Luth ES - Search Results

1

Parkinson-causing α-synuclein missense mutations shift native tetramers to monomers as a mechanism for disease initiation.

Dettmer U, Newman AJ, Soldner F, Luth ES, Kim NC, von Saucken VE, Sanderson JB, Jaenisch R, Bartels T, Selkoe D. Dettmer U, et al. Among authors: luth es. Nat Commun. 2015 Jun 16;6:7314. doi: 10.1038/ncomms8314. Nat Commun. 2015. PMID: 26076669 Free PMC article.

2

Defining the native state of α-synuclein.

Selkoe D, Dettmer U, Luth E, Kim N, Newman A, Bartels T. Selkoe D, et al. Neurodegener Dis. 2014;13(2-3):114-7. doi: 10.1159/000355516. Epub 2013 Oct 30. Neurodegener Dis. 2014. PMID: 24192542 Review.

3

In vivo cross-linking reveals principally oligomeric forms of α-synuclein and β-synuclein in neurons and non-neural cells.

Dettmer U, Newman AJ, Luth ES, Bartels T, Selkoe D. Dettmer U, et al. Among authors: luth es. J Biol Chem. 2013 Mar 1;288(9):6371-85. doi: 10.1074/jbc.M112.403311. Epub 2013 Jan 14. J Biol Chem. 2013. PMID: 23319586 Free PMC article.

4

Purification of α-synuclein from human brain reveals an instability of endogenous multimers as the protein approaches purity.

Luth ES, Bartels T, Dettmer U, Kim NC, Selkoe DJ. Luth ES, et al. Biochemistry. 2015 Jan 20;54(2):279-92. doi: 10.1021/bi501188a. Epub 2014 Dec 23. Biochemistry. 2015. PMID: 25490121 Free PMC article.

5

Corrigendum: Parkinson-causing α-synuclein missense mutations shift native tetramers to monomers as a mechanism for disease initiation.

Dettmer U, Newman AJ, Soldner F, Luth ES, Kim NC, von Saucken VE, Sanderson JB, Jaenisch R, Bartels T, Selkoe D. Dettmer U, et al. Among authors: luth es. Nat Commun. 2015 Jul 30;6:8008. doi: 10.1038/ncomms9008. Nat Commun. 2015. PMID: 26224447 Free PMC article. No abstract available.

6

Soluble, prefibrillar α-synuclein oligomers promote complex I-dependent, Ca2+-induced mitochondrial dysfunction.

Luth ES, Stavrovskaya IG, Bartels T, Kristal BS, Selkoe DJ. Luth ES, et al. J Biol Chem. 2014 Aug 1;289(31):21490-507. doi: 10.1074/jbc.M113.545749. Epub 2014 Jun 18. J Biol Chem. 2014. PMID: 24942732 Free PMC article.

7

N-alpha-acetylation of α-synuclein increases its helical folding propensity, GM1 binding specificity and resistance to aggregation.

Bartels T, Kim NC, Luth ES, Selkoe DJ. Bartels T, et al. Among authors: luth es. PLoS One. 2014 Jul 30;9(7):e103727. doi: 10.1371/journal.pone.0103727. eCollection 2014. PLoS One. 2014. PMID: 25075858 Free PMC article.

8

Biochemical and functional interaction of disrupted-in-schizophrenia 1 and amyloid precursor protein regulates neuronal migration during mammalian cortical development.

Young-Pearse TL, Suth S, Luth ES, Sawa A, Selkoe DJ. Young-Pearse TL, et al. Among authors: luth es. J Neurosci. 2010 Aug 4;30(31):10431-40. doi: 10.1523/JNEUROSCI.1445-10.2010. J Neurosci. 2010. PMID: 20685985 Free PMC article.

9

Measuring Mitochondrial Dysfunction Caused by Soluble α-Synuclein Oligomers.

Luth ES, Stavrovskaya IG. Luth ES, et al. Methods Mol Biol. 2019;1948:183-198. doi: 10.1007/978-1-4939-9124-2_14. Methods Mol Biol. 2019. PMID: 30771178

10

The WD40-Repeat Protein WDR-20 and the Deubiquitinating Enzyme USP-46 Promote Cell Surface Levels of Glutamate Receptors.

Hodul M, Rennich BJ, Luth ES, Dahlberg CL, Juo P. Hodul M, et al. Among authors: luth es. J Neurosci. 2021 Apr 7;41(14):3082-3093. doi: 10.1523/JNEUROSCI.1074-20.2021. Epub 2021 Feb 23. J Neurosci. 2021. PMID: 33622778 Free PMC article.

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