Mutations in the parkin gene result in an autosomal recessive juvenile-onset form of Parkinson's disease. As an E3 ubiquitin-ligase, parkin promotes the attachment of ubiquitin onto specific substrate proteins. Defects in the ubiquitination of parkin substrates are therefore believed to lead to neurodegeneration in Parkinson's disease.
View Article and Find Full Text PDFA monoclonal antibody raised against adenovirus E1A-associated cellular proteins recognized Nek9, a NimA-related protein kinase. Subcellular fractionation and immunofluorescence indicated that Nek9 was primarily cytoplasmic with a small portion located in the nucleus whereas E1A was primarily nuclear. Although co-immunoprecipitation experiments indicated that nuclear Nek9 interacted, directly or indirectly, with E1A, the major effect of E1A was to diminish the amount of Nek9 in the nucleus suggesting that E1A alters the subcellular distribution of Nek9 and that the interaction is transient.
View Article and Find Full Text PDFBackground: The purpose of this study was to describe the functional status and quality of life (QOL) of patients at 12 months after injury.
Methods: Retrospective study consisting of patients treated at three tertiary trauma centers for injuries. Functional capacity (FC) was measured using the Sickness Impact Profile and QOL was measured using the Medical Outcomes Study Short Form (MOS SF-36) at approximately 12 months after the date of injury.