A5002756707- Parkinson's Disease Mechanisms and Treatments
- Cellular transport and secretion
- Lysosomal Storage Disorders Research
- Phytoplasmas and Hemiptera pathogens
- Autophagy in Disease and Therapy
- RNA regulation and disease
Biomedical Research Foundation of the Academy of Athens
2021-2022
Academy of Athens
2021-2022
Leucine-rich repeat kinase 2 (LRRK2) is a involved in different cellular functions, including autophagy, endolysosomal pathways, and immune function. Mutations LRRK2 cause autosomal-dominant forms of Parkinson's disease (PD). Heterozygous mutations GBA1, the gene encoding lysosomal enzyme glucocerebrosidase (GCase), are most common genetic risk factors for PD. Moreover, GCase function altered idiopathic PD other disease. Recent work suggests that activity can regulate However, both positive...
Despite several advances in the field, pharmacodynamic outcome measures reflective of LRRK2 kinase activity clinical biofluids remain urgently needed. A variety targets and approaches have been utilized including assessments itself (levels, phosphorylation), or its substrates (e.g. Rab10 other Rab GTPases). We previously shown that intrinsic isolated from PBMCs G2019S carriers is elevated, irrespective disease status. In present study we find phosphorylation also elevated carriers, but only...
Abstract LRRK2 is a kinase involved in different cellular functions, including autophagy, endolysosomal pathways and vesicle trafficking. Mutations cause autosomal dominant forms of Parkinson’s disease (PD). Heterozygous mutations GBA1 , the gene encoding lysosomal enzyme glucocerebrosidase (GCase), are most common genetic risk factors for PD. Moreover, GCase function altered idiopathic PD other disease. Recent work suggests that activity can regulate function. However, both positive...
Abstract Despite several advances in the field, pharmacodynamic outcome measures reflective of LRRK2 kinase activity clinical biofluids remain urgently needed. A variety targets and approaches have been utilized including assessments itself (levels, phosphorylation), or its substrates (e.g. Rab10 other Rab GTPases). We previously shown that intrinsic isolated from PBMCs G2019S carriers is elevated, irrespective disease status. In present study we find phosphorylation also elevated carriers,...