adrenal gland shows strong nuclear and cytoplasmic positivity in cortical cells.
First, Kim et al used a c-Fos antibody to show that c-Jun and c-Fos functionally interact with the JC Virus early regulatory protein Large T Antigen. To begin, Kim et al established that c-Jun and c-Fos suppressed T-Ag-mediated viral DNA replication using a reported plasmid containing the JCV gene transfected into U-87MG cells containing c-Fos or c-Jun expression plasmids. Next, a c-Fos antibody was used to show that c-Jun and c-Fos physically interact with T-Ag in a GST pull-down assay using nuclear extracts from U-87MG cells. Further research is required in order to better understand whether c-Fos and c-Jun act together or independently of one another to regulate this antigen.
Another use of the c-Fos antibody in JCV research comes from Sadowska et al in their research of the regulation of JCV gene transcription by the AP-1 complex in glial cells. Similar to Kim et al, Sadowska first established an interaction between AP-1 proteins and the JCV promoter using DNA band shift assays. A co-transfection experiment on c-Jun and c-Fos further confirmed that these proteins do activate transcription of the JCV promoter as well. While Sadowska did find that the binding site between JCV and AP-1 responds to activation by either c-Jun or c-Fos, western blot analysis using a c-Jun antibody was used to confirm that c-Jun levels are modulated during the viral infection cycle.
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