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Items: 1 to 20 of 63

1.

Cytoplasmic penetration and persistent infection of mammalian cells by polyglutamine aggregates.

Ren PH, Lauckner JE, Kachirskaia I, Heuser JE, Melki R, Kopito RR.

Nat Cell Biol. 2009 Feb;11(2):219-25. doi: 10.1038/ncb1830. Epub 2009 Jan 18.

2.

Differential activities of the ubiquitin-proteasome system in neurons versus glia may account for the preferential accumulation of misfolded proteins in neurons.

Tydlacka S, Wang CE, Wang X, Li S, Li XJ.

J Neurosci. 2008 Dec 3;28(49):13285-95. doi: 10.1523/JNEUROSCI.4393-08.2008.

3.

Expanded polyglutamine stretches form an 'aggresome'.

Shimohata T, Sato A, Burke JR, Strittmatter WJ, Tsuji S, Onodera O.

Neurosci Lett. 2002 May 3;323(3):215-8.

PMID:
11959423
4.

Polyglutamine-mediated aggregation and cell death.

de Cristofaro T, Affaitati A, Feliciello A, Avvedimento EV, Varrone S.

Biochem Biophys Res Commun. 2000 Jun 16;272(3):816-21.

PMID:
10860836
5.

Molecular morphology and toxicity of cytoplasmic prion protein aggregates in neuronal and non-neuronal cells.

Grenier C, Bissonnette C, Volkov L, Roucou X.

J Neurochem. 2006 Jun;97(5):1456-66.

6.
8.

[Identification and significance of a novel degradation system for polyglutamine aggregates].

Iwata A.

Rinsho Shinkeigaku. 2013;53(1):1-8. Review. Japanese.

PMID:
23328059
9.

Polyglutamine aggregation behavior in vitro supports a recruitment mechanism of cytotoxicity.

Chen S, Berthelier V, Yang W, Wetzel R.

J Mol Biol. 2001 Aug 3;311(1):173-82.

PMID:
11469866
10.

VCP/p97 in abnormal protein aggregates, cytoplasmic vacuoles, and cell death, phenotypes relevant to neurodegeneration.

Hirabayashi M, Inoue K, Tanaka K, Nakadate K, Ohsawa Y, Kamei Y, Popiel AH, Sinohara A, Iwamatsu A, Kimura Y, Uchiyama Y, Hori S, Kakizuka A.

Cell Death Differ. 2001 Oct;8(10):977-84.

11.

Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.

Sánchez I, Mahlke C, Yuan J.

Nature. 2003 Jan 23;421(6921):373-9.

PMID:
12540902
12.

Intranuclear degradation of polyglutamine aggregates by the ubiquitin-proteasome system.

Iwata A, Nagashima Y, Matsumoto L, Suzuki T, Yamanaka T, Date H, Deoka K, Nukina N, Tsuji S.

J Biol Chem. 2009 Apr 10;284(15):9796-803. doi: 10.1074/jbc.M809739200. Epub 2009 Feb 13.

13.

Polyglutamine and polyalanine expansions in ataxin7 result in different types of aggregation and levels of toxicity.

Latouche M, Fragner P, Martin E, El Hachimi KH, Zander C, Sittler A, Ruberg M, Brice A, Stevanin G.

Mol Cell Neurosci. 2006 Mar;31(3):438-45. Epub 2005 Dec 1.

PMID:
16325416
14.

Inhibition of 26S proteasome activity by huntingtin filaments but not inclusion bodies isolated from mouse and human brain.

Díaz-Hernández M, Valera AG, Morán MA, Gómez-Ramos P, Alvarez-Castelao B, Castaño JG, Hernández F, Lucas JJ.

J Neurochem. 2006 Sep;98(5):1585-96. Epub 2006 Jun 19.

15.

Cyclosporin-A-induced prion protein aggresomes are dynamic quality-control cellular compartments.

Ben-Gedalya T, Lyakhovetsky R, Yedidia Y, Bejerano-Sagie M, Kogan NM, Karpuj MV, Kaganovich D, Cohen E.

J Cell Sci. 2011 Jun 1;124(Pt 11):1891-902. doi: 10.1242/jcs.077693. Epub 2011 May 10.

16.

Toxic proteins in neurodegenerative disease.

Taylor JP, Hardy J, Fischbeck KH.

Science. 2002 Jun 14;296(5575):1991-5. Review.

PMID:
12065827
17.

Fibrillar structure and charge determine the interaction of polyglutamine protein aggregates with the cell surface.

Trevino RS, Lauckner JE, Sourigues Y, Pearce MM, Bousset L, Melki R, Kopito RR.

J Biol Chem. 2012 Aug 24;287(35):29722-8. doi: 10.1074/jbc.M112.372474. Epub 2012 Jun 29.

18.

The transcellular spread of cytosolic amyloids, prions, and prionoids.

Aguzzi A, Rajendran L.

Neuron. 2009 Dec 24;64(6):783-90. doi: 10.1016/j.neuron.2009.12.016. Review.

19.

[Can prion-like propagation occur in neurodegenerative diseases?: in view of transmissible systemic amyloidosis].

Yoshida K, Higuchi K, Ikeda S.

Brain Nerve. 2012 Jun;64(6):665-74. Review. Japanese.

PMID:
22647474
20.

Neuronal toxicity of expanded polyglutamine depends on intracellular distribution in addition to the expression level.

Satoh M, Shimada A, Kawamura N, Chiba Y, Yoshikawa K, Ishii S, Furukawa A, Kumagai N, Hosokawa M.

Neuropathology. 2008 Oct;28(5):485-96. doi: 10.1111/j.1440-1789.2008.00908.x. Epub 2008 Mar 31.

PMID:
18384512

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