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Potential for functional redundancy in EGF and TGFalpha signaling in desmoid cells: a cDNA microarray analysis.
Trang, Sylvia H; Joyner, David E; Damron, Timothy A; Aboulafia, Albert J; Randall, R Lor.
Afiliação
  • Trang SH; SARC Laboratory, Sarcoma Services, Department of Orthopaedics and Huntsman Cancer Institute, University of Utah, Salt Lake City, UT 84112, USA.
Growth Factors ; 28(1): 10-23, 2010 Feb.
Article em En | MEDLINE | ID: mdl-20092031
Genes that replace or duplicate the function of other genes are considered functionally redundant. In this cDNA microarray study, using an Agilent microarray platform and GeneSifter analysis software, we evaluated (1) the degree of downstream transcriptional redundancy and (2) the level of genetic uniqueness apparent in desmoid tumor cells stimulated in vitro for 3 h or for 24 h with 100 ng/ml of exogenous recombinant human EGF (rhEGF) or with recombinant human transforming growth factor alpha (rhTGFalpha). Our intent was to identify genes costimulated, or genes unique to, desmoid cells stimulated in vitro with rhEGF and rhTGFalpha. This experimental approach demonstrated a 55% transcriptional redundancy in the number of desmoid genes significantly upregulated or downregulated following 3 h of stimulation with rhEGF or with rhTGFalpha, and a 65% transcriptional redundancy following 24 h of growth factor stimulation. Approximately 150 genes costimulated by rhEGF and rhTGFalpha were identified. This study suggests that EGF and TGFalpha retain some level of functional redundancy, possibly resulting from their divergence from a common ancestral gene.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Regulação Neoplásica da Expressão Gênica / Fator de Crescimento Transformador alfa / Fibromatose Agressiva / Duplicação Gênica / Fator de Crescimento Epidérmico Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Ano de publicação: 2010 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Transdução de Sinais / Regulação Neoplásica da Expressão Gênica / Fator de Crescimento Transformador alfa / Fibromatose Agressiva / Duplicação Gênica / Fator de Crescimento Epidérmico Tipo de estudo: Prognostic_studies Limite: Humans Idioma: En Ano de publicação: 2010 Tipo de documento: Article