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Eya1-deficient mice lack ears and kidneys and show abnormal apoptosis of organ primordia

Published in: Nature Genetics

Date of publication: September 1, 1999

Language: English

Main subject: apoptotic process, EYA transcriptional coactivator and phosphatase 1

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Cites articles 17

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WT-1 is required for early kidney development
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A human homologue of the Drosophila eyes absent gene underlies branchio-oto-renal (BOR) syndrome and identifies a novel gene family

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Clustering of mutations responsible for branchio-oto-renal (BOR) syndrome in the eyes absent homologous region (eyaHR) of EYA1

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Glial cell line-derived neurotrophic factor-dependent RET activation can be mediated by two different cell-surface accessory proteins

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The eye-specification proteins So and Eya form a complex and regulate multiple steps in Drosophila eye development

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Pax9-deficient mice lack pharyngeal pouch derivatives and teeth and exhibit craniofacial and limb abnormalities
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Inner ear and kidney anomalies caused by IAP insertion in an intron of the Eya1 gene in a mouse model of BOR syndrome

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