Enrique Calvo

The paper shows that modifying ionic interactions with phospholipids prevents hypoxic adaptation by preserving inner mitochondrial membrane fluidity and CoQ transfer.

This paper introduces a normalization framework to decouple protocol and instrument effects in multicenter proteomics studies, demonstrating its application to the PME13 dataset.

This study shows that myosin inhibition with mavacamten is effective in treating HCM caused by both truncating and missense variants in MYBPC3, despite different pathomechanisms.

This study shows that SHED-derived extracellular factors enhance axonal regeneration and neuronal survival in retinal ganglion cells through distinct paracrine mechanisms.

This study shows that glycation of cardiac titin increases in diabetes, leading to protein and cardiomyocyte stiffening through crosslinking advanced glycation end products.

This study investigates altered myosin super-relaxation and energy metabolism in type II diabetes using muscle biopsies and proteomic analyses, finding increased super-relaxation and reduced ATP demand.

The paper introduces a workflow for analyzing post-translational modifications using proteomics data, revealing new oxidative modifications in animal models.

The paper analyzes the PeptideAtlas database to identify unannotated coding genes and aberrant translation, finding 34 novel ORFs with peptide evidence.

This study uses CRISPR/Cas9 screening to identify novel regulators of mitochondrial oxidative metabolism, revealing key genes involved in complex I assembly and BCAA catabolism.

The paper shows that in-gel protein digestion with acidic methanol selectively methylates glutamic acid residues, not other methylable residues like aspartic acid.

ReCom improves peptide identification by using a semi-supervised approach with a reference database, increasing performance by 68% over Comet-PTM.

This study investigates the role of SCAF1 in mitochondrial respiratory supercomplexes in mice, showing its structural role in respirasome formation and its impact on respiration and ROS production.

The paper develops algorithms to comprehensively identify and quantify protein modifications, revealing oxidative damage in heart mitochondria due to mtDNA heteroplasmy.