F
Fermín A. Goytisolo
Researcher at Spanish National Research Council
Publications - 7
Citations - 1098
Fermín A. Goytisolo is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: Telomere & Telomerase. The author has an hindex of 7, co-authored 7 publications receiving 1083 citations. Previous affiliations of Fermín A. Goytisolo include Complutense University of Madrid.
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Mammalian Ku86 protein prevents telomeric fusions independently of the length of TTAGGG repeats and the G‐strand overhang
TL;DR: Results indicate that mammalian Ku86 plays a fundamental role at the telomere by preventing telomeric fusions independently of the length of TTAGGG repeats and the integrity of the G‐strand overhang.
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Short Telomeres Result in Organismal Hypersensitivity to Ionizing Radiation in Mammals
Fermín A. Goytisolo,Enrique Samper,Juan Martín-Caballero,Paul Finnon,Eloisa Herrera,Juana M. Flores,Simon Bouffler,Maria A. Blasco +7 more
TL;DR: The IR-sensitive phenotype of G5 mTR−/− mice suggests that telomere function is one of the determinants of radiation sensitivity of whole animals and that short telomeres do not significantly affect the efficiency of DNA double strand break repair in mammals.
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The absence of the dna-dependent protein kinase catalytic subunit in mice results in anaphase bridges and in increased telomeric fusions with normal telomere length and G-strand overhang.
TL;DR: A role for DNA-PKcs is to protect telomeres, which in turn are essential for chromosomal stability, which is reminiscent of the one recently described for Ku86-defective cells.
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Normal telomere length and chromosomal end capping in poly(ADP-ribose) polymerase–deficient mice and primary cells despite increased chromosomal instability
Enrique Samper,Fermín A. Goytisolo,Josiane Ménissier-de Murcia,Eva González-Suárez,Juan C. Cigudosa,Gilbert de Murcia,Maria A. Blasco +6 more
TL;DR: The results presented here indicate that PARp-1 does not play a major role in regulating telomere length or in telomeric end capping, and the chromosomal instability of PARP-1−/− primary cells can be explained by the repair defect associated to PARP -1 deficiency.
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Many ways to telomere dysfunction: in vivo studies using mouse models.
TL;DR: This review will focus on mammalian telomeres and, in particular, on the analysis of different mouse models for proteins that are important forTelomere function, such as telomerase and various telomere-binding proteins.