Novel Molecular Pathways Elicited by Mutant FGFR2 May Account for Brain Abnormalities in Apert Syndrome (2013)
- Authors:
- USP affiliated authors: ALONSO, NIVALDO - FM ; BUENO, MARIA RITA DOS SANTOS E PASSOS - IB ; ROCHA, KATIA MARIA DA - IB
- Unidades: FM; IB
- DOI: 10.1371/journal.pone.0060439
- Subjects: FATORES DE CRESCIMENTO (DEFICIÊNCIA); MUTAÇÃO GENÉTICA; FENÓTIPOS; GENÓTIPOS; BIOLOGIA MOLECULAR; CRANIOSSINOSTOSE (GENÉTICA)
- Language: Inglês
- Imprenta:
- Publisher place: San Francisco
- Date published: 2013
- Source:
- Este periódico é de acesso aberto
- Este artigo é de acesso aberto
- URL de acesso aberto
- Cor do Acesso Aberto: gold
- Licença: cc-by
-
ABNT
YEH, Erika et al. Novel Molecular Pathways Elicited by Mutant FGFR2 May Account for Brain Abnormalities in Apert Syndrome. PLOS ONE, v. 8, n. 4, p. 7 , 2013Tradução . . Disponível em: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0060439. Acesso em: 23 abr. 2024. -
APA
Yeh, E., Fanganiello, R. D., Sunaga, D. Y., Zhou, X., Holmes, G., Rocha, K. M., et al. (2013). Novel Molecular Pathways Elicited by Mutant FGFR2 May Account for Brain Abnormalities in Apert Syndrome. PLOS ONE, 8( 4), 7 . doi:10.1371/journal.pone.0060439 -
NLM
Yeh E, Fanganiello RD, Sunaga DY, Zhou X, Holmes G, Rocha KM, Alonso N, Matushita H, Wang Y, Jabs EW, Passos-Bueno MR. Novel Molecular Pathways Elicited by Mutant FGFR2 May Account for Brain Abnormalities in Apert Syndrome [Internet]. PLOS ONE. 2013 ; 8( 4): 7 .[citado 2024 abr. 23 ] Available from: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0060439 -
Vancouver
Yeh E, Fanganiello RD, Sunaga DY, Zhou X, Holmes G, Rocha KM, Alonso N, Matushita H, Wang Y, Jabs EW, Passos-Bueno MR. Novel Molecular Pathways Elicited by Mutant FGFR2 May Account for Brain Abnormalities in Apert Syndrome [Internet]. PLOS ONE. 2013 ; 8( 4): 7 .[citado 2024 abr. 23 ] Available from: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0060439 - FGFR2 mutation confers a less drastic gain of function in mesenchymal stem cells than in fibroblasts
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Informações sobre o DOI: 10.1371/journal.pone.0060439 (Fonte: oaDOI API)
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