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Diego Miranda-Saavedra

Researcher at Spanish National Research Council

Publications -  60
Citations -  8478

Diego Miranda-Saavedra is an academic researcher from Spanish National Research Council. The author has contributed to research in topics: Gene & Phosphorylation. The author has an hindex of 38, co-authored 59 publications receiving 7559 citations. Previous affiliations of Diego Miranda-Saavedra include University of Oxford & Genome Institute of Singapore.

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Comparative genomics reveals mobile pathogenicity chromosomes in Fusarium

Li-Jun Ma, +65 more
- 18 Mar 2010 - 
TL;DR: Comparison of genomes of three phenotypically diverse Fusarium species revealed lineage-specific genomic regions in F. oxysporum that include four entire chromosomes and account for more than one-quarter of the genome, putting the evolution of fungal pathogenicity into a new perspective.
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The Ectocarpus genome and the independent evolution of multicellularity in brown algae

J. Mark Cock, +76 more
- 03 Jun 2010 - 
TL;DR: The Ectocarpus genome sequence represents an important step towards developing this organism as a model species, providing the possibility to combine genomic and genetic approaches to explore these and other aspects of brown algal biology further.
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Draft genome sequence of the sexually transmitted pathogen Trichomonas vaginalis

Jane M. Carlton, +64 more
- 12 Jan 2007 - 
TL;DR: The genome sequence of the protist Trichomonas vaginalis predicts previously unknown functions for the hydrogenosome, which support a common evolutionary origin of this unusual organelle with mitochondria.
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Draft Genome of the Filarial Nematode Parasite Brugia malayi

Elodie Ghedin, +71 more
- 21 Sep 2007 - 
TL;DR: In this article, the authors sequenced the ∼90 megabase (Mb) genome of the human filarial parasite Brugia malayi and predicted ∼11,500 protein coding genes in 71 Mb of robustly assembled sequence.
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Emerging roles of pseudokinases.

TL;DR: Evidence that the pseudokinase STRAD controls the function of the tumour suppressor kinase LKB1 is reviewed and that a single amino acid substitution within the pseudokerase domain of the tyrosine kinase JAK2 leads to several malignant myeloproliferative disorders.