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Digenic inheritance of mutations in EPHA2 and SLC26A4 in Pendred syndrome

MPS-Authors
/persons/resource/persons239438

Li,  Mengnan
Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Riddell,  Meghan
Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons251139

Sapski,  Sabrina
Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons239435

Hikita,  Takao
Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224373

Mizapourshafiyi,  Fatemeh
Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224044

Boettger,  Thomas
Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224068

Krueger,  Marcus
Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224397

Wietelmann,  Astrid
Small Animal Magnetic Resonance Imaging, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Graumann,  Johannes
Biomolecular Mass Spectrometry, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224185

Offermanns,  Stefan
Pharmacology, Max Planck Institute for Heart and Lung Research, Max Planck Society;

/persons/resource/persons224376

Nakayama,  Masanori
Cell Polarity and Organogenesis, Max Planck Institute for Heart and Lung Research, Max Planck Society;

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Citation

Li, M., Nishio, S.-y., Naruse, C., Riddell, M., Sapski, S., Katsuno, T., et al. (2020). Digenic inheritance of mutations in EPHA2 and SLC26A4 in Pendred syndrome. NATURE COMMUNICATIONS, 11(1): 1343. doi:10.1038/s41467-020-15198-9.


Cite as: https://hdl.handle.net/21.11116/0000-0007-1A78-6
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