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Enrique Viguera

Researcher at University of Málaga

Publications -  30
Citations -  2233

Enrique Viguera is an academic researcher from University of Málaga. The author has contributed to research in topics: DNA replication & Control of chromosome duplication. The author has an hindex of 17, co-authored 27 publications receiving 2100 citations. Previous affiliations of Enrique Viguera include Institut national de la recherche agronomique & Spanish National Research Council.

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Journal ArticleDOI

Reductive genome evolution in Buchnera aphidicola

TL;DR: A computational study of protein folding predicts that proteins in Buchnera, as well as proteins of other intracellular bacteria, are generally characterized by smaller folding efficiency compared with proteins of free living bacteria.
Journal ArticleDOI

Rescue of arrested replication forks by homologous recombination.

TL;DR: Observations that link replication hindrance with DNA rearrangements and the possible underlying molecular processes are reviewed.
Journal ArticleDOI

Replication slippage involves DNA polymerase pausing and dissociation.

TL;DR: This work has analysed the molecular mechanism of slippage between short direct repeats, using in vitro replication of a single‐stranded DNA template that mimics the lagging strand synthesis and presents evidence that, upon polymerase dissociation, only the terminal portion of the newly synthesized strand separates from the template and anneals to another direct repeat.
Journal ArticleDOI

The helicases DinG, Rep and UvrD cooperate to promote replication across transcription units in vivo

TL;DR: It is shown that when rRNA operons are inverted to face replication, the viability of the dinG mutant is affected and over‐expression of RNase H rescues the growth defect, showing that DinG acts in vivo to remove R‐loops.

The helicases DinG, Rep and UvrD cooperate to promote replication across transcription units in vivo This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits distribution,andreproductioninanymedium,providedtheoriginalauthorandsourcearecredited.Thislicensedoesnot permit commercial exploitation without specific permission.

TL;DR: In this article, the DinG, Rep and UvrD helicases are shown to be essential for efficient replication across highly transcribed regions and the viability of the dinG mutant is affected and over expression of RNase H rescues the growth defect.