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Graber, M.

Publications and source records attributed to Graber, M..

2 recordsLinked to original sources

Unifying the analysis of bottom-up proteomics data with CHIMERYS

Proteomic workflows generate vastly complex peptide mixtures that are analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS), creating thousands of spectra, most of which are chimeric and contain fragment ions from more than one peptide. Because of differences in data acquisition strategies such as data-dependent (DDA), data-independent (DIA) or parallel reaction monitoring (PRM), separate software packages employing different analysis concepts are used for peptide identification and quantification, even though the underlying information is principally the same. Here, we introduce CHIMERYS, a novel, spectrum-centric search algorithm designed for the deconvolution of chimeric spectra that unifies proteomic data analysis. Using accurate predictions of peptide retention time, fragment ion intensities and applying regularized linear regression, it explains as much fragment ion intensity as possible with as few peptides as possible. Together with rigorous false discovery rate control, CHIMERYS accurately identifies and quantifies multiple peptides per tandem mass spectrum in DDA, DIA and PRM experiments.

biochemistry↗

Toll-like receptor 3 orchestrates a conserved mechanism of heart regeneration

The humans heart responds to tissue damage with persistent fibrotic scarring. Unlike humans, zebrafish can repair cardiac injury and re-grow heart tissue throughout life. Recently, Toll-like receptor 3 (Tlr3) was identified as an important mediator of cardiac regeneration in neonatal mice. However, no functional analysis of tlr3 knock-out mutant zebrafish in respect to cardiac regeneration has yet been performed. We hypothesize that TLR3 signalling plays a central, conserved role in driving cardiac regeneration upon injury. Therefore, we focused on tlr3 mediated cardiac regeneration in zebrafish, ultimately discovering an evolutionary conserved mechanism of heart repair. Using histological, behavioural, and RNA-Sequencing analysis, we uncovered a conserved mechanism of tlr3 mediated cardiac repair after myocardial injury. Upon myocardial cryoinjury subjection, survival is decreased in tlr3-/- fish as compared to wildtype controls. Tlr3-/- zebrafish fail to recruit immune cells to the injured ventricle, resulting in impaired DNA repair and transcriptional reprogramming of cardiomyocytes. Mechanistically, we uncover an evolutionary conserved mechanism of tlr3 activation in fibroblasts promoting monocyte migration towards an injured ventricular area. Our data reveal tlr3 as a novel therapeutic target to promote cardiac regeneration. Every experiment including human participants has been approved by the ethics committee of the Medical University of Innsbruck (Ref. Nr.: 1262/2023). All experiments including the use of laboratory animals have been approved by the federal ministry of education, science, and research of Austria (Ref. Nr.: 2020-0.345.504).

molecular biology↗