|1.||Fernandez-Funez, Pedro: 1 article (11/2013)|
|2.||Rincon-Limas, Diego E: 1 article (11/2013)|
|3.||Jensen, Kurt: 1 article (11/2013)|
|4.||Sanchez-Garcia, Jonatan: 1 article (11/2013)|
|5.||Arbelaez, Daniela: 1 article (11/2013)|
|6.||Hamdan, Shyma: 1 article (01/2013)|
|7.||Asante, Emmanuel A: 1 article (01/2013)|
|8.||Jakubcova, Tatiana: 1 article (01/2013)|
|9.||Powell, Caroline: 1 article (01/2013)|
|10.||Tomlinson, Andrew: 1 article (01/2013)|
|1.||Prion Diseases (Transmissible Spongiform Encephalopathies)
11/01/2013 - "These results uncover a new role for the hydrophobic domain in promoting oxidative folding and preventing the formation of neurotoxic Ctm PrP, mechanisms that may be relevant in the pathogenesis of both inherited and sporadic prion diseases. "
01/01/2013 - "We conclude that GSS A117V is indeed a prion disease although the relative contributions of (Ctm)PrP and prion propagation in neurodegeneration and their pathogenetic interaction remains to be established."
03/12/2010 - "Interestingly, the mutant G113V, corresponding to a hereditary form of prion disease in humans, displayed increased (Ctm)PrP topology and decreased alpha-cleavage in our in vitro assay. "
03/12/2010 - "A mutation in HC is associated with prion disease resulting in an enhanced formation of a transmembrane form ((Ctm)PrP), which has thus been postulated to be a neurotoxic molecule besides PrP(Sc). "
04/15/2007 - "Based on recent experimental evidences of the transmission of prion diseases due to a particular transmembrane form (termed (Ctm)PrP), we propose a theoretical model for the molecular mechanism of such conformational diseases, in which a misfolded (Ctm)PrP induces a similar misfolding of another (Ctm)PrP. "
|2.||Neurodegenerative Diseases (Neurodegenerative Disease)
11/01/2002 - "These results delineate the sequence of events involved in PrP biogenesis, explain the mechanism of action of (Ctm)PrP-favoring mutations associated with neurodegenerative disease, and more generally, reveal that translocation substrates can be cotranslationally partitioned into multiple populations at the translocon."
07/13/2001 - "Increased generation of (Ctm)PrP in either transgenic mice or humans is associated with the development of neurodegenerative disease. "