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Miguel Godinho Ferreira

Researcher at Instituto Gulbenkian de Ciência

Publications -  51
Citations -  2569

Miguel Godinho Ferreira is an academic researcher from Instituto Gulbenkian de Ciência. The author has contributed to research in topics: Telomere & Telomerase. The author has an hindex of 21, co-authored 50 publications receiving 2145 citations. Previous affiliations of Miguel Godinho Ferreira include Lincoln's Inn & University of Manchester.

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Positive epistasis drives the acquisition of multidrug resistance.

TL;DR: In an antibiotic-free environment the cost of multiple resistance is smaller than expected, a signature of pervasive positive epistasis among alleles that confer resistance to antibiotics, and a significant fraction of resistant mutations can be beneficial in certain resistant genetic backgrounds.
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Single-cell functional and chemosensitive profiling of combinatorial colorectal therapy in zebrafish xenografts.

TL;DR: The results suggest that zebrafish larvae xenografts constitute a promising fast assay for precision medicine, bridging the gap between genotype and phenotype in an in vivo setting.
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The fission yeast Taz1 protein protects chromosomes from Ku-dependent end-to-end fusions.

TL;DR: The data suggest a model whereby taz1(-) telomeres are exposed to the prevailing mode of DNA repair, which is dictated by the cell cycle, and Taz1 caps chromosome ends and provides the telome Respecific interaction that prevents Ku from treating telomere breaks as double-strand breaks.
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The exoribonuclease Dis3L2 defines a novel eukaryotic RNA degradation pathway.

TL;DR: The results suggest that in S. pombe, and possibly in most other eukaryotes, Dis3L2 is an important factor in mRNA degradation, and this novel 3′‐5′ RNA decay pathway represents an alternative to degradation by Xrn1 and the exosome.
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Two modes of DNA double-strand break repair are reciprocally regulated through the fission yeast cell cycle

TL;DR: It is shown that G1 arrest is the specific nitrogen starvation-induced event that promotes NHEJ between taz1(-) telomeres, and the general levels of N HEJ and HR are reciprocally regulated through the cell cycle, so that NHEj is 10-fold higher in early G1 than in other cell cycle stages; the reverse is true for HR.