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José A. García-Salcedo

Researcher at University of Granada

Publications -  60
Citations -  1520

José A. García-Salcedo is an academic researcher from University of Granada. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 17, co-authored 47 publications receiving 1198 citations. Previous affiliations of José A. García-Salcedo include Spanish National Research Council & Free University of Brussels.

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Circulating Levels of Sclerostin Are Increased in Patients with Type 2 Diabetes Mellitus

TL;DR: Circulating sclerostin is increased in T2DM independently of gender and age, and its relationship with bone metabolism and calciotropic hormones, bone turnover markers, bone mineral density (BMD), and morphometric vertebral fractures is analyzed.
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A differential role for actin during the life cycle of Trypanosoma brucei

TL;DR: Results indicate that actin is required for the formation of coated vesicles from the flagellar pocket membrane, which is the first step in the endocytic pathway, and suggest that trypanosomes have different functional requirements for actin during the bloodstream and procyclic phases of the life cycle.
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A chromosomal SIR2 homologue with both histone NAD-dependent ADP-ribosyltransferase and deacetylase activities is involved in DNA repair in Trypanosoma brucei

TL;DR: It is proposed that histone modification by TbSIR2RP1 is involved in DNA repair, which is in contrast to other known proteins of this family.
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Atherosclerotic Disease in Type 2 Diabetes Is Associated With an Increase in Sclerostin Levels

TL;DR: Serum sclerostin levels could be a major modulator of Wnt signaling in AD with implications in type 2 diabetes mellitus patients, and Circulating sclerOSTin is increased in T2DM patients with atherosclerotic lesions.
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Neuropeptides kill African trypanosomes by targeting intracellular compartments and inducing autophagic-like cell death

TL;DR: Neuropeptides exerted their trypanolytic activity through an unusual mechanism that involves peptide uptake by the parasite, disruption of lysosome integrity and cytosolic accumulation of glycolytic enzymes, which promotes an energetic metabolism failure that initiates an autophagic-like cell death.