Zobrazeno 1 - 10
of 60
pro vyhledávání: '"Hardy J Rideout"'
Autor:
Katerina Melachroinou, Emmanouela Leandrou, Polytimi-Eleni Valkimadi, Anna Memou, Georgios Hadjigeorgiou, Leonidas Stefanis, Hardy J Rideout
Publikováno v:
PLoS ONE, Vol 11, Iss 11, p e0166053 (2016)
Despite the plethora of sequence variants in LRRK2, only a few clearly segregate with PD. Even within this group of pathogenic mutations, the phenotypic profile can differ widely.We examined multiple properties of LRRK2 behavior in cellular models ov
Externí odkaz:
https://doaj.org/article/ed751423893843bfb4c676d2114bec17
Autor:
Nathan D Jorgensen, Yong Peng, Cherry C-Y Ho, Hardy J Rideout, Donald Petrey, Peng Liu, William T Dauer
Publikováno v:
PLoS ONE, Vol 4, Iss 12, p e8463 (2009)
BACKGROUND:Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most common genetic cause of Parkinson disease (PD). LRRK2 contains an "enzymatic core" composed of GTPase and kinase domains that is flanked by leucine-rich repeat (LRR) and WD40 p
Externí odkaz:
https://doaj.org/article/46e6a5e35fda4c749b2d483255b7fbe9
Autor:
Nicole Comfort, Meethila Gade, Madeleine Strait, Samantha J. Merwin, Daphne Antoniou, Chiara Parodi, Lina Marcinczyk, Lea Jean‐Francois, Tessa R. Bloomquist, Anna Memou, Hardy J. Rideout, Stefania Corti, Shingo Kariya, Diane B. Re
Publikováno v:
Journal of Cachexia, Sarcopenia and Muscle, Vol 14, Iss 3, Pp 1322-1336 (2023)
Abstract Background Sarcopenia, the age‐associated decline in skeletal muscle mass and strength, has long been considered a disease of muscle only, but accumulating evidence suggests that sarcopenia could originate from the neural components contro
Externí odkaz:
https://doaj.org/article/971c856039ca453e86c53bf33c9ab51e
Autor:
Hardy J. Rideout, Marie-Christine Chartier-Harlin, Matthew J. Fell, Warren D. Hirst, Sarah Huntwork-Rodriguez, Cheryl E. G. Leyns, Omar S. Mabrouk, Jean-Marc Taymans
Publikováno v:
Frontiers in Neuroscience, Vol 14 (2020)
Evidence is mounting that LRRK2 function, particularly its kinase activity, is elevated in multiple forms of Parkinson’s disease, both idiopathic as well as familial forms linked to mutations in the LRRK2 gene. However, sensitive quantitative marke
Externí odkaz:
https://doaj.org/article/9b99a1e11ad44ba693fc6e89a5f08950
Autor:
Nasia Antoniou, Dimitrios Vlachakis, Anna Memou, Emmanouela Leandrou, Polytimi-Eleni Valkimadi, Katerina Melachroinou, Diane B. Re, Serge Przedborski, William T. Dauer, Leonidas Stefanis, Hardy J. Rideout
Publikováno v:
Scientific Reports, Vol 8, Iss 1, Pp 1-17 (2018)
Abstract In experimental models, both in vivo and cellular, over-expression of Parkinson’s linked mutant leucine-rich repeat kinase 2 (LRRK2) is sufficient to induce neuronal death. While several cell death associated proteins have been linked to L
Externí odkaz:
https://doaj.org/article/023f75cba7e141e794a505571ddc8b16
Autor:
Athina Simitsi, Christos Koros, Hardy J. Rideout, Alexandros Papadimitriou, Maria Kedariti, Politymi-Eleni Valkimadi, Lampros Dimitrakopoulos, Lilian Peptropoulou-Vathi, Leonidas Stefanis, Roy N. Alcalay, Dimitra Papadimitriou
Publikováno v:
npj Parkinson's Disease. 8
Despite several advances in the field, pharmacodynamic outcome measures reflective of LRRK2 kinase activity in clinical biofluids remain urgently needed. A variety of targets and approaches have been utilized including assessments of LRRK2 itself (le
Autor:
Marco A. S. Baptista, Katerina Melachroinou, Sushma Narayan, Leonidas Stefanis, Katie Kopil, Najah Levers, Roy N. Alcalay, Neal Joshi, Shalini Padmanabhan, Christopher Liong, Samantha J. Hutten, Min Suk Kang, Un Jung Kang, Hardy J. Rideout
Publikováno v:
Movement Disorders. 35:2095-2100
Background Leucine-rich repeat kinase 2 kinase inhibitors are being vigorously pursued as potential therapeutic options; however, there is a critical need for sensitive and quantitative assays of leucine-rich repeat kinase 2 function and target engag
Autor:
Nicole Comfort, Meethila Gade, Madeleine Strait, Samantha J. Merwin, Daphne Antoniou, Anna Memou, Hardy J. Rideout, Stefania Corti, Shingo Kariya, Diane B. Re
BackgroundSarcopenia, the age-associated decline in skeletal muscle mass and strength, has long been considered a disease of muscle only, but accumulating evidence suggests that sarcopenia could originate from the neural components controlling muscle
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::5dc225c8f92d9569560431276fe7540d
https://doi.org/10.1101/2022.02.01.478571
https://doi.org/10.1101/2022.02.01.478571
Autor:
Leah G. Helton, Panagiotis S Athanasopoulos, Bernd K Gilsbach, Scotty Hall, Ranjan Kumar Singh, Ahmed Soliman, Hardy J. Rideout, Felix von Zweydorf, Christian Johannes Gloeckner, Francesco Raimondi, Franz Y. Ho, Eileen J. Kennedy, Arjan Kortholt, Jascha Tobias Manschwetus, Timothy J LeClair, Friedrich W. Herberg, Wim Versées, Michalis Kentros
Publikováno v:
ACS chemical biology 16(11), 2326-2338 (2021). doi:10.1021/acschembio.1c00487
ACS chemical biology, 16(11). AMER CHEMICAL SOC
ACS chemical biology, 16(11). AMER CHEMICAL SOC
Leucine-Rich Repeat Kinase 2 (LRRK2) is a large, multidomain protein with dual kinase and GTPase function that is commonly mutated in both familial and idiopathic Parkinson's Disease (PD). While dimerization of LRRK2 is commonly detected in PD models
Autor:
Alessio Di Fonzo, Hardy J. Rideout, Nicoletta Plotegher, Maria Kedariti, Roy N. Alcalay, Leonidas Stefanis, Elena Ziviani, Massimo Aureli, Elisa Greggio, Laura Civiero, Matthew Surface, Alice Kaganovich, Emanuele Frattini, Pascale Baden, Mark R. Cookson, Michela Deleidi, Susanna Cogo
LRRK2 is a kinase involved in different cellular functions, including autophagy, endolysosomal pathways and vesicle trafficking. Mutations inLRRK2cause autosomal dominant forms of Parkinson’s disease (PD). Heterozygous mutations inGBA1, the gene en
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::c1fc9161f6c56dd675818cd90924e942
https://doi.org/10.1101/2021.09.27.461935
https://doi.org/10.1101/2021.09.27.461935