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Items: 1 to 20 of 92

1.

Cellular inclusion bodies of mutant huntingtin exon 1 obscure small fibrillar aggregate species.

Sahl SJ, Weiss LE, Duim WC, Frydman J, Moerner WE.

Sci Rep. 2012;2:895. doi: 10.1038/srep00895. Epub 2012 Nov 28.

2.

14-3-3zeta is indispensable for aggregate formation of polyglutamine-expanded huntingtin protein.

Omi K, Hachiya NS, Tanaka M, Tokunaga K, Kaneko K.

Neurosci Lett. 2008 Jan 24;431(1):45-50. Epub 2007 Nov 17.

PMID:
18078716
3.

Mutant huntingtin promotes the fibrillogenesis of wild-type huntingtin: a potential mechanism for loss of huntingtin function in Huntington's disease.

Busch A, Engemann S, Lurz R, Okazawa H, Lehrach H, Wanker EE.

J Biol Chem. 2003 Oct 17;278(42):41452-61. Epub 2003 Jul 29.

4.

Super-resolution fluorescence of huntingtin reveals growth of globular species into short fibers and coexistence of distinct aggregates.

Duim WC, Jiang Y, Shen K, Frydman J, Moerner WE.

ACS Chem Biol. 2014 Dec 19;9(12):2767-78. doi: 10.1021/cb500335w. Epub 2014 Oct 20.

5.

Putting huntingtin "aggregation" in view with windows into the cellular milieu.

Hatters DM.

Curr Top Med Chem. 2012;12(22):2611-22. Review.

PMID:
23339311
6.

Quantitative relationships between huntingtin levels, polyglutamine length, inclusion body formation, and neuronal death provide novel insight into huntington's disease molecular pathogenesis.

Miller J, Arrasate M, Shaby BA, Mitra S, Masliah E, Finkbeiner S.

J Neurosci. 2010 Aug 4;30(31):10541-50. doi: 10.1523/JNEUROSCI.0146-10.2010.

7.

Serine phosphorylation suppresses huntingtin amyloid accumulation by altering protein aggregation properties.

Mishra R, Hoop CL, Kodali R, Sahoo B, van der Wel PC, Wetzel R.

J Mol Biol. 2012 Nov 23;424(1-2):1-14. doi: 10.1016/j.jmb.2012.09.011. Epub 2012 Sep 18.

8.

Suppression of mutant Huntingtin aggregate formation by Cdk5/p35 through the effect on microtubule stability.

Kaminosono S, Saito T, Oyama F, Ohshima T, Asada A, Nagai Y, Nukina N, Hisanaga S.

J Neurosci. 2008 Aug 27;28(35):8747-55. doi: 10.1523/JNEUROSCI.0973-08.2008.

9.

Accumulation of mutant huntingtin fragments in aggresome-like inclusion bodies as a result of insufficient protein degradation.

Waelter S, Boeddrich A, Lurz R, Scherzinger E, Lueder G, Lehrach H, Wanker EE.

Mol Biol Cell. 2001 May;12(5):1393-407.

10.

Tumor necrosis factor receptor-associated factor 6 (TRAF6) associates with huntingtin protein and promotes its atypical ubiquitination to enhance aggregate formation.

Zucchelli S, Marcuzzi F, Codrich M, Agostoni E, Vilotti S, Biagioli M, Pinto M, Carnemolla A, Santoro C, Gustincich S, Persichetti F.

J Biol Chem. 2011 Jul 15;286(28):25108-17. doi: 10.1074/jbc.M110.187591. Epub 2011 Mar 25.

11.

Protein aggregates in Huntington's disease.

Arrasate M, Finkbeiner S.

Exp Neurol. 2012 Nov;238(1):1-11. doi: 10.1016/j.expneurol.2011.12.013. Epub 2011 Dec 19. Review.

12.

Complex interplay between the length and composition of the huntingtin-derived peptides modulates the intracellular behavior of the N-terminal fragments of mutant huntingtin.

Milewski M, Gawliński P, Bąk D, Matysiak A, Bal J.

Eur J Cell Biol. 2015 May;94(5):179-89. doi: 10.1016/j.ejcb.2015.02.001. Epub 2015 Feb 20.

PMID:
25773959
13.

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death.

Arrasate M, Mitra S, Schweitzer ES, Segal MR, Finkbeiner S.

Nature. 2004 Oct 14;431(7010):805-10.

14.

Huntingtin disrupts lipid bilayers in a polyQ-length dependent manner.

Burke KA, Hensal KM, Umbaugh CS, Chaibva M, Legleiter J.

Biochim Biophys Acta. 2013 Aug;1828(8):1953-61. doi: 10.1016/j.bbamem.2013.04.025. Epub 2013 May 2.

15.

Huntington's Disease.

Finkbeiner S.

Cold Spring Harb Perspect Biol. 2011 Jun 1;3(6). pii: a007476. doi: 10.1101/cshperspect.a007476. Review.

16.

Dynamic recruitment of active proteasomes into polyglutamine initiated inclusion bodies.

Schipper-Krom S, Juenemann K, Jansen AH, Wiemhoefer A, van den Nieuwendijk R, Smith DL, Hink MA, Bates GP, Overkleeft H, Ovaa H, Reits E.

FEBS Lett. 2014 Jan 3;588(1):151-9. doi: 10.1016/j.febslet.2013.11.023. Epub 2013 Nov 26.

17.

Mutant huntingtin fragments form oligomers in a polyglutamine length-dependent manner in vitro and in vivo.

Legleiter J, Mitchell E, Lotz GP, Sapp E, Ng C, DiFiglia M, Thompson LM, Muchowski PJ.

J Biol Chem. 2010 May 7;285(19):14777-90. doi: 10.1074/jbc.M109.093708. Epub 2010 Mar 10.

18.

Folding Landscape of Mutant Huntingtin Exon1: Diffusible Multimers, Oligomers and Fibrils, and No Detectable Monomer.

Sahoo B, Arduini I, Drombosky KW, Kodali R, Sanders LH, Greenamyre JT, Wetzel R.

PLoS One. 2016 Jun 6;11(6):e0155747. doi: 10.1371/journal.pone.0155747. eCollection 2016.

20.

Soluble polyglutamine oligomers formed prior to inclusion body formation are cytotoxic.

Takahashi T, Kikuchi S, Katada S, Nagai Y, Nishizawa M, Onodera O.

Hum Mol Genet. 2008 Feb 1;17(3):345-56. Epub 2007 Oct 18.

PMID:
17947294

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