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Prochownik EV 《Cellular and molecular life sciences : CMLS》2005,62(21):2438-2459
The discovery of oncogenes (c-onc’s) and tumor suppressors (TS’s) has led to the concept that cancer arises from defects in
each of these classes of genes or their products. More recently, it has been appreciated that c-onc and TS proteins often
affect one another’s functions. Within this context, I review the two classical TS’s, p53 and the retinoblastoma protein,
and the consequences of their inactivation. The various forms of genomic instability (GI) that underly the high mutation rates
of transformed cells are then discussed. Particular emphasis is placed upon the concept that GI is not only an integral part
of the transformed state but is a prerequisite. Increased oxidative DNA damage, and/or an inabiliy to repair it, can lead
to GI. The review then discusses recent observations showing that loss of the TS protein peroxiredoxin 1 (prdx1) and increased
expression of the c-onc protein c-Myc, each leads to increased oxidative DNA damage. The critical nature of the c-onc-TS interaction
is underscored by that occurring between prdx1 and c-Myc, with the former protein regulating the production of DNA-damaging
reactive oxygen species by the latter. The intimate association between these proteins and others serves as a paradigm for
the exquisite balancing act that c-onc’s and TS’s must maintain in order to properly control normal DNA replication and cellular
proliferation while simultaneously minimizing the acquisition of potentially neoplastic mutations.
Received 10 May 2005; received after revision 3 July 2005; accepted 19 July 2005 相似文献
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