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Natalia de la Fuente

Researcher at Autonomous University of Madrid

Publications -  6
Citations -  315

Natalia de la Fuente is an academic researcher from Autonomous University of Madrid. The author has contributed to research in topics: ATPase & Saccharomyces cerevisiae. The author has an hindex of 6, co-authored 6 publications receiving 296 citations. Previous affiliations of Natalia de la Fuente include Spanish National Research Council.

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Regulation of yeast H(+)-ATPase by protein kinases belonging to a family dedicated to activation of plasma membrane transporters.

TL;DR: Two genes from Saccharomyces cerevisiae are characterized that encode protein kinases implicated in activation of the yeast plasma membrane H+-ATPase (Pma1) in response to glucose metabolism, and ptk2 mutants exhibited reduced uptake of lithium and methylammonium.
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Head morphogenesis genes of the Bacillus subtilis bacteriophage SPP1.

TL;DR: In this article, the phage cistrons required for assembly of SPP1 heads were identified and characterized, and a DNA fragment containing most of the head morphogenesis genes was cloned and sequenced.
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Glucose activation of the yeast plasma membrane H+-ATPase requires the ubiquitin-proteasome proteolytic pathway.

TL;DR: It is proposed that glucose triggers degradation of an inhibitory protein resulting in enzyme activation, and that ATPase activation by glucose requires the ubiquitin–proteasome proteolytic pathway.
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Yeast gene YOR137c is involved in the activation of the yeast plasma membrane H+-ATPase by glucose

TL;DR: It is proposed that at least two independent mechanisms are involved in glucose activation of the H+‐ATPase and that YOR137c gene product is implicated in this activation.
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The cell wall integrity/remodeling MAPK cascade is involved in glucose activation of the yeast plasma membrane H(+)-ATPase.

TL;DR: In a genetic screening for multicopy suppressors of the rsp5 mutation, the WSC2/YNL283c gene was identified, a component of the PKC1-MPK1 mitogen-activated protein kinase (MAPK) signaling pathway that controls the cell wall integrity, and deletion of the MPK1/SLT2 gene disturbs the glucose-triggered K(m) decrease in ATPase.