Aina Bernal
Autonomous University of Barcelona
7 Papers
19 Citations
Aina Bernal is an academic researcher from Autonomous University of Barcelona. The author has contributed to research in topics: Telomere & Telomerase. The author has an hindex of 4, co-authored 5 publications.
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Papers
The HASTER lncRNA promoter is a cis-acting transcriptional stabilizer of HNF1A
Anthony Beucher,Irene Miguel-Escalada,Diego Balboa,Matias G. De Vas,Miguel A. Maestro,Javier García-Hurtado,Aina Bernal,Roser Gonzalez-Franco,Pierfrancesco Vargiu,Holger Heyn,Philippe Ravassard,Sagrario Ortega,Jorge Ferrer +12 more
TL;DR: In this paper , the HASTER promoter DNA, rather than the lncRNA, modulates HNF1A promoter-enhancer interactions in cis and thereby regulates HNF 1A transcription.
Pancreas agenesis mutations disrupt a lead enhancer controlling a developmental enhancer cluster
Irene Miguel-Escalada,Miguel A. Maestro,Diego Balboa,Anamaria Elek,Aina Bernal,Edgar Bernardo,Vanessa Grau,Javier García-Hurtado,Arnau Sebé-Pedrós,Jorge Ferrer +9 more
TL;DR: In this article , an epigenetic cascade that is required for duct and endocrine differentiation was shown to activate an entire PTF1A enhancer cluster in early pancreatic multipotent progenitors, which revealed an enhancer that acts as a regulatory master key and is thus vulnerable to pathogenic loss of function mutations.
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Generation of Immortalised But Unstable Cells after hTERT Introduction in Telomere-Compromised and p53-Deficient vHMECs.
TL;DR: This study provides evidence that while immortalisation of vHMECs at early stages results in an almost stable karyotypes, a transient telomere-dependent CIN period—aggravated by p53 deficiency—and followed by hTERT overexpression serves as a mechanism for the generation of immortal unstable cells which, due to their evolving karyotype, could attain additional promoting properties permissive to malignancy.
7
Centrosome aberrations in human mammary epithelial cells driven by cooperative interactions between p16INK4a deficiency and telomere-dependent genotoxic stress.
Daniel Domínguez,Purificación Feijoo,Aina Bernal,Amaia Ercilla,Neus Agell,Anna Genescà,Laura Tusell +6 more
TL;DR: This study shows that TP53 proficient vHMECs cells develop centrosome aberrations when telomere-dysfunction genotoxic stress is produced in the presence of a defective p16INK4a setting and in parallel with an activation of the DNA damage checkpoint response.