Results 71 to 80 of about 28,054 (245)

S100A9 promotes pulmonary arterial hypertension by regulating mitochondria–endoplasmic reticulum interaction‐mediated inflammatory injury of endothelial cells

Interdisciplinary Medicine, EarlyView.
Macrophage‐derived S100 calcium‐binding protein A9 (S100A9) promotes the pathological progression of pulmonary arterial hypertension (PAH). S100A9 upregulates the interaction between signal‐transducing adaptor protein 2 and leucine‐rich repeat kinase 2, thereby regulating mitochondria–endoplasmic reticulum (ER) contact.
Chen Gong, Long Chen, Yiting Zhao, Xiaohe Wang, Qiang Yuan, Xiaofeng Fang, Liuyi Li, Yinbo Xu, Shumei Jiang, Guangwen Xu, Ke Meng, Delong Wang, Kangli Cao, Jianlong Sheng, Liling Guo, Shichun Shen   +15 more
wiley   +1 more source

Electron microscopy analysis of alpha-synuclein and LRRK2 transgenic C. elegans [PDF]

, 2013
Thesis (M.A.)--Boston UniversityMutations in alpha-synuclein and leucine-rich repeat kinase 2 (LRRK2) have been implicated in the cause of Parkinson’s disease (PD).
Nguyen, Andrew Huy
core   +1 more source

Clinical features and progression of Parkinson's disease with LRRK2 variants: A prospective study

Annals of Clinical and Translational Neurology
Objective We established a prospective cohort study to investigate the differences in motor and non‐motor symptoms between idiopathic Parkinson's disease (IPD) and Parkinson's disease in carriers of leucine‐rich repeat kinase 2 (LRRK2) gene risk variants
Tingwei Song, Xiaoxia Zhou, Chunyu Wang, Heng Wu, Xinxiang Yan, Jifeng Guo, Beisha Tang, Lifang Lei, Qian Xu, Parkinson's Disease & Movement Disorders Multicenter Database and Collaborative Network in China (PD‐MDCNC)   +9 more
doaj   +1 more source

Alpha‐Synuclein Promotes Anterograde Vesicle Transport in Melanocytes and Melanoma Cells: A Pro‐Survival Function

Journal of the Chinese Chemical Society, EarlyView.
Model for how α‐syn modulates the positioning of endolysosomes in melanoma cells. (a) α‐syn tethers endolysosomes to the plasma membrane, a last step in anterograde transport. (b) Loss of α‐syn expression causes the loss of the tethering function, which leads to perinuclear vesicle clustering. Reproduced from the open access article.
Stephan N. Witt
wiley   +1 more source

PAK6 phosphorylates 14-3-3γ to regulate steady state phosphorylation of LRRK2 [PDF]

, 2017
Mutations in Leucine-rich repeat kinase 2 (LRRK2) are associated with Parkinson's disease (PD) and, as such, LRRK2 is considered a promising therapeutic target for age-related neurodegeneration.
Adeosun, Aitken, Anneleen Kiekens, Bastea, Beccano-Kelly, Belluzzi, Berg, Chen, Chia, Cinzia Franchin, Civiero, Civiero, Civiero, Civiero, Claudia Morganti, Clokie, Denison, Dzamko, Dzamko, Elisa Greggio, Evy Lobbestael, Fuji, Giorgio Arrigoni, Giovanni Piccoli, Gloeckner, Greggio, Greggio, Greggio, Gu, Guaitoli, Ha, Isabella Tessari, Ito, Jean-Marc Taymans, Kaplan, Kaur, Kumar, Laura Civiero, Lavalley, Li, Li, Liu, Lobbestael, Longo, Longo, Luigi Bubacco, Mackintosh, MacLeod, Marie-Christine Chartier-Harlin, Mark R. Cookson, Matikainen-Ankney, Melrose, Muda, Nekrasova, Nichols, Paolo Pinton, Patrick A. Lewis, Rennefahrt, Schrantz, Sepulveda, Sheng, Sluchanko, Sluchanko, Sluchanko, Steger, Susanna Cogo, Taus, Tinti, Tzivion, Veerle Baekelandt, Winner, Woodcock, Yue, Zhou   +73 more
core   +3 more sources

G2019S selective LRRK2 kinase inhibitor abrogates mitochondrial DNA damage

npj Parkinson's Disease
Pathogenic mutations in LRRK2 cause Parkinson’s disease (PD). The G2019S variant is the most common, which results in abnormally high kinase activity. Compounds that target LRRK2 kinase activity are currently being developed and tested in clinical trials.
Nicholas Pena, Tara Richbourg, Claudia P. Gonzalez-Hunt, Rui Qi, Paul Wren, Carrolee Barlow, Natalie F. Shanks, Holly J. Carlisle, Laurie H. Sanders   +8 more
doaj   +1 more source

Genetic and Pathological Testing Attitudes for Parkinson's Disease in At‐Risk Relatives

Movement Disorders Clinical Practice, EarlyView.
Abstract Background Parkinson's disease (PD) is increasingly recognized as a neurodegenerative disorder with a broad clinical spectrum and diverse biomarkers enabling early detection. α‐synuclein seed amplification assays (SAA) and genetic testing now allow identification of PD pathology in asymptomatic individuals.
Tal Weil, Anat Mirelman, Roy N. Alcalay, Nurit Omer, Penina Ponger, Avner Thaler   +5 more
wiley   +1 more source

Rab29 activation of the Parkinson's disease-associated LRRK2 kinase [PDF]

, 2017
Parkinson's disease predisposing LRRK2 kinase phosphorylates a group of Rab GTPase proteins including Rab29, within the effector‐binding switch II motif. Previous work indicated that Rab29, located within the PARK16 locus mutated in Parkinson's patients,
Adil R Sarhan, Dario R Alessi, Elena Purlyte, Francesca Tonelli, Hatcher JM, Herschel S Dhekne, Lis P, Melanie Wightman, Pawel Lis, Rachel Gomez, Suzanne R Pfeffer, Terina N Martinez   +11 more
core   +2 more sources

Alzheimer's Biomarkers and Visuospatial Cognition in Parkinson's Disease: Modification by α‐Synuclein and Mediation of Age Effects

Movement Disorders Clinical Practice, EarlyView.
Abstract Background Visuospatial deficits in Parkinson's disease (PD) often precede dementia and complicate daily functioning. Alzheimer's disease (AD) pathology and α‐synuclein aggregation frequently co‐occur in PD, but their combined impact on cognition is unclear.
David Ledingham, Sahana Sathyanarayana, Charlotte B. Stewart, Robyn Iredale, Victoria Foster, Debra Galley, Meher Lad, Mark R. Baker, Nicola Pavese   +8 more
wiley   +1 more source

Overexpression of Parkinson's Disease-Associated Mutation LRRK2 G2019S in Mouse Forebrain Induces Behavioral Deficits and alpha-Synuclein Pathology [PDF]

, 2017
Citation: Xiong, Y. L., Neifert, S., Karuppagounder, S. S., Stankowski, J. N., Lee, B. D., Grima, J. C., . . . Dawson, V. L. (2017). Overexpression of Parkinson's Disease-Associated Mutation LRRK2 G2019S in Mouse Forebrain Induces Behavioral Deficits and
Chen, G. X., Dawson, T. M., Dawson, V. L., Grima, J. C., Karuppagounder, S. S., Ko, H. S., Lee, B. D., Lee, Y., Neifert, S., Stankowski, J. N., Swing, D., Tessarollo, L., Xiong, Y. L.   +12 more
core   +1 more source