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Javier Calvo-Garrido

Researcher at Spanish National Research Council

Publications -  12
Citations -  4754

Javier Calvo-Garrido is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: Autophagy & Dictyostelium. The author has an hindex of 10, co-authored 10 publications receiving 3840 citations. Previous affiliations of Javier Calvo-Garrido include Autonomous University of Madrid.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy 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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Autophagy in Dictyostelium: Genes and pathways, cell death and infection

Javier Calvo-Garrido, +7 more
- 16 Aug 2010 - 
TL;DR: This review focuses on the identification and annotation of the putative Dictyostelium autophagy genes and on the role of Autophagy in development, cell death and infection by bacterial pathogens.
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Autophagy dysfunction and ubiquitin-positive protein aggregates in Dictyostelium cells lacking Vmp1.

Javier Calvo-Garrido, +1 more
- 01 Jan 2010 - 
TL;DR: The results suggest that Vmp1 is required for the clearance of these ubiquitinated protein aggregates through autophagy and highlight a potential role for VMP1 in protein-aggregation diseases.
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Vacuole Membrane Protein 1 Is an Endoplasmic Reticulum Protein Required for Organelle Biogenesis, Protein Secretion, and Development

Javier Calvo-Garrido, +4 more
- 01 Aug 2008 - 
TL;DR: Transmission electron microscopy of vmp1(-) cells showed the accumulation of autophagic features that suggests a role of Vmp1 in macroautophagy, suggesting a functional conservation of the protein among evolutionarily distant species and highlights Dictyostelium as a valid experimental system to address the function of this gene.
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MidA is a putative methyltransferase that is required for mitochondrial complex I function

Sergio Carilla-Latorre, +10 more
- 15 May 2010 - 
TL;DR: Interestingly, this complex I deficiency in a Dictyostelium midA− mutant causes a complex phenotypic outcome, which includes phototaxis and thermotaxis defects, which is mediated by a chronic activation of AMPK.