E
Elena I. Rugarli
Researcher at University of Cologne
Publications - 86
Citations - 7063
Elena I. Rugarli is an academic researcher from University of Cologne. The author has contributed to research in topics: Mitochondrion & Hereditary spastic paraplegia. The author has an hindex of 43, co-authored 81 publications receiving 6260 citations. Previous affiliations of Elena I. Rugarli include Baylor University & University of Milan.
Papers
More filters
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.
Journal ArticleDOI
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.
Journal ArticleDOI
Mitochondrial quality control: a matter of life and death for neurons
TL;DR: The role of the mitochondrial QC network for neuronal survival and neurodegeneration is discussed and mitochondrial proteases emerge as central regulators that coordinate different quality control pathways within an interconnected network of mechanisms.
Journal ArticleDOI
The m-AAA Protease Defective in Hereditary Spastic Paraplegia Controls Ribosome Assembly in Mitochondria
TL;DR: A regulatory role of an AAA protease for mitochondrial protein synthesis in yeast is described and mitochondrial defects associated with m-AAA protease mutants in yeast are rationalize and shed new light on the mechanism of axonal degeneration in HSP.
Journal ArticleDOI
Opitz G/BBB syndrome, a defect of midline development, is due to mutations in a new RING finger gene on Xp22
Nandita Quaderi,Susann Schweiger,Karin Gaudenz,Brunella Franco,Elena I. Rugarli,Wolfgang Berger,George J. Feldman,Manuela Volta,Grazia Andolfi,S. Gilgenkrantz,Robert W. Marion,Raoul C.M. Hennekam,John M. Opitz,Maximilian Muenke,H.H. Ropers,H.H. Ropers,Andrea Ballabio +16 more
TL;DR: A new gene on Xp22f MIDI (Midline 1), which is disrupted in an OS patient carrying an X-chromosome inversion and is also mutated in several OS families, suggests an important role for this gene in midline development.