Erratum p300-mediated acetylation of the Rothmund-Thomson-syndrome gene product RECQL4 regulates its subcellular localization

Introduction Genome instability plays a major role in the development and progression of cancer. All organisms have developed pathways to mitigate DNA damage by employing enzymes that are involved in all DNA metabolic processes, including replication, recombination and repair (Tuteja and Tuteja, 2001). The fundamental importance of these enzymes, such as DNA helicases and acetyltransferases, is highlighted by the variety of genetic instability disorders caused by enzymes defective in these functions (Iyer et al., 2004; Khakhar et al., 2003). One family of proteins required to maintain genome stability is the RecQ helicase family (Hickson, 2003). Humans possess five RecQ homologues: RECQL1, BLM, WRN, RECQL4 and RECQL5. Five autosomal recessive disorders (which have been characterized by genomic instability, cancer progression and developmental abnormalities) have been associated with defects in the gene products BLM (causing Bloom syndrome) (Ellis et al.