In vitro scratch assay: a convenient and inexpensive method for analysis of cell migration in vitro.
In PLoS ONE, 2006
... CA), actin, phospho-Akt, Akt and PTEN antibodies (Santa Cruz, CA), Caspase-9 antibody (Millipore, Billerica, MA), DJ-1 antibody (MBL International, Woburn, MA), HRP ...
Neural stem cells in Parkinson's disease: a role for neurogenesis defects in onset and progression.
Esch-sur-Alzette, Luxembourg. In Cell Mol Life Sci, 18 Dec 2014
Finally, the roles of PD-related genes, SNCA, LRRK2, VPS35, Parkin, PINK1 and DJ-1 have been studied in NSCs, progenitor cells and induced pluripotent stem cells, demonstrating a role for some of these genes in stem/progenitor cell proliferation and maintenance.
Protective and toxic roles of dopamine in Parkinson's disease.
Santiago, Chile. In J Neurochem, Jun 2014
The discovery of genes associated with Parkinson's disease (such as alpha synuclein (SNCA), E3 ubiquitin protein ligase (parkin), DJ-1 (PARK7), ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL-1), serine/threonine-protein kinase (PINK-1), leucine-rich repeat kinase 2 (LRRK2), cation-transporting ATPase 13A1 (ATP13A), etc.) contributed enormously to basic research towards understanding the role of these proteins in the sporadic form of the disease.
Mitochondria in the aetiology and pathogenesis of Parkinson's disease.
London, United Kingdom. In Lancet Neurol, 2008
The proteins that are associated with familial PD--PTEN-induced putative kinase 1 (PINK1), DJ-1, alpha-synuclein, leucine-rich repeat kinase 2, and, possibly, parkin--are either mitochondrial proteins or are associated with mitochondria, and all interface with the pathways of oxidative stress and free radical damage.
London, United Kingdom. In Lancet, 2006
Recently identified nuclear gene mutations of mitochondrial proteins include mutations of frataxin causing Friedreich's ataxia, PINK1, DJ1 causing Parkinson's disease and POLG causing infantile mtDNA depletion syndrome, ophthalmoplegia, parkinsonism, male subfertility and, in a transgenic mouse model, premature senescence.