Molecular determinants of the aggregation behavior of α- and β-synuclein
نویسندگان
چکیده
منابع مشابه
The Aggregation of Huntingtin and α-Synuclein
Huntington's and Parkinson's diseases are neurodegenerative disorders associated with unusual protein interactions. Although the origin and evolution of these diseases are completely different, characteristic deposits of protein aggregates (huntingtin and α-synuclein resp.), are a common feature in both diseases. After these observations, many studies are performed with both proteins. Some of t...
متن کاملUnveiling a Selective Mechanism for the Inhibition of α-Synuclein Aggregation by β-Synuclein
α-Synuclein (αS) is an intrinsically disordered protein that is associated with Parkinson's disease (PD) through its ability to self-assemble into oligomers and fibrils. Inhibition of this oligomerization cascade is an interesting approach to developing therapeutical strategies and β-synuclein (βS) has been described as a natural negative regulator of this process. However, the biological backg...
متن کاملan inverstigation into the shrinkage behavior (kinetics) of microfilled hybrid and nano dental composites
چکیده ندارد.
15 صفحه اولA Relationship between the Transient Structure in the Monomeric State and the Aggregation Propensities of α-Synuclein and β-Synuclein
α-Synuclein is an intrinsically disordered protein whose aggregation is implicated in Parkinson's disease. A second member of the synuclein family, β-synuclein, shares significant sequence similarity with α-synuclein but is much more resistant to aggregation. β-Synuclein is missing an 11-residue stretch in the central non-β-amyloid component region that forms the core of α-synuclein amyloid fib...
متن کاملSIRT1 protects against α-synuclein aggregation by activating molecular chaperones.
α-Synuclein is a key molecule in the pathogenesis of synucleinopathy including dementia with Lewy bodies, Parkinson's disease, and multiple system atrophy. Sirtuins are NAD(+)-dependent protein deacetylases that are highly conserved and counter aging in lower organisms. We show that the life span of a mouse model with A53T α-synuclein mutation is increased by overexpressing SIRT1 and decreased ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Protein Science
سال: 2008
ISSN: 0961-8368
DOI: 10.1110/ps.073181508