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Alvaro J. Obaya
Researcher at Brown University
Publications - 8
Citations - 1871
Alvaro J. Obaya is an academic researcher from Brown University. The author has contributed to research in topics: Cell cycle & Cyclin-dependent kinase. The author has an hindex of 7, co-authored 7 publications receiving 1791 citations.
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Journal ArticleDOI
Identification of CDK4 as a target of c-MYC.
Heiko Hermeking,Carlo Rago,Marino Schuhmacher,Qing Li,John Barrett,Alvaro J. Obaya,Brenda C. O'Connell,Maria K. Mateyak,Wanny Tam,Franz Kohlhuber,Chi V. Dang,John M. Sedivy,Dirk Eick,Bert Vogelstein,Kenneth W. Kinzler +14 more
TL;DR: Serial analysis of gene expression has identified the cyclin-dependent kinase 4 (CDK4) gene as a transcriptional target of c-MYC, and it is shown that CDK4 provides a direct link between the oncogenic effects of c -MYC and cell-cycle regulation.
Journal Article
Phenotypes of c-Myc-deficient rat fibroblasts isolated by targeted homologous recombination
TL;DR: The c-myc null cell lines reported here are a new experimental system in which to investigate the importance of putative c-Myc target genes and to identify novel downstream genes involved in cell cycle progression and apoptosis.
Journal ArticleDOI
c-Myc regulates cyclin D-Cdk4 and -Cdk6 activity but affects cell cycle progression at multiple independent points.
TL;DR: It is proposed that c-Myc functions as a crucial link in the coordinate adjustment of growth rate to environmental conditions and reduces coordinately the activities of all cyclin–cyclin-dependent kinase complexes in exponentially cycling cells.
Journal ArticleDOI
Mysterious liaisons: the relationship between c-Myc and the cell cycle.
TL;DR: The mechanisms by which c-Myc interacts with the intrinsic cyclin/Cdk cell cycle machinery remain undefined.
Journal ArticleDOI
c-myc null cells misregulate cad and gadd45 but not other proposed c-Myc targets
Andrew B. G. Bush,Maria K. Mateyak,Kerri A Dugan,Alvaro J. Obaya,Susumu Adachi,John M. Sedivy,Michael D. Cole +6 more
TL;DR: It is reported here that the expression of virtually all proposed c-Myc target genes is unchanged in cells containing a homozygous null deletion of c-myc, and it is demonstrated that a loss-of-function approach is critical for the evaluation of potential c- MYC target genes.