Thomas Langer

This study investigates the role of PHB2 in T cell proliferation, differentiation, and effector functions, finding that PHB2 deficiency causes cell cycle arrest and metabolic dysfunction.

This study shows that loss of CHCHD2 and CHCHD10 causes tissue-specific bioenergetic defects in cardiac and skeletal muscle, leading to distinct pathological outcomes.

The paper identifies AIFM1 as an OMA1 substrate that, when cleaved under mitochondrial stress, reduces OXPHOS activity and suppresses cell growth.

The paper shows OMA1 regulates mitochondrial protein import and OXPHOS biogenesis under stress by degrading DNAJC15, affecting protein translocation and organelle communication.

This study investigates the role of the CHCHD2-CHCHD10 protein complex in mitochondrial dysfunction and lipid homeostasis in mice, showing its importance in motor function and disease resistance.

This study shows that mutant CHCHD10 causes mitochondrial dysfunction and cardiomyopathy by disrupting cytochrome c oxidation and activating retrograde signaling.

This study identifies AFG3L2-mediated proteolysis as a mechanism that restricts mitochondrial biogenesis and gene expression under hypoxia by degrading key mitochondrial proteins.

This study maps the MCU-mediated mitochondrial calcium signaling network using proteomics, identifying 89 new interactors and their roles in disease-related pathways.

This study shows CLUH is essential for maintaining mitochondrial function and translation in motoneuronal axons, preventing peripheral neuropathy in mice.

The paper shows that the mitochondrial proton gradient regulates the m-AAA protease AFG3L2 through TMBIM5, linking protein turnover to mitochondrial energy status and Ca2+ signaling.

This study identifies YME1L as a mitochondrial protease that regulates metabolic state transitions in adult neural stem cells, ensuring self-renewal and preventing premature differentiation.