T
Thomas Langer
Researcher at Max Planck Society
Publications - 253
Citations - 26029
Thomas Langer is an academic researcher from Max Planck Society. The author has contributed to research in topics: Mitochondrion & mitochondrial fusion. The author has an hindex of 82, co-authored 222 publications receiving 23219 citations. Previous affiliations of Thomas Langer include Heidelberg University & Ludwig Maximilian University of Munich.
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Journal ArticleDOI
The i-AAA protease YME1L and OMA1 cleave OPA1 to balance mitochondrial fusion and fission
Ruchika Anand,Timothy Wai,Michael J. Baker,Nikolay Kladt,Astrid Schauss,Elena I. Rugarli,Thomas Langer,Thomas Langer +7 more
TL;DR: OPA1 processing by YEM1L and OMA1 is dispensable for mitochondrial fusion and instead drives mitochondrial fragmentation, which is crucial for mitochondrial integrity and quality control.
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Making heads or tails of phospholipids in mitochondria
TL;DR: The discovery of proteins that regulate mitochondrial membrane lipid composition and of a multiprotein complex tethering ER to mitochondrial membranes has unveiled novel mechanisms of mitochondrial membrane biogenesis.
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The ATP hydrolysis-dependent reaction cycle of the Escherichia coli Hsp70 system DnaK, DnaJ, and GrpE
TL;DR: A model reaction in which DnaK, DnaJ, and GrpE mediate the folding of denatured firefly luciferase is analyzed to gain a biologically relevant understanding of the mechanism of Hsp70 action.
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Regulation of OPA1 processing and mitochondrial fusion by m-AAA protease isoenzymes and OMA1
Sarah Ehses,Ines Raschke,Giuseppe Mancuso,Andrea Bernacchia,Stefan Geimer,Daniel Tondera,Jean-Claude Martinou,Benedikt Westermann,Elena I. Rugarli,Thomas Langer,Thomas Langer +10 more
TL;DR: The cleavage by OMA1 causes an accumulation of the short OPA1 variants, and the role ofm-AAA proteases in ensuring a balance of long and short Opa1 isoforms is investigated.
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Quality control of mitochondria: protection against neurodegeneration and ageing
Takashi Tatsuta,Thomas Langer +1 more
TL;DR: Current knowledge on surveillance strategies that limit mitochondrial damage and ensure cellular integrity and their role in human disease are summarized.