On Prions, Proteasomes, and Mad Cows  

Oleh:

Goldberg, Alfred L.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The New England Journal of Medicine (keterangan: ada di Proquest) vol. 357 no. 11 (Sep. 2007), page 1150.

Ketersediaan

Perpustakaan FK Nomor Panggil: N08.K.2007.05 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

All cells have the capacity to selectively degrade misfolded intracellular proteins, which, if they accumulated, could interfere with normal function and could be toxic. Such proteins may arise by mutation, errors in gene expression, failure to fold correctly, spontaneous denaturation, or postsynthetic damage (for example, by oxygen radicals). How often such events occur in cells is uncertain, largely because the ubiquitin–proteasome pathway rapidly degrades such aberrant proteins, including those that cause various inherited diseases, such as cystic fibrosis and certain hemoglobinopathies.1 This pathway also protects against neurodegenerative diseases.1,2 The hallmarks of amyotrophic lateral sclerosis, Parkinson's disease, Lewy-body dementia, Huntington's disease, . . .

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