PuSH - Publication Server of Helmholtz Zentrum München

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1.
Götzl, J.K.* et al.: Opposite microglial activation stages upon loss of PGRN or TREM2 result in reduced cerebral glucose metabolism. EMBO Mol. Med. 11, e9711 (2019)
2.
van Well, E.M.* et al.: A protein quality control pathway regulated by linear ubiquitination. EMBO J. 38:e100730 (2019)
3.
Xiang, X.* et al.: The Trem2 R47H Alzheimer's risk variant impairs splicing and reduces Trem2 mRNA and protein in mice but not in humans. Mol. Neurodegener. 13:49 (2018)
4.
Kleinberger, G.* et al.: The FTD-like syndrome causing TREM2 T66M mutation impairs microglia function, brain perfusion, and glucose metabolism. EMBO J., accepted (2017)
5.
Mazaheri, F.* et al.: TREM2 deficiency impairs chemotaxis and microglial responses to neuronal injury. EMBO Rep. 18, 1186-1198 (2017)
6.
Schlepckow, K.* et al.: An Alzheimer-associated TREM2 variant occurs at the ADAM cleavage site and affects shedding and phagocytic function. EMBO Mol. Med. 9, 1356-1365 (2017)
7.
Zhou, Q.* et al.: Antibodies inhibit transmission and aggregation of C9orf72 poly-GA dipeptide repeat proteins. EMBO Mol. Med. 9, 687-702 (2017)
8.
Fleck, D.* et al.: Proteolytic processing of Neuregulin 1 type III by three intramembrane cleaving proteases. J. Biol. Chem. 291, 318-333 (2016)
9.
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)
10.
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)
11.
Xiang, X.* et al.: TREM2 deficiency reduces the efficacy of immunotherapeutic amyloid clearance. EMBO Mol. Med. 8, 992-1004 (2016)
12.
Xiang, X.* et al.: TREM2-deficiency reduces the efficacy of immunotherapeutic amyloid clearance. J. Neurochem. 138, 1, 422-422 (2016)
13.
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)
14.
Solchenberger, B.* ; Russell, C.* ; Kremmer, E. ; Haass, C.* & Schmid, B.*: Granulin knock out zebrafish lack frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis pathology. PLoS ONE 10:e0118956 (2015)
15.
Willem, M.* et al.: η-secretase processing of APP inhibits neuronal activity in the hippocampus. Nature 526, 443-447 (2015)
16.
Götzl, J.K.* et al.: Common pathobiochemical hallmarks of progranulin-associated frontotemporal lobar degeneration and neuronal ceroid lipofuscinosis. Acta Neuropathol. 127, 845-860 (2014)
17.
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)
18.
Mackenzie, I.R.* et al.: Dipeptide repeat protein pathology in C9ORF72 mutation cases: Clinico-pathological correlations. Acta Neuropathol. 126, 859-879 (2013)
19.
Mori, K.* et al.: The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS. Science 339, 1335-1338 (2013)
20.
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)