Abstract:
:Acute promyelocytic leukemia (APL) is caused by chromosomal translocations that involve the retinoic acid receptor alpha (RAR) and several other genes to yield X-RAR fusion proteins. Unlike wild-type RARs, which require heterodimerization with the retinoid X receptor (RXR) for their function as DNA-binding transcriptional regulators, X-RAR fusion proteins bind DNA and deregulate transcription as homo-oligomers. In this issue of Cancer Cell, however, Zeisig et al. and Zhu et al. show that RXR recruitment is a critical determinant for the transforming potential of oligomeric X-RAR fusion proteins and explore the possibility for targeted interventions in APL with either RAR or RXR ligands.
journal_name
Cancer Celljournal_title
Cancer cellauthors
Minucci S,Pelicci PGdoi
10.1016/j.ccr.2007.06.012subject
Has Abstractpub_date
2007-07-01 00:00:00pages
1-3issue
1eissn
1535-6108issn
1878-3686pii
S1535-6108(07)00178-Xjournal_volume
12pub_type
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