PuSH - Publication Server of Helmholtz Zentrum München

19 Records found.
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1.
van Well, E.M.* et al.: A protein quality control pathway regulated by linear ubiquitination. EMBO J. 38:e100730 (2019)
2.
Weber, A.* et al.: Epigenome-wide DNA methylation profiling in Progressive Supranuclear Palsy reveals major changes at DLX1. Nat. Commun. 9:2929 (2018)
3.
Kleinberger, G.* et al.: The FTD-like syndrome causing TREM2 T66M mutation impairs microglia function, brain perfusion, and glucose metabolism. EMBO J., accepted (2017)
4.
Lehmer, C.* et al.: Poly-GP in cerebrospinal fluid links C9orf72-associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD. EMBO Mol. Med. 9, 859-868 (2017)
5.
Schludi, M.H.* et al.: Spinal poly-GA inclusions in a C9orf72 mouse model trigger motor deficits and inflammation without neuron loss. Acta Neuropathol. 134, 241–254 (2017)
6.
Zhou, Q.* et al.: Antibodies inhibit transmission and aggregation of C9orf72 poly-GA dipeptide repeat proteins. EMBO Mol. Med. 9, 687-702 (2017)
7.
Kretner, B.* et al.: Generation and deposition of Aβ43 by the virtually inactive presenilin-1 L435F mutant contradicts the presenilin loss-of-function hypothesis of Alzheimer's disease. EMBO Mol. Med. 8, 458-465 (2016)
8.
Müller, S.H.* et al.: Genome-wide association study in essential tremor identifies three new loci. Brain 139, 3163-3169 (2016)
9.
Suárez-Calvet, M.* et al.: Monomethylated and unmethylated FUS exhibit increased binding to Transportin and distinguish FTLD-FUS from ALS-FUS. Acta Neuropathol. 131, 587-604 (2016)
10.
Schludi, M.H.* et al.: Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing. Acta Neuropathol. 130, 537-555 (2015)
11.
Schludi, M.H.* et al.: Erratum to: Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing. Acta Neuropathol. 130, 557-558 (2015)
12.
Schulte, E.C. et al.: Rare variants in β-Amyloid Precursor Protein (APP) and Parkinson's disease. Eur. J. Hum. Genet. 23, 1328-1333 (2015)
13.
Arzberger, T.* et al.: Neuropathological alterations in ftd cases with c9orf72 mutation - new insights. Eur. Psych. 29:EPA-1718 (2014)
14.
Götzl, J.K.* et al.: Common pathobiochemical hallmarks of progranulin-associated frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis. Acta Neuropathol. 127, 845-860 (2014)
15.
May, S.* et al.: C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration. Acta Neuropathol. 128, 485-503 (2014)
16.
Mackenzie, I.R.* et al.: Dipeptide repeat protein pathology in C9ORF72 mutation cases: Clinico-pathological correlations. Acta Neuropathol. 126, 859-879 (2013)
17.
Mori, K.* et al.: The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS. Science 339, 1335-1338 (2013)
18.
Mori, K.* et al.: Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins. Acta Neuropathol. 126, 881-893 (2013)
19.
Roeber, S.* et al.: Evidence for a pathogenic role of different mutations at codon 188 of PRNP. PLoS ONE 3:e2147 (2008)