Norbert Hübner

The paper identifies 25% of 7,264 non-canonical open reading frames (ncORFs) as producing translated gene products, supported by over 3,000 peptides from 3.8 billion mass spectra.

This study shows that loss of eEF1A2 in cardiomyocytes causes cardiomyopathy through proteostasis defects, and mTORC1 inhibition can reverse the condition.

The paper expands and refines a reference catalog of human non-canonical open reading frames (ncORFs) by incorporating more datasets and introducing a translation signature score framework to prioritize high-quality ncORFs.

This study shows PIEZO2 channels are critical for coronary artery development, as their absence causes vessel malformations and cardiac issues in mice.

The paper maps and validates key genetic loci influencing heart rate and function in fish, identifying potential targets for cardiac disease treatment.

This study identifies LINC01503-MP, a mitochondrial microprotein derived from an lncRNA, which promotes cell proliferation and oxidative metabolism in colorectal cancer cells.

The paper assesses MS-based identifications of unannotated human microproteins, finding large variation in reported proteins and PSM quality across studies.

This paper identifies direct cardiomyocyte toxicities of IL11 therapy, showing it causes acute heart failure by activating JAK/STAT3, which questions its continued use in patients.

The paper investigates dominance and additivity in mammalian genetics, finding dominance accounts for 25% of heritable variance and reveals novel dominance QTLs and trans-acting effects in gene expression.

This paper uses spatial transcriptomics and single-cell data to identify cellular niches in the human heart, revealing new insights into cardiac function and potential drug targets.

This study shows that inhibiting IL11 improves healthspan in aged mice by reversing metabolic dysfunction, sarcopenia, and frailty.

This study investigates the role of RPL3L in ribosome heterogeneity and mitochondrial activity in cardiomyocytes, finding that its depletion increases ribosome-mitochondria interactions and ATP levels.

This study identifies endocardial sprouting angiogenesis as a key mechanism in coronary vessel formation, revealing distinct molecular profiles that shape coronary arteries and veins.

This paper outlines a community-driven initiative to create a consolidated catalog of human Ribo-seq ORFs, addressing the lack of standardized annotation for these features.

The paper identifies 27 RBPs that regulate both mRNA abundance and translational efficiency in human hearts, with 21 affecting distinct sets of target genes through differential affinity for target length.

The paper uses CAGE sequencing to identify alternative promoter usage in a rat model of hypertension, linking promoter shifts to insulin resistance and blood pressure.

The paper identifies a trans locus in rats that causes a protein length-dependent shift in translational efficiency, affecting cardiac hypertrophy and sarcomere protein stoichiometry.

This study identifies pro-neurogenic compounds in apple peel and flesh that enhance hippocampal neurogenesis in adult mice through distinct mechanisms.

The paper identifies Pttg1 and Ulk4 as genetic modifiers that enhance SHH pathway resilience and are involved in primary cilia formation in the neuroepithelium.

The paper identifies a microprotein-independent role for LINC00261 in endocrine cell differentiation during human pancreas development through genetic ablation of lncRNAs.

The paper characterizes the cellular composition and gene expression of the adult human heart using single-cell transcriptomics, identifying distinct cell types and their functional roles.

The paper introduces Xtail, a method to identify differentially translated genes by analyzing Ribo-seq data while accounting for mRNA abundance variations.

The paper identifies translational regulators of fibrogenic genes in human cardiac fibroblasts and shows their role in cardiac fibrosis through ribosome profiling and RNA-binding protein analysis.

The paper identifies Tug1 as essential for male fertility, showing it has three distinct regulatory activities: a cis DNA repressor, a trans-acting lncRNA, and a conserved peptide affecting mitochondrial function.