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1.
Frick, P.* et al.: Novel antibodies reveal presynaptic localization of C9orf72 protein and reduced protein levels in C9orf72 mutation carriers. Acta Neuropathol. Commun. 6:72 (2018)
2.
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)
3.
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)
4.
Zhou, Q.* et al.: Antibodies inhibit transmission and aggregation of C9orf72 poly-GA dipeptide repeat proteins. EMBO Mol. Med. 9, 687-702 (2017)
5.
Fleck, D.* et al.: Proteolytic processing of Neuregulin 1 type III by three intramembrane cleaving proteases. J. Biol. Chem. 291, 318-333 (2016)
6.
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)
7.
Mackenzie, I.R.* et al.: Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers. Acta Neuropathol. 130, 845-861 (2015)
8.
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)
9.
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)
10.
Arzberger, T.* et al.: Neuropathological alterations in ftd cases with c9orf72 mutation - new insights. Eur. Psych. 29:EPA-1718 (2014)
11.
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)
12.
Fleck, D.* et al.: Dual cleavage of neuregulin 1 type III by BACE1 and ADAM17 liberates its EGF-like domain and allows paracrine signaling. J. Neurosci. 33, 7856-7869 (2013)
13.
Mackenzie, I.R.* et al.: Dipeptide repeat protein pathology in C9ORF72 mutation cases: Clinico-pathological correlations. Acta Neuropathol. 126, 859-879 (2013)
14.
Mori, K.* et al.: The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS. Science 339, 1335-1338 (2013)
15.
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)
16.
Schmid, B.* et al.: Loss of ALS-associated TDP-43 in zebrafish causes muscle degeneration, vascular dysfunction, and reduced motor neuron axon outgrowth. Proc. Natl. Acad. Sci. U.S.A. 110, 4986-4991 (2013)
17.
Lang, C.M.* et al.: Membrane orientation and subcellular localization of transmembrane protein 106B (TMEM106B), a major risk factor for frontotemporal lobar degeneration. J. Biol. Chem. 287, 19355-19365 (2012)