Results 181 to 190 of about 1,549,882 (213)
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Mapping the interactions between prion protein (PrPC) and prion protein fibrils (PrPSc)
Biophysical Journal, 2023Alyssa M. Thallemer +2 more
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Current Neurovascular Research, 2009
In the variant form of Creutzfeldt-Jakob disease (vCJD), 'florid' deposits of the protease resistant form of prion protein (PrP(sc)) were aggregated around the cerebral blood vessels suggesting the possibility that prions may spread into the brain via the cerebral microcirculation.
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In the variant form of Creutzfeldt-Jakob disease (vCJD), 'florid' deposits of the protease resistant form of prion protein (PrP(sc)) were aggregated around the cerebral blood vessels suggesting the possibility that prions may spread into the brain via the cerebral microcirculation.
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2004
Main histopathological hallmarks of TSEs are severe spongiosis, gliosis and brain tissue deposition of an abnormal isoform (PrPSc or PrPres) of the normal cellular prion protein (PrPC or PrPsen). Despite identical primary sequences, PrPC and PrPSc isoforms differ in their tertiary structures [1] and as a consequence, they exhibit distinct ...
Gregory J. Raymond, Joëlle Chabry
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Main histopathological hallmarks of TSEs are severe spongiosis, gliosis and brain tissue deposition of an abnormal isoform (PrPSc or PrPres) of the normal cellular prion protein (PrPC or PrPsen). Despite identical primary sequences, PrPC and PrPSc isoforms differ in their tertiary structures [1] and as a consequence, they exhibit distinct ...
Gregory J. Raymond, Joëlle Chabry
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2013
Transmissible spongiform encephalopathies (TSEs) are a group of fatal, neurodegenerative diseases that can affect both humans and animals. TSEs can be sporadic, familial, or acquired diseases. The prion hypothesis states that a misfolded form of the host glycoprotein, PrPC, acts as the infectious agent in TSE disease.
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Transmissible spongiform encephalopathies (TSEs) are a group of fatal, neurodegenerative diseases that can affect both humans and animals. TSEs can be sporadic, familial, or acquired diseases. The prion hypothesis states that a misfolded form of the host glycoprotein, PrPC, acts as the infectious agent in TSE disease.
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PRPSC replication, protein folding and misfolding
Neurobiology of Aging, 2000openaire +1 more source
The Effect of Plasminogen-Derived Peptides to PrPSc Formation
International Journal of Peptide Research and Therapeutics, 2022Sungeun Lee +2 more
exaly
Crossing the Species Barrier by PrPSc Replication In Vitro Generates Unique Infectious Prions
Cell, 2008Paula Saa +2 more
exaly
A PROCESS FOR ISOLATION AND PURIFICATION OF A TARGET PROTEIN FREE OF PRION PROTEIN (PRPSC)
2009GILLJAM GUSTAV +3 more
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Infectivity-associated PrPSc and disease duration-associated PrPSc of mouse BSE prions
Prion, 2015Kohtaro Miyazawa, Kentaro Masujin
exaly