Your browser doesn't support javascript.
loading
De novo alu-element insertions in FGFR2 identify a distinct pathological basis for Apert syndrome.
Oldridge, M; Zackai, E H; McDonald-McGinn, D M; Iseki, S; Morriss-Kay, G M; Twigg, S R; Johnson, D; Wall, S A; Jiang, W; Theda, C; Jabs, E W; Wilkie, A O.
Affiliation
  • Oldridge M; Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom.
Am J Hum Genet ; 64(2): 446-61, 1999 Feb.
Article in En | MEDLINE | ID: mdl-9973282
Subject(s)
Fulltext
Add to My VHL
Print
XML
PubMed Links
Search on Google

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Acrocephalosyndactylia / Mutagenesis, Insertional / Receptors, Fibroblast Growth Factor / Receptor Protein-Tyrosine Kinases / Alu Elements Type of study: Diagnostic_studies / Prognostic_studies Limits: Animals / Child / Female / Humans / Male Language: En Journal: Am J Hum Genet Year: 1999 Document type: Article Affiliation country: Reino Unido Country of publication: Estados Unidos
Fulltext
Add to My VHL
Print
XML
PubMed Links
Search on Google

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Acrocephalosyndactylia / Mutagenesis, Insertional / Receptors, Fibroblast Growth Factor / Receptor Protein-Tyrosine Kinases / Alu Elements Type of study: Diagnostic_studies / Prognostic_studies Limits: Animals / Child / Female / Humans / Male Language: En Journal: Am J Hum Genet Year: 1999 Document type: Article Affiliation country: Reino Unido Country of publication: Estados Unidos