The Ter mutation in the dead end gene causes germ cell loss and testicular germ cell tumours

Kirsten K. Youngren, Douglas Coveney, Xiaoning Peng, Chitralekha Bhattacharya, Laura S. Schmidt, Michael L. Nickerson, Bruce T. Lamb, Jian Min Deng, Richard R. Behringer, Blanche Capel, Edward M. Rubin, Joseph H. Nadeau () and Angabin Matin ()
Additional contact information
Kirsten K. Youngren: Case Western Reserve University
Douglas Coveney: Duke University
Xiaoning Peng: University of Texas, MD Anderson Cancer Center
Chitralekha Bhattacharya: University of Texas, MD Anderson Cancer Center
Laura S. Schmidt: SAIC-Frederick, Inc.
Michael L. Nickerson: NCI Frederick
Bruce T. Lamb: Case Western Reserve University
Jian Min Deng: University of Texas, MD Anderson Cancer Center
Richard R. Behringer: University of Texas, MD Anderson Cancer Center
Blanche Capel: Duke University
Edward M. Rubin: Lawrence Berkeley National Laboratory
Joseph H. Nadeau: Case Western Reserve University
Angabin Matin: University of Texas, MD Anderson Cancer Center

Nature, 2005, vol. 435, issue 7040, 360-364

Abstract: Testicular cancer The phenotype of Ter testicular germ cell tumour susceptibility gene was first described more than 30 years ago, but it has taken until now for the identity of the gene to be discovered. Ter is a mutation inducing a termination codon on the mouse version of the dead end gene, known from zebrafish embryos. It encodes a protein with an RNA recognition motif, thus implicating RNA biology in testicular tumour development.

Date: 2005
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DOI: 10.1038/nature03595

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