Inappropriate p53 activation during development induces features of CHARGE syndrome

Jeanine L. Van Nostrand, Colleen A. Brady, Heiyoun Jung, Daniel R. Fuentes, Margaret M. Kozak, Thomas M. Johnson, Chieh-Yu Lin, Chien-Jung Lin, Donald L. Swiderski, Hannes Vogel, Jonathan A. Bernstein, Tania Attié-Bitach, Ching-Pin Chang, Joanna Wysocka, Donna M. Martin and Laura D. Attardi ()
Additional contact information
Jeanine L. Van Nostrand: Stanford University School of Medicine
Colleen A. Brady: Stanford University School of Medicine
Heiyoun Jung: Stanford University School of Medicine
Daniel R. Fuentes: Stanford University School of Medicine
Margaret M. Kozak: Stanford University School of Medicine
Thomas M. Johnson: Stanford University School of Medicine
Chieh-Yu Lin: Stanford University School of Medicine
Chien-Jung Lin: Stanford University School of Medicine
Donald L. Swiderski: The University of Michigan Medical School
Hannes Vogel: Stanford University School of Medicine
Jonathan A. Bernstein: Stanford University School of Medicine
Tania Attié-Bitach: Hôpital Necker-Enfants Malades, APHP
Ching-Pin Chang: Krannert Institute of Cardiology, Indiana University School of Medicine
Joanna Wysocka: Stanford University School of Medicine
Donna M. Martin: The University of Michigan Medical School
Laura D. Attardi: Stanford University School of Medicine

Nature, 2014, vol. 514, issue 7521, 228-232

Abstract: Inappropriate activation of the tumour-suppressor protein p53 during development can promote phenotypes similar to those of CHARGE syndrome, suggesting that p53 activation not only has a beneficial function in suppressing cancer but also a deleterious function in promoting developmental syndromes.

Date: 2014
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DOI: 10.1038/nature13585

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