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Your search keyword '"Jae, Lucas T."' showing total 9 results
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9 results on '"Jae, Lucas T."'

2. FIRRM/C1orf112 is synthetic lethal with PICH and mediates RAD51 dynamics

Author

Stok, Colin, Tsaridou, Stavroula, van den Tempel, Nathalie, Everts, Marieke, Wierenga, Elles, Bakker, Femke J., Kok, Yannick, Alves, Inês Teles, Jae, Lucas T., Raas, Maximilian W.D., Huis in 't Veld, Pim J., de Boer, H. Rudolf, Bhattacharya, Arkajyoti, Karanika, Eleftheria, Warner, Harry, Chen, Mengting, van de Kooij, Bert, Dessapt, Julien, ter Morsche, Lars, Perepelkina, Polina, Fradet-Turcotte, Amelie, Guryev, Victor, Tromer, Eelco C., Chan, Kok-Lung, Fehrmann, Rudolf S.N., and van Vugt, Marcel A.T.M.

Published
2023
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4. Phosphorylation of muramyl peptides by NAGK is required for NOD2 activation

Author

Stafford, Che A., Gassauer, Alicia-Marie, de Oliveira Mann, Carina C., Tanzer, Maria C., Fessler, Evelyn, Wefers, Benedikt, Nagl, Dennis, Kuut, Gunnar, Sulek, Karolina, Vasilopoulou, Catherine, Schwojer, Sophia J., Wiest, Andreas, Pfautsch, Marie K., Wurst, Wolfgang, Yabal, Monica, Fröhlich, Thomas, Mann, Matthias, Gisch, Nicolas, Jae, Lucas T., and Hornung, Veit

Published
2022
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6. OMA1 mediates local and global stress responses against protein misfolding in CHCHD10 mitochondrial myopathy

Author

Shammas, Mario K., Huang, Xiaoping, Wu, Beverly P., Fessler, Evelyn, Song, Insung Y., Randolph, Nicholas P., Li, Yan, Bleck, Christopher K.E., Springer, Danielle A., Fratter, Carl, Barbosa, Ines A., Powers, Andrew F., Quiros, Pedro M., Lopez-Otin, Carlos, Jae, Lucas T., Poulton, Joanna, and Narendra, Derek P.

Subjects
Proteins -- Denaturation, Stress (Physiology) -- Health aspects, Mitochondrial myopathies -- Models -- Causes of, Health care industry
Abstract

Mitochondrial stress triggers a response in the cell's mitochondria and nucleus, but how these stress responses are coordinated in vivo is poorly understood. Here, we characterize a family with myopathy caused by a dominant p.G58R mutation in the mitochondrial protein CHCHD10. To understand the disease etiology, we developed a knockin (KI) mouse model and found that mutant CHCHD10 aggregated in affected tissues, applying a toxic protein stress to the inner mitochondrial membrane. Unexpectedly, the survival of CHCHD10-KI mice depended on a protective stress response mediated by the mitochondrial metalloendopeptidase OMA1. The OMA1 stress response acted both locally within mitochondria, causing mitochondrial fragmentation, and signaled outside the mitochondria, activating the integrated stress response through cleavage of DAP3-binding cell death enhancer 1 (DELE1). We additionally identified an isoform switch in the terminal complex of the electron transport chain as a component of this response. Our results demonstrate that OMA1 was critical for neonatal survival conditionally in the setting of inner mitochondrial membrane stress, coordinating local and global stress responses to reshape the mitochondrial network and proteome., Introduction Mitochondria produce energy by coupling the transport of protons across the inner mitochondrial membrane (IMM) to the production of ATP (1). The integrity of the IMM is sensed by [...]

Published
2022

8. The FIGNL1-interacting protein C1orf112 is synthetic lethal with PICH and mediates RAD51 retention on chromatin

Author

Stok, Colin, primary, van den Tempel, Nathalie, additional, Everts, Marieke, additional, Wierenga, Elles, additional, Bakker, Femke, additional, Kok, Yannick, additional, Alves, Inês Teles, additional, Jae, Lucas T., additional, Bhattacharya, Arkajyoti, additional, Karanika, Elefteria, additional, Perepelkina, Polina, additional, Bergink, Steven, additional, Chan, Kok-Lung, additional, de Boer, H. Rolf, additional, Fehrmann, Rudolf S.N., additional, and van Vugt, Marcel A.T.M., additional

Published
2022
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