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Antonio Postigo
Researcher at University of Louisville
Publications - 56
Citations - 8099
Antonio Postigo is an academic researcher from University of Louisville. The author has contributed to research in topics: Transcription factor & Integrin. The author has an hindex of 34, co-authored 53 publications receiving 7582 citations. Previous affiliations of Antonio Postigo include Autonomous University of Madrid & Catalan Institution for Research and Advanced Studies.
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Journal ArticleDOI
Cdk phosphorylation triggers sequential intramolecular interactions that progressively block Rb functions as cells move through G1
TL;DR: Evidence is presented that phosphorylation of the C-terminal region of Rb by Cdk4/6 initiates successive intramolecular interactions that lead to phosphorylated histone deacetylase from the pocket and disruption of pocket structure.
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Rb Interacts with Histone Deacetylase to Repress Transcription
TL;DR: It is demonstrated that Rb can also repress transcription of endogenous cell cycle genes containing E2F sites through recruitment of histone deacetylase, which de acetylates histones on the promoter, thereby promoting formation of nucleosomes that inhibit transcription.
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Exit from G1 and S phase of the cell cycle is regulated by repressor complexes containing HDAC-Rb-hSWI/SNF and Rb-hSWI/SNF.
H.Steven Zhang,Mark Gavin,Anjali Dahiya,Antonio Postigo,Duanduan Ma,Robin X. Luo,J. William Harbour,Douglas C. Dean +7 more
TL;DR: Evidence is presented that Rb forms a repressor containing histone deacetylase (HDAC) and the hSWI/SNF nucleosome remodeling complex, which inhibits transcription of genes for cyclins E and A and arrests cells in the G1 phase of the cell cycle.
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EMT-activating transcription factors in cancer: beyond EMT and tumor invasiveness.
Ester Sánchez-Tilló,Yongqing Liu,Oriol de Barrios,Laura Siles,Lucia Fanlo,Miriam Cuatrecasas,Douglas S. Darling,Douglas C. Dean,Antoni Castells,Antonio Postigo +9 more
TL;DR: EMT-ATFs have been shown to cooperate in oncogenic transformation, regulate cancer cell stemness, override safeguard programs against cancer like apoptosis and senescence, determine resistance to chemotherapy and promote tumor angiogenesis.
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ZEB1 represses E-cadherin and induces an EMT by recruiting the SWI/SNF chromatin-remodeling protein BRG1.
Ester Sánchez-Tilló,A Lázaro,R Torrent,Miriam Cuatrecasas,Eva C. Vaquero,Antoni Castells,Pablo Engel,Antonio Postigo +7 more
TL;DR: ZEB1/BRG1 is identified as a new transcriptional mechanism regulating E-cadherin expression and epithelial-to-mesenchymal transdifferentiation that may be involved during the initial stages of tumor invasion.