Johan H. Auwerx

This study maps proteome-wide QTLs in a MASLD mouse model to construct gene-protein-phenotype metabolic networks, identifying Ubr1 as a central regulator of proteostasis and lipid metabolism.

This study identifies genetic loci affecting lifespan dynamics, sex differences, and body weight trade-offs in mice using an actuarial approach.

This study identifies SIRT2 as a regulator of β-cell proliferation, showing its role in controlling β-cell expansion during hyperglycemia while preserving feedback mechanisms.

The paper identifies a UPRmt modulator, fipp-1/FIP1L1, that extends lifespan in C. elegans and is associated with metabolic homeostasis in humans.

The paper identifies modifier pathways for inborn errors of metabolism using multiomic data and gene regulatory networks from healthy populations.

This study identifies a pro-myogenic domain in CYTOR and shows that chemically modified RNA delivery improves dystrophic myotube function.

The paper identifies genetic and molecular regulators of lifespan in C. elegans using a recombinant inbred population and validates their relevance to human age-related diseases.

This study identifies the GFRAL neuronal axis as critical for GDF15-mediated adaptive thermogenesis in white adipose tissue under mitochondrial stress.

The paper identifies genetic and dietary factors influencing intestinal inflammation in BXD mice, finding MUC4 and EPHA6 as potential mediators of IBD susceptibility.

The paper integrates multi-omics data from two C. elegans strains to show that doxycycline-induced UPRmt affects mitochondrial function and lifespan through shared and strain-specific pathways.

The paper examines how diet and genetics interact to affect longevity and weight gain in mice, finding that genetic differences significantly influence the impact of high-fat diets on lifespan.

This study examines how genetic background and sex influence metabolic responses to high-fat diet in mice, highlighting the role of mitochondrial function in physiological diversity.

This paper demonstrates that gene replacement therapy using AAV-PHP.B vector improves survival and corrects metabolic and behavioral deficits in a mouse model of Leigh syndrome.

This study identifies TBK1 as a kinase that phosphorylates mutant huntingtin, reduces its aggregation and toxicity in multiple HD models.

The paper introduces GeneBridge, a method for imputing gene function and predicting module connections using multi-species expression data, and demonstrates its application across 1,700 datasets.

BXD mouse family doubled to 150 inbred strains segregating over 6 million variants, with roughly 10,000 located recombinations and a public phenome exceeding 7000 traits.

The paper identifies evolutionarily conserved functional modules related to proteostasis in normal aging across species and links them to age-related GWAS and caloric restriction.

The paper analyzes mitochondrial variation in the DGRP, identifies haplotype-specific phenotypic associations, and finds no major fitness effects from mito-nuclear incompatibilities.

This study identifies a homozygous ERAL1 mutation as the cause of Perrault syndrome, showing it disrupts mitochondrial ribosome assembly and function.