List of works - Max Koppers

A large genome scan for rare CNVs in amyotrophic lateral sclerosis

scientific article

ALS-associated mutations in FUS disrupt the axonal distribution and function of SMN.

scientific article published on 15 May 2013

Angiogenin variants in Parkinson disease and amyotrophic lateral sclerosis

scientific article published on December 2011

C9orf72 ablation in mice does not cause motor neuron degeneration or motor deficits

scientific article published on 5 June 2015

C9orf72 and UNC13A are shared risk loci for amyotrophic lateral sclerosis and frontotemporal dementia: a genome-wide meta-analysis

scientific article

CGG-repeat expansion in FMR1 is not associated with amyotrophic lateral sclerosis

scientific article published on 15 April 2012

Comparative interactomics analysis of different ALS-associated proteins identifies converging molecular pathways

scientific article published on 10 May 2016

ER - lysosome contacts at a pre-axonal region regulate axonal lysosome availability

scientific article published on 23 July 2021

Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis

scientific article published on 25 July 2016

Late Endosomes Act as mRNA Translation Platforms and Sustain Mitochondria in Axons

scientific article published on 03 January 2019

Molecular control of local translation in axon development and maintenance

scientific article published on 14 March 2018

Mutations in the profilin 1 gene cause familial amyotrophic lateral sclerosis

scientific article

NIPA1 polyalanine repeat expansions are associated with amyotrophic lateral sclerosis

scientific article published on 28 February 2012

Protein aggregation in amyotrophic lateral sclerosis.

scientific article published on 15 May 2013

Receptor-specific interactome as a hub for rapid cue-induced selective translation in axons

scientific article published on 20 November 2019

Screening for rare variants in the coding region of ALS-associated genes at 9p21.2 and 19p13.3.

scientific article published on 8 November 2012

UNC13A is a modifier of survival in amyotrophic lateral sclerosis

scientific article published on 25 November 2011

VAPB and C9orf72 mutations in 1 familial amyotrophic lateral sclerosis patient

scientific article published on 09 August 2012

VCP mutations in familial and sporadic amyotrophic lateral sclerosis

scientific article published on 10 November 2011

List of works by Max Koppers

A large genome scan for rare CNVs in amyotrophic lateral sclerosis

ALS-associated mutations in FUS disrupt the axonal distribution and function of SMN.

Angiogenin variants in Parkinson disease and amyotrophic lateral sclerosis

C9orf72 ablation in mice does not cause motor neuron degeneration or motor deficits

C9orf72 and UNC13A are shared risk loci for amyotrophic lateral sclerosis and frontotemporal dementia: a genome-wide meta-analysis

CGG-repeat expansion in FMR1 is not associated with amyotrophic lateral sclerosis

Comparative interactomics analysis of different ALS-associated proteins identifies converging molecular pathways

ER - lysosome contacts at a pre-axonal region regulate axonal lysosome availability

Genome-wide association analyses identify new risk variants and the genetic architecture of amyotrophic lateral sclerosis

Late Endosomes Act as mRNA Translation Platforms and Sustain Mitochondria in Axons

Molecular control of local translation in axon development and maintenance

Mutations in the profilin 1 gene cause familial amyotrophic lateral sclerosis

NIPA1 polyalanine repeat expansions are associated with amyotrophic lateral sclerosis

Protein aggregation in amyotrophic lateral sclerosis.

Receptor-specific interactome as a hub for rapid cue-induced selective translation in axons

Screening for rare variants in the coding region of ALS-associated genes at 9p21.2 and 19p13.3.

UNC13A is a modifier of survival in amyotrophic lateral sclerosis

VAPB and C9orf72 mutations in 1 familial amyotrophic lateral sclerosis patient

VCP mutations in familial and sporadic amyotrophic lateral sclerosis