Publications by authors named "E Dassa"

Article Synopsis
  • ABC transporters are a superfamily that move a wide range of substances across cell membranes, combining conserved ATP-binding features with diverse transmembrane structures.
  • The different structural forms of the transmembrane domains (TMDs) suggest that these transporters evolved by pairing ancient motor domains with various mechanical systems.
  • A new classification for ABC transporters is proposed that emphasizes structural similarities in their TMDs for better categorization.
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Article Synopsis
  • Staphylococcus sciuri is an ancient species in the Staphylococcus genus, diverging from macrococci around 250 million years ago and lacking host-specific colonization strategies.
  • Genome analysis of S. sciuri reveals unique genetic traits that facilitate its transition between free-living and infective states, including an abundance of phosphoenolpyruvate:carbohydrate phosphotransferase systems.
  • The strain lacks major virulence factors seen in Staphylococcus aureus, but contains systems for heme and iron acquisition, as well as genes involved in signaling networks that may provide insight into how S. aureus developed its virulence.
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Isolated complex I deficiencies are one of the most commonly observed biochemical features in patients suffering from mitochondrial disorders. In the majority of these clinical cases the molecular bases of the diseases remain unknown suggesting the involvement of unidentified factors that are critical for complex I function. The Saccharomyces cerevisiae NDI1 gene, encoding the mitochondrial internal NADH dehydrogenase was previously shown to complement a complex I deficient strain in Caenorhabditis elegans with notable improvements in reproduction and whole organism respiration.

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Mitochondrial calcium is an important modulator of cellular metabolism. CCDC90A was reported to be a regulator of the mitochondrial calcium uniporter (MCU) complex, a selective channel that controls mitochondrial calcium uptake, and hence was renamed MCUR1. Here we show that suppression of CCDC90A in human fibroblasts produces a specific cytochrome c oxidase (COX) assembly defect, resulting in decreased mitochondrial membrane potential and reduced mitochondrial calcium uptake capacity.

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