GPMDB00245OtherHornburg D, et al.InstrumentNot AvailableNot availableMus_musculus_viruses, Mousemmann@biochem.mpg.de25193168Max Planck Institute of Biochemistry, Germany, et al.http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003425http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003403http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003404http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003423http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003424http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003402http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003429http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003407http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003408http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003405http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003406http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003428http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003421http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003422http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003444http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003420http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003409http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003414http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003415http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003412http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003457http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003413http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003419http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003416http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003417http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003410http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003411http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003430Not availableGPMDBThe fatal neurodegenerative disorders amyotrophic lateral sclerosis and spinal muscular atrophy are, respectively, the most common motoneuron disease and genetic cause of infant death. Various in vitro model systems have been established to investigate motoneuron disease mechanisms, in particular immortalized cell lines and primary neurons. Using quantitative mass-spectrometry-based proteomics, we compared the proteomes of primary motoneurons to motoneuron-like cell lines NSC-34 and N2a, as well as to non-neuronal control cells, at a depth of 10,000 proteins. We used this resource to evaluate the suitability of murine in vitro model systems for cell biological and biochemical analysis of motoneuron disease mechanisms. Individual protein and pathway analysis indicated substantial differences between motoneuron-like cell lines and primary motoneurons, especially for proteins involved in differentiation, cytoskeleton, and receptor signaling, whereas common metabolic pathways were more similar. The proteins associated with amyotrophic lateral sclerosis also showed distinct differences between cell lines and primary motoneurons, providing a molecular basis for understanding fundamental alterations between cell lines and neurons with respect to neuronal pathways with relevance for disease mechanisms. Our study provides a proteomics resource for motoneuron research and presents a paradigm of how mass-spectrometry-based proteomics can be used to evaluate disease model systems.Deep proteomic evaluation of primary and cell line motoneuron disease models delineates major differences in neuronal characteristics.Hornburg Daniel D,Drepper Carsten C,Butter Falk F,Meissner Felix F,Sendtner Michael M,Mann Matthias M,Hornburg Daniel D, Drepper Carsten C, Butter Falk F, Meissner Felix F, Sendtner Michael M, Mann Matthias Manterior horn cell, deep, human disease, Diseases., Line, Cell Lines, Homo sapiens disease, cell line cell, cell_line, motor neuron, motoneuron, Cell, cell line, LinesBCD541, AA003644, GEMIN1, PLXN5, mol, Gehrigs Disease, Sclerosis, Nerve, number, Nl1, Amyotrophic Lateral Sclerosis, AA009236, PLEXIN-B1, motoneuron, Spectrum Analyses, IPOA, presence, SeP, Charcot Disease, NSC, bulbar, SMA, CEH, Line, Mass, Gene Products, NEPII, NL1, NL2, SMN, motor neuron, Analysis, SEH, Lou Gehrig's disease, Mass Spectroscopy, LOU GEHRIGS DIS, SEP, Gehrig Disease, Mass Spectrum Analysis, neural stem cell, ALS (Amyotrophic Lateral Sclerosis), human disease, Motor neuron disease, Guam Disease, Lou-Gehrigs, Infant, reference sample, Analyses, cell, GEHRIGS DIS, Guam Form of Amyotrophic Lateral Sclerosis, cell line cell, proteins, Lateral Scleroses, Deaths, cell line, sEP, anterior horn cell, Parkinsonism Dementia Complex of Guam, Amyotrophic lateral sclerosis, SOD, SELP, Homo sapiens disease, Neuron, Nerve Cell, Lou Gehrig Disease, Controlled, homodimer, Bulbar motor neuron disease, Gene., Amyotrophic lateral sclerosis (disorder), data, Amyotrophic Lateral Sclerosis-Parkinsonism-Dementia Complex 1, Disease, Controlling, SMNT, ALS, dJ353E16.2, MGCR1-PEN, amyotrophic lateral sclerosis, Amyotrophic Lateral Sclerosis Parkinsonism Dementia Complex 1, Guam Form, Proteins, mKIAA4111, Cell Lines, Parkinsonism/Dementia complex of Guam, Mell1, MGCR1, cell_line, Guam, RGD1565571, Spectrum Analysis, Cell, Lou Gehrigs Disease, Spectroscopy, polypeptide, count in organism, Lou Gehrig's Disease, count, MMEL2, MGCR, Protein, Amyotrophic Lateral, Diseases, ALS1, Death, Mass Spectrum Analyses, Lines, T-BCD541, Mass Spectrum, Albs, LOU GEHRIG DIS, Motor Neuron Disease, Nerve Cells, SMA3, Dementia With Amyotrophic Lateral Sclerosis, Gehrig's Disease, Parkinsonism-Dementia Complex of Guam, SMA4, Spinal Muscular Atrophy, SMA1, Lou-Gehrigs Disease, SMA2, AMYOTROPHIC SCLEROSIS, hSod1, Spectrometry, ALS - Amyotrophic lateral sclerosis, Infant Deaths, Amyotrophic, SMA@, Protein Gene Products, TDRD16A, Gene Proteins, HEL-S-44, MOTOR NEURON DIS AMYOTROPHIC LATERAL SCLEROSIS, Cells, Eph2, Charcot disease, quantitative, Amyotrophic Lateral Sclerosis With Dementia, Proteomes, NEP2, Amyotrophic Lateral Sclerosis-Parkinsonism/dementia Complex 1, presence or absence in organismanterior horn cell, deep, human disease, Diseases., Line, Cell Lines, Homo sapiens disease, cell line cell, cell_line, motor neuron, motoneuron, Cell, cell line, Linesbiological signaling, Lattices, Microtrabecular, Activity, determination, Laboratory, Cytoplasmic Filaments, Gehrigs Disease, Sclerosis, Nerve, number, Amyotrophic Lateral Sclerosis, FBN, Gene, motoneuron, presence, Charcot Disease, NSC, Filament, bulbar, Readability, Cytoskeletons, ECTOL1, Cytoskeletal Filaments, Line, Gene Products, motor neuron, Analysis, Research Activity, Laboratory Research, Microtrabecular Lattice, Lou Gehrig's disease, WMS, LOU GEHRIGS DIS, Gehrig Disease, Priorities, neural stem cell, study, ALS (Amyotrophic Lateral Sclerosis), human disease, Motor neuron disease, Guam Disease, Lou-Gehrigs, Infant, reference sample, Cytoplasmic Filament, Research, cell, Cytoskeletal, Spectrum, GEHRIGS DIS, Guam Form of Amyotrophic Lateral Sclerosis, cell line cell, proteins, Lateral Scleroses, Deaths, cell line, anterior horn cell, OCTD, Cytoplasmic, Parkinsonism Dementia Complex of Guam, Amyotrophic lateral sclerosis, Microtrabecular Lattices, signaling process, Homo sapiens disease, Neuron, Development and Research, Research Priority, associated, Nerve Cell, GPHYSD2, Lou Gehrig Disease, SGS, Controlled, single organism signaling, Bulbar motor neuron disease, Amyotrophic lateral sclerosis (disorder), Amyotrophic Lateral Sclerosis-Parkinsonism-Dementia Complex 1, Disease, Controlling, ALS, amyotrophic lateral sclerosis, Amyotrophic Lateral Sclerosis Parkinsonism Dementia Complex 1, Guam Form, Proteins, Cell Lines, Parkinsonism/Dementia complex of Guam, Research Priorities, cell_line, Guam, Cell, Lou Gehrigs Disease, ACMICD, Spectroscopy, polypeptide, count in organism, Lou Gehrig's Disease, Priority, count, Diseases., Protein, chemical analysis, Amyotrophic Lateral, Diseases, Research Activities, Cytoskeletal Filament, MFS1, Death, WMS2, Lines, Research and Development, LOU GEHRIG DIS, Motor Neuron Disease, Nerve Cells, distinct, Dementia With Amyotrophic Lateral Sclerosis, Gehrig's Disease, Parkinsonism-Dementia Complex of Guam, Spinal Muscular Atrophy, Lou-Gehrigs Disease, AMYOTROPHIC SCLEROSIS, Spectrometry, ALS - Amyotrophic lateral sclerosis, Filaments, MASS, Understanding, Infant Deaths, Amyotrophic, signalling, Protein Gene Products, Activities, Gene Proteins, signalling process, MOTOR NEURON DIS AMYOTROPHIC LATERAL SCLEROSIS, Cells, SSKS, Lattice, assay, Charcot disease, quantitative, Amyotrophic Lateral Sclerosis With Dementia, Proteomes, Amyotrophic Lateral Sclerosis-Parkinsonism/dementia Complex 1, presence or absence in organism2405http://gpmdb.thegpm.org/~/dblist_gpmnum/gpmnum=GPM32320003403dbgap_ncbi~0patentfamilies~0rfam~0merops~0complex-portal~0uniprot~0wormbaseparasite~0embl-covid19~0reactome~0emdb~0wgs_masters~0ebiweb_resources~0opentargets_genetics~0biomodels_all~0ipd-mhc~0ebiweb_teams~0taxonomy~0genome_assembly~0sc-experiments~0ebiweb_people~0enzymeportal_enzymes~0ipd-nhkir~0cellosaurus~0pdbe~0chebi~0patentproteins~0interpro7~0uniref~0chembl~0pdbekb~0gpcrdb~0hgnc~0sc-genes~0intact~0rhea~0ebiweb_training~0alphafold~0imgt-hla~0patentnucleotides~0ensemblroot~0eva_studies~0non-coding~0europepmc~0pubmed~1identifiers_registry~0pdbechem~0hpa-covid19~0eva-variants-covid19~0biosamples~0gwas_catalog~0biotools~0tls_masters~0mesh~0coding~0sra~0opentargets~0efo~0embl-pathogen~0project~0pride~1human_diseases~0geo_datasets~0embl~0treefam~0uniparc~0ols~0dgva~0intenz~0go~0tsa_masters~0biosamples-covid19~0ebiweb_corporate~0omim~0lrg~0earlycause-molecular-sequences~0ipd-kir~0empiar~0rnacentral~0orcid_data_claims~0gpmdb~2lineage-covid19~0metagenomics~0pfam~0pride archive~1varsite~00Resource Reanalysis0.00.00.0074028377544725480.01.0falseDeep proteomic evaluation of primary and cell line motoneuron disease models delineates major differences in neuronal characteristicsData from ProteomeXchange, PXD ID: PXD000666. File: 20120710_EXQ4_DaHo_SA_labelfree_7D_MN1_3_12_2.mzml. Published as part of Mol Cell Proteomics. 2014 Sep 5 . From the Abstract: {{i}} The fatal neurodegenerative disorders amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA) are the most common motoneuron disease and genetic cause of infant death, respectively. Various in vitro model systems have been established to investigate motoneuron disease mechanisms - in particular immortalized cell lines and primary neurons. By quantitative mass spectrometry (MS)-based proteomics we here compare the proteomes of primary motoneurons to motoneuron-like cell lines NSC-34 and N2a as well as to non-neuronal control cells at a depth of 10,000 proteins ... {{/i}}2014-09-10GPM3232000340325193168PXD000666PXD000666