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Dolores Pérez-Sala

Researcher at Spanish National Research Council

Publications -  133
Citations -  9805

Dolores Pérez-Sala is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: Vimentin & Cyclopentenone prostaglandins. The author has an hindex of 40, co-authored 119 publications receiving 8992 citations.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Glutathionylation of the p50 subunit of NF-kappaB: a mechanism for redox-induced inhibition of DNA binding.

TL;DR: New oxidative modifications in Cys62 involved in the redox regulation of the NF-kappaB subunit p50 are identified and could represent a molecular basis for the coupling of pro-oxidative stimuli to gene expression.
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15-Deoxy-Δ12,14-prostaglandin J2Inhibition of NF-κB-DNA Binding through Covalent Modification of the p50 Subunit

TL;DR: Results clearly show that p50 is a target for covalent modification by 15d-PGJ2 that results in inhibition of DNA binding.
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The cyclopentenone 15-deoxy-delta 12,14-prostaglandin J2 binds to and activates H-Ras.

TL;DR: A mechanism for the activation of the Ras signaling pathway is described, which results from the chemical modification of H-Ras by formation of a covalent adduct with cyclopentenone prostaglandins.
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Molecular basis for the direct inhibition of AP-1 DNA binding by 15-deoxy-Δ12,14-prostaglandin J2. Vol. 278 (2003) 51251-51260

TL;DR: It is shown that 15d-PGJ2 covalently modifies c-Jun and directly inhibits the DNA binding activity of AP-1, which may contribute to the complex effects of cyclopentenone prostaglandins on the cellular response to pro-inflammatory agents.