Model systems are important tools for the investigation of pathogenic processes. Especially
for diseases with a late onset of symptoms and slow progression, like most spinocerebellar
ataxias (SCA), it is time-consuming or even impossible to analyze all aspects of the
pathogenesis in humans.
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Mesenchymal stem cell transplantation ameliorates motor function deterioration of spinocerebellar ataxia by rescuing cerebellar Purkinje cells...
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Minireview cung cấp cho các bạn kiến thức về ngành y đề tài: Protein-protein interaction networks in the spinocerebellar ataxias...
Many risks that we face on a daily basis may be unavoidable, so there is an expectation
by individuals that the level of risk is being managed and reduced to safe levels
through evidence-based risk assessments and public health interventions. There has
been a growing recognition that risks need to be viewed in their public health context
to ensure that the most important risks are prioritized and addressed. Under a
broader public health imperative, risk assessments are used as an important process to
quantify the probability of harmful effects to individuals, sub-populations (eg.
The protein ataxin-3 is responsible for spinocerebellar ataxia type 3, a neu-rodegenerative disease triggered when the length of a stretch of consecutive
glutamines exceeds a critical threshold. Different physiologic roles have
been suggested for this protein. More specifically, recent papers have
shown that the highly conserved N-terminal Josephin domain of ataxin-3
binds ubiquitin and has ubiquitin hydrolase activity, thanks to a catalytic
device specific to cysteine proteases.
Spinocerebellar ataxia types 2 (SCA2) and 3 (SCA3) are
autosomal-dominantly inherited, neurodegenerative dis-eases caused by CAG repeat expansions in the coding
regions of the genes encoding ataxin-2 and ataxin-3,
respectively. To provide a rationale for further functional
experiments, we explored the proteinarchitectures of ataxin-2 and ataxin-3. Using structure-based multiple sequence
alignments of homologous proteins, we investigated
domains, sequence motifs, and interaction partners.