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Cited by 143

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Inappropriate p53 activation during development induces features of CHARGE syndrome

Van Nostrand, Jeanine L., Brady, Colleen A., Jung, Heiyoun, Fuentes, Daniel R., Kozak, Margaret M., Johnson, Thomas M., Lin, Chieh-Yu, Lin, Chien-Jung, Swiderski, Donald L., Vogel, Hannes, Bernstein, Jonathan A., Attié-Bitach, Tania, Chang, Ching-Pin, Wysocka, Joanna, Martin, Donna M., Attardi, Laura D.·2014·Nature
DOI 10.1038/nature13585
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Show all 6 references

Research works printed but not linked: 31

  1. Davenport, S. L. H., Hefner, M. A. & Mitchell, J. A. The spectrum of clinical features in CHARGE syndrome. Clin. Genet. 29, 298–310 (1986) · DOI
  2. Jongmans, M. C. J. et al. CHARGE syndrome: the phenotypic spectrum of mutations in the CHD7 gene. J. Med. Genet. 43, 306–314 (2006) · DOI · Paper page
  3. Brady, C. A. et al. Distinct p53 transcriptional programs dictate acute DNA-damage responses and tumor suppression. Cell 145, 571–583 (2011) · DOI · Paper page
  4. Johnson, T. M., Hammond, E. M., Giaccia, A. & Attardi, L. D. The p53QS transactivation-deficient mutant shows stress-specific apoptotic activity and induces embryonic lethality. Nature Genet. 37, 145–152 (2005) · DOI
  5. Brock, K. E., Mathiason, M. A., Rooney, B. L. & Williams, M. S. Quantitative analysis of limb anomalies in CHARGE syndrome: correlation with diagnosis and characteristic CHARGE anomalies. Am. J. Med. Genet. A. 123A, 111–121 (2003) · DOI
  6. Zentner, G. E., Layman, W. S., Martin, D. M. & Scacheri, P. C. Molecular and phenotypic aspects of CHD7 mutation in CHARGE syndrome. Am. J. Med. Genet. A. 152A, 674–686 (2010) · DOI · Paper page
  7. Lalani, S. R. et al. Spectrum of CHD7 mutations in 110 individuals with CHARGE syndrome and genotype–phenotype correlation. Am. J. Hum. Genet. 78, 303–314 (2006) · DOI · Paper page
  8. Ragan, D. C., Casale, A. J., Rink, R. C., Cain, M. P. & Weaver, D. D. Genitourinary anomalies in the CHARGE association. J. Urol. 161, 622–625 (1999) · DOI
  9. Inoue, H. et al. Successful cord blood transplantation for a CHARGE syndrome with CHD7 mutation showing DiGeorge sequence including hypoparathyroidism. Eur. J. Pediatr. 169, 839–844 (2010) · DOI
  10. Corsten-Janssen, N. et al. The cardiac phenotype in patients with a CHD7 mutation. Circ. Cardiovasc. Genet. 6, 248–254 (2013) · DOI
  11. Rinon, A. et al. p53 coordinates cranial neural crest cell growth and epithelial–mesenchymal transition/delamination processes. Development 138, 1827–1838 (2011) · DOI
  12. Armstrong, J. F., Kaufman, M. H., Harrison, D. J. & Clarke, A. R. High-frequency developmental abnormalities in p53-deficient mice. Curr. Biol. 5, 931–936 (1995) · DOI · Paper page
  13. Lengner, C. J. et al. Osteoblast differentiation and skeletal development are regulated by Mdm2–p53 signaling. J. Cell Biol. 172, 909–921 (2006) · DOI · Paper page
  14. Sanlaville, D. et al. Phenotypic spectrum of CHARGE syndrome in fetuses with CHD7 truncating mutations correlates with expression during human development. J. Med. Genet. 43, 211–217 (2006) · DOI · Paper page
  15. Legendre, M. et al. Antenatal spectrum of CHARGE syndrome in 40 fetuses with CHD7 mutations. J. Med. Genet. 49, 698–707 (2012) · DOI
  16. Veprintsev, D. B. & Fersht, A. R. Algorithm for prediction of tumour suppressor p53 affinity for binding sites in DNA. Nucleic Acids Res. 36, 1589–1598 (2008) · DOI
  17. Bajpai, R. et al. CHD7 cooperates with PBAF to control multipotent neural crest formation. Nature 463, 958–962 (2010) · DOI · Paper page
  18. Schnetz, M. P. et al. CHD7 targets active gene enhancer elements to modulate ES cell-specific gene expression. PLoS Genet. 6, e1001023 (2010) · DOI · Paper page
  19. Bosman, E. A. et al. Multiple mutations in mouse Chd7 provide models for CHARGE syndrome. Hum. Mol. Genet. 14, 3463–3476 (2005) · DOI · Paper page
  20. Hurd, E. et al. Loss of Chd7 function in gene-trapped reporter mice is embryonic lethal and associated with severe defects in multiple developing tissues. Mamm. Genome 18, 94–104 (2007) · DOI · Paper page
  21. Adams, M. E. et al. Defects in vestibular sensory epithelia and innervation in mice with loss of Chd7 function: implications for human CHARGE syndrome. J. Comp. Neurol. 504, 519–532 (2007) · doi:10.1002/cne.21460
  22. Morimoto, A. K. et al. Absent semicircular canals in CHARGE syndrome: radiologic spectrum of findings. AJNR Am. J. Neuroradiol. 27, 1663–1671 (2006)
  23. Mendrysa, S. M. et al. mdm2 is critical for inhibition of p53 during lymphopoiesis and the response to ionizing irradiation. Mol. Cell. Biol. 23, 462–472 (2003) · DOI · Paper page
  24. Balow, S. A. et al. Knockdown of fbxl10/kdm2bb rescues chd7 morphant phenotype in a zebrafish model of CHARGE syndrome. Dev. Biol. 382, 57–69 (2013) · DOI
  25. Corsten-Janssen, N. et al. More clinical overlap between 22q11.2 deletion syndrome and CHARGE syndrome than often anticipated. Mol. Syndromol. 4, 235–245 (2013) · doi:10.1159/000351127
  26. Jones, N. C. et al. Prevention of the neurocristopathy Treacher Collins syndrome through inhibition of p53 function. Nature Med.14. 125–133 (2008) · DOI · Paper page
  27. Sato, T. & Bartunkova, S. Analysis of embryonic vascular morphogenesis. Methods Mol. Biol. 137, 223–233 (2000)
  28. Ovchinnikov, D. Alcian blue/alizarin red staining of cartilage and bone in mouse. Cold Spring Harb. Protoc. http://dx.doi.org/10.1101/pdb.prot5170 (March 2009) · DOI
  29. Hurd, E. A., Poucher, H. K., Cheng, K., Raphael, Y. & Martin, D. M. The ATP-dependent chromatin remodeling enzyme CHD7 regulates pro-neural gene expression and neurogenesis in the inner ear. Development 137, 3139–3150 (2010) · DOI
  30. Lane, D. et al. Epitope analysis of the murine p53 tumour suppressor protein. Oncogene 12, 2461–2466 (1996)
  31. Kenzelmann Broz, D. et al. Global genomic profiling reveals an extensive p53-regulated autophagy program contributing to key p53 responses. Genes Dev. 27, 1016–1031 (2013) · DOI · Paper page

Cited by

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Metadata

Authors
Van Nostrand, J. L., Brady, C. A., Jung, H., Fuentes, D. R., Kozak, M. M., Johnson, T. M., Lin, C.-Y., Lin, C.-J., Swiderski, D. L., Vogel, H., Bernstein, J. A., Attié-Bitach, T., Chang, C.-P., Wysocka, J., Martin, D. M., & Attardi, L. D.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
2014-08-03
Volume
514
Issue
7521
Pages
228-232
ISSN
  • 0028-0836
  • 1476-4687
DOI
10.1038/nature13585
Cited by
143
References
6
Language
en
Licence
www.springer.com/tdm (tdm)

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CoChat. (2026). Citation check: Inappropriate p53 activation during development induces features of CHARGE syndrome. https://app.cochat.ai/papers/10.1038/nature13585
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Van Nostrand, J. L., Brady, C. A., Jung, H., Fuentes, D. R., Kozak, M. M., Johnson, T. M., Lin, C.-Y., Lin, C.-J., Swiderski, D. L., Vogel, H., Bernstein, J. A., Attié-Bitach, T., Chang, C.-P., Wysocka, J., Martin, D. M., & Attardi, L. D. (2014). Inappropriate p53 activation during development induces features of CHARGE syndrome. Nature. https://doi.org/10.1038/nature13585

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.