D. Edbauer

发表

Genetic modifications of the adeno-associated virus type 2 capsid reduce the affinity and the neutralizing effects of human serum antibodies

M. Hallek, J. Kleinschmidt, L. Perabò, 2003, Gene Therapy.

microRNA‐34c is a novel target to treat dementias

P. Falkai, L. Farinelli, A. Schmitt, 2011, The EMBO journal.

In Situ Structure of Neuronal C9orf72 Poly-GA Aggregates Reveals Proteasome Recruitment

W. Baumeister, F. Beck, Q. Guo, 2018, Cell.

C9ORF72 repeat expansions in mice cause TDP-43 pathology, neuronal loss, and behavioral deficits

Kevin F. Bieniek, L. Petrucelli, M. Murray, 2015, Science.

Loss of ALS-associated TDP-43 in zebrafish causes muscle degeneration, vascular dysfunction, and reduced motor neuron axon outgrowth

E. Kremmer, C. van Broeckhoven, M. Cruts, 2013, Proceedings of the National Academy of Sciences.

C9orf72 FTLD/ALS-associated Gly-Ala dipeptide repeat proteins cause neuronal toxicity and Unc119 sequestration

M. Mann, E. Kremmer, Daniel Hornburg, 2014, Acta Neuropathologica.

Insulin-degrading Enzyme Rapidly Removes the β-Amyloid Precursor Protein Intracellular Domain (AICD)*

C. Haass, D. Edbauer, M. Willem, 2002, The Journal of Biological Chemistry.

Presenilin-1 mutations of leucine 166 equally affect the generation of the Notch and APP intracellular domains independent of their effect on Aβ42 production

B. Ghetti, Hui Zheng, C. Haass, 2002, Proceedings of the National Academy of Sciences of the United States of America.

Identification of Distinct γ-Secretase Complexes with Different APH-1 Variants*

C. Haass, D. Edbauer, S. Prokop, 2004, Journal of Biological Chemistry.

Requirement of PEN-2 for Stabilization of the Presenilin N-/C-terminal Fragment Heterodimer within the γ-Secretase Complex*

C. Haass, D. Edbauer, S. Prokop, 2004, Journal of Biological Chemistry.

Co-expression of Nicastrin and Presenilin Rescues a Loss of Function Mutant of APH-1*

C. Haass, C. Kaether, D. Edbauer, 2004, Journal of Biological Chemistry.

Identification of distinct gamma-secretase complexes with different APH-1 variants.

C. Haass, D. Edbauer, S. Prokop, 2004, The Journal of biological chemistry.

Monomethylated and unmethylated FUS exhibit increased binding to Transportin and distinguish FTLD-FUS from ALS-FUS

E. Kremmer, T. Arzberger, I. Mackenzie, 2016, Acta Neuropathologica.

Active poly‐GA vaccination prevents microglia activation and motor deficits in a C9orf72 mouse model

H. Blum, T. Arzberger, C. Haass, 2019, EMBO molecular medicine.

Poly‐GP in cerebrospinal fluid links C9orf72‐associated dipeptide repeat expression to the asymptomatic phase of ALS/FTD

E. Kremmer, J. Kornhuber, B. Landwehrmeyer, 2017, EMBO molecular medicine.

Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD

Kevin F. Bieniek, B. Miller, C. Geula, 2019, Acta Neuropathologica.

PEN-2 Is an Integral Component of the γ-Secretase Complex Required for Coordinated Expression of Presenilin and Nicastrin*

Harald Steiner, Edith Winkler, Christian Haass, 2002, The Journal of Biological Chemistry.

Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins

E. Kremmer, C. Broeckhoven, M. Cruts, 2013, Acta Neuropathologica.

Good guy or bad guy: the opposing roles of microRNA 125b in cancer

D. Edbauer, Julia Banzhaf-Strathmann, 2014, Cell Communication and Signaling.

Clinico-genetic findings in 509 frontotemporal dementia patients

K. Fliessbach, H. Obrig, A. Winkler, 2021, Molecular Psychiatry.

FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations

A. Spottke, K. Fliessbach, A. Drzezga, 2019, Translational Psychiatry.

The C9orf72 repeat size correlates with onset age of disease, DNA methylation and transcriptional downregulation of the promoter

C. Broeckhoven, C. van Broeckhoven, S. Engelborghs, 2015, Molecular Psychiatry.

Dipeptide repeat protein pathology in C9ORF72 mutation cases: clinico-pathological correlations

S. Lorenzl, E. Kremmer, D. Troost, 2013, Acta Neuropathologica.

Loss of TMEM106B potentiates lysosomal and FTLD‐like pathology in progranulin‐deficient mice

W. Wurst, K. Wind, M. Damme, 2020, EMBO reports.

Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs

C. Heyser, L. Petrucelli, C. Shaw, 2016, Neuron.

C9ORF72 poly(GA) aggregates sequester and impair HR23 and nucleocytoplasmic transport proteins

L. Petrucelli, M. Murray, D. Dickson, 2016, Nature Neuroscience.

Nuclear Import Receptors Directly Bind to Arginine-Rich Dipeptide Repeat Proteins and Suppress Their Pathological Interactions

Sinem Usluer, T. Madl, J. Shorter, 2020, Cell reports.

Quantitative analysis and clinico-pathological correlations of different dipeptide repeat protein pathologies in C9ORF72 mutation carriers

L. Petrucelli, E. Kremmer, D. Troost, 2015, Acta Neuropathologica.

Dual Cleavage of Neuregulin 1 Type III by BACE1 and ADAM17 Liberates Its EGF-Like Domain and Allows Paracrine Signaling

E. Kremmer, C. Haass, D. Edbauer, 2013, The Journal of Neuroscience.

Drug screen in iPSC-Neurons identifies nucleoside analogs as inhibitors of (G4C2)n expression in C9orf72 ALS/FTD.

P. Heutink, T. Carell, Markus Müller, 2022, Cell reports.

Proteolytic Processing of Neuregulin 1 Type III by Three Intramembrane-cleaving Proteases

E. Kremmer, M. Rossner, C. Haass, 2015, The Journal of Biological Chemistry.

Novel antibodies reveal presynaptic localization of C9orf72 protein and reduced protein levels in C9orf72 mutation carriers

M. Oulad-Abdelghani, I. Mackenzie, J. Prudlo, 2018, Acta Neuropathologica Communications.

hnRNP A3 binds to GGGGCC repeats and is a constituent of p62-positive/TDP43-negative inclusions in the hippocampus of patients with C9orf72 mutations

C. Broeckhoven, M. Cruts, H. Kretzschmar, 2013, Acta Neuropathologica.

Novel clinical associations with specific C9ORF72 transcripts in patients with repeat expansions in C9ORF72

L. Petrucelli, R. Petersen, B. Boeve, 2015, Acta Neuropathologica.

Early dipeptide repeat pathology in a frontotemporal dementia kindred with C9ORF72 mutation and intellectual disability

I. Mackenzie, J. Rankin, D. Edbauer, 2014, Acta Neuropathologica.

Multi-omics profiling identifies a deregulated FUS-MAP1B axis in ALS/FTD–associated UBQLN2 mutants

J. Dengjel, Jochen H Weishaupt, E. Graf, 2022, Life Science Alliance.

The porphyrin TMPyP4 inhibits elongation during the noncanonical translation of the FTLD/ALS-associated GGGGCC repeat in the C9orf72 gene

S. Tagami, C. Haass, D. Edbauer, 2021, The Journal of biological chemistry.

Poly-glycine–alanine exacerbates C9orf72 repeat expansion-mediated DNA damage via sequestration of phosphorylated ATM and loss of nuclear hnRNPA3

T. Arzberger, C. Haass, Markus Weber, 2019, Acta Neuropathologica.

Glycine-alanine dipeptide repeat protein contributes to toxicity in a zebrafish model of C9orf72 associated neurodegeneration

K. Kawakami, C. Haass, D. Edbauer, 2017, Molecular Neurodegeneration.

Reduced hnRNPA3 increases C9orf72 repeat RNA levels and dipeptide‐repeat protein deposition

T. Arzberger, I. Mackenzie, C. Haass, 2016, EMBO reports.

Retraction Note to: A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

J. V. van Swieten, R. Willemsen, D. Edbauer, 2016, Acta Neuropathologica Communications.

A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

J. V. van Swieten, R. Willemsen, D. Edbauer, 2014, Acta neuropathologica communications.

The C9orf72 GGGGCC Repeat Is Translated into Aggregating Dipeptide-Repeat Proteins in FTLD/ALS

E. Kremmer, C. van Broeckhoven, M. Cruts, 2013, Science.

Three novel presenilin 1 mutations marking the wide spectrum of age at onset and clinical patterns in familial Alzheimer’s disease

A. Danek, H. Kretzschmar, T. Arzberger, 2015, Journal of neural transmission.

Targeting RNA G‐quadruplexes as new treatment strategy for C9orf72 ALS/FTD

D. Edbauer, Martin H. Schludi, 2017, EMBO molecular medicine.

RNA versus protein toxicity in C9orf72 ALS/FTLD

T. Arzberger, D. Edbauer, Martin H. Schludi, 2018, Acta Neuropathologica.

A perturbed network in neurodegeneration

D. Edbauer, J. Gallo, 2022, Science.

FUS-mediated alternative splicing in the nervous system: consequences for ALS and FTLD

D. Edbauer, Denise Orozco, 2013, Journal of Molecular Medicine.

Regulation of Synaptic Structure and Function by FMRP-Associated MicroRNAs miR-125 b and miR-132

P. Sharp, J. Neilson, M. Sheng, 2010 .

Loss of TREM2 function increases amyloid seeding but reduces plaque associated ApoE

D. Holtzman, M. Meyer-Luehmann, T. Arzberger, 2018, Nature Neuroscience.

Distinct Roles of NR2A and NR2B Cytoplasmic Tails in Long-Term Potentiation

M. Sheng, K. Foster, N. Mclaughlin, 2010, The Journal of Neuroscience.

Distinct Roles of NR 2 A and NR 2 B Cytoplasmic Tails in Long-Term Citation

M. Sheng, K. Foster, N. Mclaughlin, 2010 .

Molecular Distinct Roles of NR 2 A and NR 2 B Cytoplasmic Tails in Long-Term Potentiation

M. Sheng, K. Foster, N. Mclaughlin, 2010 .

Reconstitution of γ-secretase activity

J. Regula, C. Haass, D. Edbauer, 2003, Nature Cell Biology.

Good guy or bad guy: the opposing roles of microRNA 125b in cancer

D. Edbauer, Julia Banzhaf-Strathmann, 2014, Cell Communication and Signaling.

Regulation of Synaptic Structure and Function by FMRP-Associated MicroRNAs miR-125b and miR-132

P. Sharp, J. Neilson, M. Sheng, 2010, Neuron.

The FTLD risk factor TMEM106B and MAP6 control dendritic trafficking of lysosomes

C. Hoogenraad, C. Haass, D. Edbauer, 2013, The EMBO journal.

Presenilin-dependent Intramembrane Proteolysis of CD44 Leads to the Liberation of Its Intracellular Domain and the Secretion of an Aβ-like Peptide*

Harald Steiner, Masatoshi Takeda, Christian Haass, 2002, The Journal of Biological Chemistry.

MicroRNA-132 dysregulation in schizophrenia has implications for both neurodevelopment and adult brain function

B. H. Miller, R. Roth, Shibing Deng, 2012, Proceedings of the National Academy of Sciences.

ALS‐associated fused in sarcoma (FUS) mutations disrupt Transportin‐mediated nuclear import

I. Mackenzie, C. Haass, M. Neumann, 2010, The EMBO journal.

Loss of fused in sarcoma (FUS) promotes pathological Tau splicing

C. Haass, D. Edbauer, S. Tahirovic, 2012, EMBO reports.

Promoter DNA methylation regulates progranulin expression and is altered in FTLD

C. Plass, C. van Broeckhoven, S. Engelborghs, 2013, Acta neuropathologica communications.

Disease‐linked TDP‐43 hyperphosphorylation suppresses TDP‐43 condensation and aggregation

G. Hummer, V. Dötsch, D. Edbauer, 2022, The EMBO journal.

Disease‐linked TDP‐43 hyperphosphorylation suppresses TDP‐43 condensation and aggregation

G. Hummer, V. Dötsch, D. Edbauer, 2021, bioRxiv.

Cell‐to‐cell transmission of C9orf72 poly‐(Gly‐Ala) triggers key features of ALS/FTD

F. Hartl, T. Arzberger, F. Frottin, 2020, The EMBO journal.

TDP‐43 loss of function inhibits endosomal trafficking and alters trophic signaling in neurons

Daniel Hornburg, T. Arzberger, F. Meissner, 2016, The EMBO journal.

Sequestration of multiple RNA recognition motif-containing proteins by C9orf72 repeat expansions

Stuart A. Wilson, A. Higginbottom, S. Wharton, 2014, Brain : a journal of neurology.

Antibodies inhibit transmission and aggregation of C9orf72 poly‐GA dipeptide repeat proteins

T. Arzberger, C. Haass, D. Edbauer, 2017, EMBO molecular medicine.

miR-132, an experience-dependent microRNA, is essential for visual cortex plasticity.

M. Sur, S. Levine, H. Sugihara, 2011, Nature neuroscience.

Identification and Characterization of Neuronal Mitogen-activated Protein Kinase Substrates Using a Specific Phosphomotif Antibody*S⃞

M. Yaffe, M. Sheng, Chi-Fong Wang, 2009, Molecular & Cellular Proteomics.

Gel-like inclusions of C-terminal fragments of TDP-43 sequester and inhibit proteasomes in neurons

M. Mann, W. Baumeister, F. Hartl, 2021, bioRxiv.

A novel CHCHD10 mutation implicates a Mia40‐dependent mitochondrial import deficit in ALS

C. van Broeckhoven, M. Heneka, J. van der Zee, 2018, EMBO molecular medicine.

Congenic expression of poly-GA but not poly-PR in mice triggers selective neuron loss and interferon responses found in C9orf72 ALS

W. Wurst, W. Enard, T. Arzberger, 2020, Acta Neuropathologica.

Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing

E. Kremmer, T. Arzberger, D. Edbauer, 2015, Acta Neuropathologica.

Spinal poly-GA inclusions in a C9orf72 mouse model trigger motor deficits and inflammation without neuron loss

H. Fuchs, L. Petrucelli, T. Strom, 2017, Acta Neuropathologica.

Atrophy in the Thalamus But Not Cerebellum Is Specific for C9orf72 FTD and ALS Patients – An Atlas-Based Volumetric MRI Study

K. Fliessbach, H. Huppertz, A. Danek, 2018, Front. Aging Neurosci..

RNA-Dependent Intergenerational Inheritance of Enhanced Synaptic Plasticity after Environmental Enrichment

Cemil Kerimoglu, R. Stilling, D. Edbauer, 2017, bioRxiv.

Presenilin-1 affects trafficking and processing of βAPP and is targeted in a complex with nicastrin to the plasma membrane

J. Rietdorf, C. Haass, C. Kaether, 2002, The Journal of cell biology.

Presenilin and nicastrin regulate each other and determine amyloid β-peptide production via complex formation

C. Haass, D. Edbauer, H. Steiner, 2002, Proceedings of the National Academy of Sciences of the United States of America.

Membrane Orientation and Subcellular Localization of Transmembrane Protein 106B (TMEM106B), a Major Risk Factor for Frontotemporal Lobar Degeneration*♦

E. Kremmer, C. Haass, D. Edbauer, 2012, The Journal of Biological Chemistry.

MicroRNA‐125b induces tau hyperphosphorylation and cognitive deficits in Alzheimer's disease

Eva Benito, Thomas Arzberger, Stephanie May, 2014, The EMBO journal.

Reconstitution of gamma-secretase activity.

J. Regula, C. Haass, D. Edbauer, 2003, Nature cell biology.

Low-degree trisomy 21 mosaicism promotes early-onset Alzheimer disease

A. Danek, Georg S. Nuebling, A. Rominger, 2021, Neurobiology of Aging.

γ-Secretase Activity Is Associated with a Conformational Change of Nicastrin*

J. Schmitz, C. Haass, D. Edbauer, 2003, The Journal of Biological Chemistry.

The presenilin C‐terminus is required for ER‐retention, nicastrin‐binding and γ‐secretase activity

C. Haass, C. Kaether, D. Edbauer, 2004, The EMBO journal.

Synaptic dysfunction induced by glycine‐alanine dipeptides in C9orf72‐ALS/FTD is rescued by SV2 replenishment

D. Edbauer, Le Ma, K. Krishnamurthy, 2020, EMBO molecular medicine.

Cytoplasmic poly-GA aggregates impair nuclear import of TDP-43 in C9orf72 ALS/FTLD

D. Edbauer, S. May, D. Dormann, 2016, Human molecular genetics.

OP-HMGJ160421 790..800

D. Edbauer, S. May, D. Dormann, 2017 .

Cerebellar c9RAN proteins associate with clinical and neuropathological characteristics of C9ORF72 repeat expansion carriers

Kevin F. Bieniek, L. Petrucelli, R. Petersen, 2015, Acta Neuropathologica.

An amyloid-like cascade hypothesis for C9orf72 ALS/FTD

C. Haass, D. Edbauer, 2016, Current Opinion in Neurobiology.

Proteomics and C9orf72 neuropathology identify ribosomes as poly-GR/PR interactors driving toxicity

M. Mann, Daniel Hornburg, T. Arzberger, 2018, Life Science Alliance.

Gel‐like inclusions of C‐terminal fragments of TDP‐43 sequester stalled proteasomes in neurons

W. Baumeister, F. Meissner, Q. Guo, 2022, EMBO reports.

In Situ Structure of Neuronal C 9 orf 72 Poly-GA Aggregates Reveals Proteasome Recruitment Graphical

Florian Beck, Wolfgang Baumeister, Till Rudack, 2018 .

Staufen2 regulates neuronal target RNAs.

Q. Morris, M. Kiebler, Xiao Li, 2013, Cell reports.

A new inducible transgenic mouse model for C9orf72-associated GGGGCC repeat expansion supports a gain-of-function mechanism in C9orf72-associated ALS and FTD

J. V. van Swieten, R. Willemsen, D. Edbauer, 2014, Acta neuropathologica communications.

Knocking out C9ORF72 Exacerbates Axonal Trafficking Defects Associated with Hexanucleotide Repeat Expansion and Reduces Levels of Heat Shock Proteins

M. Bickle, S. Petri, D. Edbauer, 2020, Stem cell reports.

MicroRNA-125 b induces tau hyperphosphorylation and cognitive deficits in Alzheimer ’ s disease

H. Kretzschmar, T. Arzberger, D. Edbauer, 2014 .

Gain of Toxicity from ALS / F TD-Linked Repeat Expansions in C 9 ORF 72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs Highlights

C. Heyser, L. Petrucelli, C. Shaw, 2016 .

Role of Septin Cytoskeleton in Spine Morphogenesis and Dendrite Development in Neurons

M. Sheng, D. Edbauer, A. Simonetta, 2007, Current Biology.

Loss of TDP-43 causes ectopic endothelial sprouting and migration defects through increased fibronectin, vcam 1 and integrin α4/β1

S. Bonn, C. Haass, D. Edbauer, 2023, Frontiers in Cell and Developmental Biology.

Identi cation and temporal stability of conformational epitopes of autoantibodies against Myelin Oligodendrocyte Glycoprotein recognized by patients with di erent in ammatory central nervous system diseases

U. Schüller, R. Hohlfeld, L. Klein, 2014 .

The ER under rapid fire

D. Edbauer, Benjamin M. Schwenk, 2014, The EMBO journal.

Have you seen ? The ER under rapid fire

D. Edbauer, Benjamin M. Schwenk, 2014 .

Nicastrin Interacts with γ-Secretase Complex Components via the N-terminal Part of Its Transmembrane Domain*

C. Haass, C. Kaether, D. Edbauer, 2003, Journal of Biological Chemistry.

Immature nicastrin stabilizes APH‐1 independent of PEN‐2 and presenilin: identification of nicastrin mutants that selectively interact with APH‐1

Harald Steiner, Christian Haass, C. Haass, 2004, Journal of neurochemistry.

C9orf72 protein quality control by UBR5‐mediated heterotypic ubiquitin chains

C. Behrends, D. Edbauer, Julia Jülg, 2023, EMBO reports.

Erratum to: Distribution of dipeptide repeat proteins in cellular models and C9orf72 mutation cases suggests link to transcriptional silencing

E. Kremmer, T. Arzberger, D. Edbauer, 2015, Acta Neuropathologica.

Multiomic ALS signatures highlight sex differences and molecular subclusters and identify the MAPK pathway as therapeutic target

H. Rehrauer, R. Schlapbach, M. Sturm, 2023, bioRxiv.

Rescue of FTLD-associated TDP-43 pathology and neurodegeneration by peripheral AAV-mediated expression of brain-penetrant progranulin

T. Sandmann, M. Simon, C. Haass, 2023, bioRxiv.

Multimodal and Longitudinal Bioimaging Methods for Characterizing the Progressive Course of Dementia

K. Fliessbach, B. Landwehrmeyer, M. Schroeter, 2019, Frontiers Research Topics.

Targeting the glycine-rich domain of TDP-43 with antibodies prevents its aggregation in vitro and reduces neurofilament levels in vivo

T. Arzberger, J. Herms, A. Schepers, 2023, Acta Neuropathologica Communications.

Chronic T cell proliferation in brains after stroke could interfere with the efficacy of immunotherapies

T. Hortobágyi, T. Arzberger, P. Nelson, 2021, The Journal of experimental medicine.

FUS-mediated alternative splicing in the nervous system: consequences for ALS and FTLD

D. Edbauer, Denise Orozco, 2013, Journal of Molecular Medicine.

microRNA‐34c is a novel target to treat dementias

P. Falkai, L. Farinelli, A. Schmitt, 2011, The EMBO journal.

miR-132, an experience-dependent microRNA, is essential for visual cortex plasticity

M. Sur, S. Levine, H. Sugihara, 2011, Nature Neuroscience.

Gain of Toxicity from ALS/FTD-Linked Repeat Expansions in C9ORF72 Is Alleviated by Antisense Oligonucleotides Targeting GGGGCC-Containing RNAs

C. Heyser, L. Petrucelli, F. Rigo, 2016, Neuron.

Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD

C. Geula, M. Mesulam, J. Grafman, 2019, Acta Neuropathologica.

Enhanced legumain activity links progranulin deficiency to TDP-43 pathology in frontotemporal lobar degeneration

M. Damme, D. Edbauer, C. Broeckhoven, 2024, bioRxiv.

Presenilin-1 affects trafficking and processing of βAPP and is targeted in a complex with nicastrin to the plasma membrane

J. Rietdorf, C. Haass, C. Kaether, 2002, The Journal of cell biology.