@article{oai:nagoya.repo.nii.ac.jp:00001376,
 author = {SUN, Xue-Zhi and HARADA, Yoshi-Nobu and GUI, Chun and ZHANG, Rui and TAKAHASHI, Sentaro and Fukui, Yoshihiro and MURATA, Yoshiharu},
 issue = {1/2},
 journal = {Environmental medicine : annual report of the Research Institute of Environmental Medicine, Nagoya University},
 month = {Dec},
 note = {A new mutant mice that carried the nonfunctional xeroderma pigmentosum group G gene (the mouse counterpart of the human XPG gene) alleles have been generated through a gene-targeting and embryonic stem cell technology. The developmental characteristics of the -/- homozygous mice identified by PCR and Northern blotting were studied. Body size of mutants was clearly smaller than normal littermates from the age of 6 days. Such postnatal growth failure became more and more obvious with developmental proceeding. By postnatal day 23, all of the mutants died after showing great weakness and emaciation. These symptoms in the mutants were similar to the clinical phenotypes of Cockayne syndrome. Moreover, some progressive neurological signs also appeared in the homozygous mice around 2 weeks after birth. When compared development of brains at postnatal day 19, both cerebrum and cerebellum of the xpg-mutants were smaller and significant difference from the wild-types. Their weights only accounted for 79.5% and 66.9% of those in the wild-types, respectively. Such microcephaly and progressive neurological signs mimicked the clinical phenotype of the patients with XPG. We believe that the xpg null mice will be an animal model for studying mechanisms concerning the clinic symptoms and Cockayne syndrome in XPG patients., 国立情報学研究所で電子化したコンテンツを使用している。},
 pages = {66--69},
 title = {Developmental Characteristics of Mice Lacking the DNA Excision Repair Gene XPG},
 volume = {46},
 year = {2002}
}