Jesper Foged Havelund

STEP-PTM enables integrated quantitative analysis of proteome, metabolome, and multiple PTM classes from single biological samples using a modular TMT-multiplexed workflow.

This paper identifies SLC25A34 as a key regulator of interorganellar lipid cycling, integrating circadian rhythms, diet, and temperature to control thermogenic metabolism.

This study uses forebrain organoids to show that schizophrenia involves sex-specific protein-state dysregulation, with changes in post-translational modifications and proteomic pathways rather than transcript levels.

This study shows that male obesity affects adipose mitochondrial function in offspring via the let-7-DICER axis, with reversible effects observed in both mice and human semen.

This study compares guided and unguided forebrain organoids using multi-omic analyses, revealing differences in cellular composition, metabolic profiles, and post-translational modifications.

This study shows that ACBP is not essential for adipose tissue function or systemic energy metabolism in mice, as knockout mice show no significant metabolic changes.

The paper presents the cryo-EM structure of HsNHE6, revealing its dimeric architecture, ion-binding site, and lipid-stabilized gate, along with insights into its disordered C-terminus and functional roles in ion exchange and disease.

This study presents a temporal atlas of protein and PTM abundance in cerebral organoids, showing significant changes during development related to neuronal differentiation and energy metabolism.

This study shows that modulating pseudoexon splicing in the PCCA gene with antisense oligonucleotides restores enzyme activity in propionic acidemia by rescuing PCCA and PCCB protein levels.

The paper examines the temporal response to maternal pulmonary immune activation across maternal and fetal organs using multi-omics, finding that the placenta protects the fetus through metabolic adaptations rather than immune responses.

This study identifies altered mitochondrial and energy metabolism in PARK2 mutant human iPSC-derived dopaminergic neurons through metabolomic analysis.