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J. Biol. Chem., Vol. 277, Issue 1, 535-543, January 4, 2002
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,
From the Growth Factor Division, National Cancer Center Research
Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
In extraskeletal myxoid chondrosarcoma,
chromosomal translocation creates a gene fusion between EWS
and the orphan nuclear receptor NOR1. The resulting fusion
gene product, EWS/NOR1, has been believed to lead to malignant
transformation by functioning as a transcriptional activator, but an
alternative mechanism may also be involved. Here, using a newly
developed functional complementation screening in yeast, we found that
EWS/NOR1, but not EWS or NOR1, complemented the loss of function of the
small nuclear ribonucleoprotein Snu23p, an essential factor for
pre-mRNA splicing in yeast. To verify the potential function of
EWS/NOR1 in mammalian cells, we next showed that overexpression of
EWS/NOR1 caused increased usage of the distal 5'-splice site of
pre-mRNA splicing and that EWS/NOR1 interacted with the human
splicing protein U1C; neither EWS nor NOR1 had the same activity or
interaction as EWS/NOR1. Altogether, our findings reveal that EWS/NOR1
gains a novel activity affecting pre-mRNA splicing.
To whom correspondence should be addressed. Tel.: 81-3-3542-2511 (ext. 4302); Fax: 81-3-3542-8170; E-mail: nohkura@gan2.ncc.go.jp.
§
Recipient of a research resident fellowship from the Foundation for
Promotion of Cancer Research of Japan.
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