||Takuya Takafuji, Kota Kayama, Nozomi Sugimoto, Masatoshi Fujita, GRWD1, a new player among oncogenesis-related ribosomal/nucleolar proteins, Cell Cycle, 10.1080/15384101.2017.1338987, 2017.08, Increasing attention has been paid to certain ribosomal or ribosome biosynthesis-related proteins involved in oncogenesis. Members of one group are classified as “tumor suppressive factors” represented by RPL5 and RPL11; loss of their functions leads to cancer predisposition. RPL5 and RPL11 prevent tumorigenesis by binding to and inhibiting the MDM2 ubiquitin ligase and thereby up-regulating p53. Many other candidate tumor suppressive ribosomal/nucleolar proteins have been suggested. However, it remains to be experimentally clarified whether many of these factors can actually prevent tumorigenesis and if so, how they do so. Conversely, some ribosomal/nucleolar proteins promote tumorigenesis. For example, PICT1 binds to and anchors RPL11 in nucleoli, down-regulating p53 and promoting tumorigenesis. GRWD1 was recently identified as another such factor. When overexpressed, GRWD1 suppresses p53 and transforms normal human cells, probably by binding to RPL11 and sequestrating it from MDM2. However, other pathways may also be involved..
||Mitsunori Higa, Masatoshi Fujita, Kazumasa Yoshida, DNA Replication Origins and Fork Progression at Mammalian Telomeres, Genes (Basel). 2017 Mar 28;8(4). pii: E112. doi: 10.3390/genes8040112., 2017.03.
||Fujita M, Cdt1 revisited: complex and tight regulation during the cell cycle and consequences of deregulation in mammalian cells, Cell Div. 1: 22, 2006.
||Fujita M., DNA Replication Initiation., Encyclopedic Reference of Genomics and Proteomics in Molecular Medicine (edited by Ganten, D. and Ruckpaul, K.). Springer, Berlin Heidelberg & New York, pp446-449, 2006.
||Tsurumi T, Fujita M and Kudoh A., Latent and lytic Epstein-Barr virus replication strategies., Rev. Med. Virol. 15: 3-15, 2005.