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Andrea Daga

Researcher at Laboratory of Molecular Biology

Publications -  36
Citations -  3023

Andrea Daga is an academic researcher from Laboratory of Molecular Biology. The author has contributed to research in topics: Endoplasmic reticulum & Atlastin. The author has an hindex of 24, co-authored 36 publications receiving 2761 citations. Previous affiliations of Andrea Daga include University of Padua & California Institute of Technology.

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MELAS mutation in mtDNA binding site for transcription termination factor causes defects in protein synthesis and in respiration but no change in levels of upstream and downstream mature transcripts.

TL;DR: The pathogenetic mechanism of the mitochondrial tRNA(LeuUUR) gene mutation responsible for the MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) syndrome was investigated in transformants obtained by transfer of mitochondria from three genetically unrelated M ELAS patients into human mitochondrial DNA-less (rho 0) cells.
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Homotypic fusion of ER membranes requires the dynamin-like GTPase Atlastin

TL;DR: It is demonstrated that Atlastin mediates membrane tethering and fusion and strongly suggest that it is the GTPase activity that is required for ER homotypic fusion, which is shown to depend on GTP hydrolysis.
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Natural selection favors a newly derived timeless allele in Drosophila melanogaster

TL;DR: It is reported that a mutation in the circadian clock gene timeless in Drosophila melanogaster has arisen and spread by natural selection relatively recently in Europe and when introduced into different genetic backgrounds, natural and artificial alleles of the timeless gene affect the incidence of diapause.
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The hereditary spastic paraplegia gene, spastin, regulates microtubule stability to modulate synaptic structure and function.

TL;DR: In vivo data strongly support previous reports, providing a probable cause for the neuronal dysfunction in spastin-linked HSP disease and suggests therapeutic targets for HSP treatment and may provide insight into neurological disorders linked to microtubule dysfunction.
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Patterning of cells in the Drosophila eye by Lozenge, which shares homologous domains with AML1.

TL;DR: The strategies involved in cell fate determination in the Drosophila eye are remarkably similar to those utilized during vertebrate hematopoietic development and require the coordinate action of growth factor and AML1-like pathways.