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The premature ageing syndrome protein, WRN, is a 3′→5′ exonuclease

The premature ageing syndrome protein, WRN, is a 3′→5′ exonuclease © 1998 Nature America Inc. • http://genetics.nature.com correspondence de Lille rue Calmette 59000 Lille, France. 22 kg/m , range 14.8–25) and to test for obesity with a monogenic dominant form Laboratoire de Nutrition et Service de the inheritance of this frameshift mutation of inheritance in humans. Médecine et Nutrition, Hôtel-Dieu place du in the proband’s family (Fig. 2). The muta- Parvis Notre Dame 75004 Paris, France. tion was not found in the control popula- Correspondence should be adressed to K.C. (e- Acknowledgements mail: [email protected]). tion. The mutation co-segregated with the We thank G. Bonhomme, A. Legall and E. Rocca- Serra for technical help and C. Dina for severe obesity phenotype in the proband’s 1. Comuzzie, A.G & Allison, D.B. Science 280, statistical advice. This work was supported by the family over three generations (lod score 1374–1377 (1998). Direction de la Recherche Clinique/Assistance 1.5). All subjects bearing the mutation had 2. Fan, W., Boston, B., Kesterson, V., Hruby, V. & Cone, Publique-Hopitaux de Paris and the Programme R. Nature 385, 165–168 (1997). a Z score at least four standard deviations 3. Huazar, D. et al. Cell 88, 131–141 (1997). Hospitalier de Recherche Clinique (PHRC). We above a normal BMI (ref. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Genetics Springer Journals

The premature ageing syndrome protein, WRN, is a 3′→5′ exonuclease

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References (13)

Publisher
Springer Journals
Copyright
Copyright © 1998 by Nature America Inc.
Subject
Biomedicine; Biomedicine, general; Human Genetics; Cancer Research; Agriculture; Gene Function; Animal Genetics and Genomics
ISSN
1061-4036
eISSN
1546-1718
DOI
10.1038/2410
Publisher site
See Article on Publisher Site

Abstract

© 1998 Nature America Inc. • http://genetics.nature.com correspondence de Lille rue Calmette 59000 Lille, France. 22 kg/m , range 14.8–25) and to test for obesity with a monogenic dominant form Laboratoire de Nutrition et Service de the inheritance of this frameshift mutation of inheritance in humans. Médecine et Nutrition, Hôtel-Dieu place du in the proband’s family (Fig. 2). The muta- Parvis Notre Dame 75004 Paris, France. tion was not found in the control popula- Correspondence should be adressed to K.C. (e- Acknowledgements mail: [email protected]). tion. The mutation co-segregated with the We thank G. Bonhomme, A. Legall and E. Rocca- Serra for technical help and C. Dina for severe obesity phenotype in the proband’s 1. Comuzzie, A.G & Allison, D.B. Science 280, statistical advice. This work was supported by the family over three generations (lod score 1374–1377 (1998). Direction de la Recherche Clinique/Assistance 1.5). All subjects bearing the mutation had 2. Fan, W., Boston, B., Kesterson, V., Hruby, V. & Cone, Publique-Hopitaux de Paris and the Programme R. Nature 385, 165–168 (1997). a Z score at least four standard deviations 3. Huazar, D. et al. Cell 88, 131–141 (1997). Hospitalier de Recherche Clinique (PHRC). We above a normal BMI (ref.

Journal

Nature Genetics – Springer Journals

Published: Oct 1, 1998

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