Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MS analysis of phosphopeptides enriched from the lumbar spinal cord of SOD1G93A mice at 20weeks.

ABSTRACT: This project is "Phosphoproteomic analysis of the lumbar spinal cord, a lesion site in the amyotrophic lateral sclerosis (ALS) mouse model SOD1G93A mice". The aim of this study is to clarify the phosphorylation changes by the lumbar spinal cord of SOD1G93A mice at 20w by applying proteomics technology. The goal of this study is to better understand the pathogenesis of ALS. lumbar spinal cord of SOD1G93A mice (n=5) and WT mice (n=4) were collected at 20w, and the phosphoproteomics were compared.

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Fumiaki Tanaka

PROVIDER: PXD030651 | JPOST Repository | Thu May 19 00:00:00 BST 2022

REPOSITORIES: jPOST

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	190401QE_P10.mznld	Other
	190401QE_P10.raw	Raw
	190401QE_P2.mznld	Other
	190401QE_P2.raw	Raw
	190401QE_P3.mznld	Other

Items per page:

1 - 5 of 20

Publications

Inhibition of Crmp1 Phosphorylation at Ser522 Ameliorates Motor Function and Neuronal Pathology in Amyotrophic Lateral Sclerosis Model Mice.

Asano Tetsuya T Nakamura Haruko H Kawamoto Yuko Y Tada Mikiko M Kimura Yayoi Y Takano Hiroshi H Yao Ryoji R Saito Hiroya H Ikeda Takuya T Komiya Hiroyasu H Kubota Shun S Hashiguchi Shunta S Takahashi Keita K Kunii Misako M Tanaka Kenichi K Goshima Yoshio Y Nakamura Fumio F Takeuchi Hideyuki H Doi Hiroshi H Tanaka Fumiaki F

eNeuro 20220523 3

Amyotrophic lateral sclerosis (ALS) is a rapidly progressive and fatal neurodegenerative disorder that affects upper and lower motor neurons; however, its pathomechanism has not been fully elucidated. Using a comprehensive phosphoproteomic approach, we have identified elevated phosphorylation of Collapsin response mediator protein 1 (Crmp1) at serine 522 in the lumbar spinal cord of ALS model mice overexpressing a human superoxide dismutase mutant (SOD1<sup>G93A</sup>). We investigated the effec ...[more]

PMID: 35523582

Similar Datasets

Transcription profiling of human post mortem spinal cord grey matter from sporadic and familial ALS patients vs controls to identify amyotrophic lateral sclerosis (ALS) associated genes

Project description:Identification of amyotrophic lateral sclerosis (ALS) associated genes. Post mortem spinal cord grey matter from sporadic and familial ALS patients compared with controls.

2007-09-26 | E-GEOD-833 | biostudies-arrayexpress

Amyotrophic lateral sclerosis

Project description:Identification of amyotrophic lateral sclerosis (ALS) associated genes. Post mortem spinal cord grey matter from sporadic and familial ALS patients compared with controls. Keywords: other

2003-11-14 | GSE833 | GEO

Gene expression profiling of resistant and vulnerable motor neuron subtypes in amyotrophic lateral sclerosis

Project description:A consistent clinical feature of amyotrophic lateral sclerosis (ALS) is the sparing of eye movements. Pathological studies have confirmed that there is relative sparing of the cranial motor nuclei of the oculomotor, trochlear and abducens nerves, although pathological changes resembling those seen in anterior horn cells are present to a lesser degree. The aim of the present study is to combine LCM and microarray analysis to study the differences between motor neurons that are selectively resistant (oculomotor neurons) and those that are vulnerable (lumbar spinal motor neurons) to the disease process in amyotrophic lateral sclerosis. We used microarray analysis to determine the differences in gene expression between oculomotor and lumbar spinal motor neurons, isolated by laser capture microdissection from the midbrain and spinal cord of neurologically normal human controls.

2013-03-01 | E-GEOD-40438 | biostudies-arrayexpress

Muscle Gene Expression Is a Marker of Amyotrophic Lateral Sclerosis Severity

Project description:This study was designed to identify gene expression changes in skeletal muscle that could define reliably the degree of the severity of Amyotrophic lateral sclerosis (ALS). All samples were from human biopsies, either from healthy muscles or from muscle whose patients were clearly diagnosed as having Amyotrophic Lateral Sclerosis (ALS)

2012-01-17 | E-MEXP-3260 | biostudies-arrayexpress

miR-155 plays a crucial role in ALS and is an immune therapeutic target [RNA-Seq]

Project description:Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. In addition, dysregulated proteins in the spinal cord of SOD1 mice that we identified in human ALS spinal cords and CSF were restored in SOD1G93A/miR155-/- mice. Treatment of SOD1 mice with anti-miR-155 SOD1 mice injected systemically or into the cerebrospinal fluid prolonged survival and restored the microglial unique genetic and microRNA profiles. Our findings provide a new avenue for immune based therapy of ALS by targeting miR-155. Total RNA was isolated from whole lumbar spinal cord homogenate from healthy control donors without known neurologic diseases and sporadic and familial ALS.

2014-11-24 | E-GEOD-52946 | biostudies-arrayexpress

Early alterations in lipid metabolism in the spinal cord of SOD1 mice

Project description:Amyotrophic lateral sclerosis (ALS) is a multifactorial and complex fatal degenerative disorder. A number of pathological mechanisms that lead to motor neuron death have been identified, although there are many unknowns in the disease aetiology of ALS. Alterations in lipid metabolism are well documented in the progression of ALS, both at the systemic level and in the spinal cord of mouse models and ALS patients. The origin of these lipid alterations remains unclear. This study aims to identify early lipid metabolic pathways altered before systemic metabolic symptoms in the spinal cord of mouse models of ALS. To do this, we performed a transcriptomic analysis of the spinal cord of SOD1G93A mice at an early disease stage(p90)

2021-09-27 | GSE184484 | GEO

Gene expression profiling of resistant and vulnerable motor neuron subtypes in amyotrophic lateral sclerosis

2013-03-01 | GSE40438 | GEO

Amyotrophic lateral sclerosis: SOD1 mouse model

Project description:Identification of familial amyotrophic lateral sclerosis (fALS) related genes. Material from three hSOD1(G93A) transgenic mice was compared to material from three non-transgenic control mice using an alternating loop design on two-colour cDNA microarrays. Statistical data management and analysis: postgreSQL relational database (www.postgresql.org), Perl, and R (www.r-project.org); pin-wise lowess-regression based normalisation (Yang et al., 2002 [PMID: 11842121]); mixed ANOVA-model. Keywords = amyotrophic lateral sclerosis, ALS, SOD1 mouse model

2010-06-05 | E-GEOD-2400 | biostudies-arrayexpress

Peripheral blood lymphocytes: ALS patients vs. healthy controls

Project description:Transcripional profiling of lymphocytes from patients with amyotrophic lateral sclerosis (ALS) (n=11) and healthy control subjects (n=11). The goal was to determine disease response expression signatures relevant of ALS pathogenesis that affect brain and spinal cord. The reference design was used: each Cy5-labeled cRNA sample from ALS patient or healthy control subject was cohybridized on Agilent-014850 Whole Human Genome Microarray 4x44K G4112F with the reference pool formed with equal amounts of Cy3-labeled cRNAs from each sample from the healthy control group. Eleven lymphocyte samples from definite sporadic ALS patients and eleven samples from healthy control subjects were used.

2011-12-11 | E-GEOD-28253 | biostudies-arrayexpress

MG400 profile of microglia from SOD miR155-KO mice

Project description:Amyotrophic lateral sclerosis (ALS) is a paralytic degenerative disease of the nervous system. In the SOD1 mouse model of ALS we found loss of the molecular and functional microglia signature associated with pronounced expression of miR-155 in SOD1 mice. We also found increased expression of miR-155 in the spinal cord of ALS subjects. Genetic ablation of miR-155 increased survival in SOD1 mice and reversed the abnormal microglial and monocyte molecular signature. In addition, dysregulated proteins in the spinal cord of SOD1 mice that we identified in human ALS spinal cords and CSF were restored in SOD1G93A/miR155-/- mice. Treatment of SOD1 mice with anti-miR-155 SOD1 mice injected systemically or into the cerebrospinal fluid prolonged survival and restored the microglial unique genetic and microRNA profiles. Our findings provide a new avenue for immune based therapy of ALS by targeting miR-155. Total RNA was isolated from FACS sorted adult FCRLS+ microglia from spinal cords of Non-Tg/miR155+/-, SOD1G93A-miR155+/- and SOD1G93A-miR155–/- mice at the age of 120d. Total RNA was extracted using mirVanaTM miRNA isolation kit (Ambion) according to the manufacturer’s protocol. nCounter Nansotring custom-made MG400 chip was used for gene expression profile

2014-11-24 | E-GEOD-52803 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data