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Oppositely imprinted genes p57(Kip2) and Igf2 interact in a mouse model for Beckwith–Wiedemann syndrome
Beckwith–Wiedemann syndrome (BWS) is a clinically variable disorder characterized by somatic overgrowth, macroglossia, abdominal wall defects, visceromegaly, and an increased susceptibility to childhood tumors. The disease has been linked to a large cluster of imprinted genes at human chromosome 11p...
保存先:
| 出版年: | Genes Dev |
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| 主要な著者: | , , , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
Cold Spring Harbor Laboratory Press
1999
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| 主題: | |
| オンライン･アクセス: | https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC317182/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/10601037/ https://ncbi.nlm.nih.govhttps://doi.org/10.1101/gad.13.23.3115 |
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