Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomics of Juvenile Huntington's disease and control BA4 cortex

ABSTRACT: Proteomics analyses of Juvenile Huntington's disease and age-matched control individuals in the BA4 motor cortex region

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Vivian Hook

PROVIDER: MSV000091664 | MassIVE | Sat Apr 08 04:14:00 BST 2023

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Proteomics analyses of Juvenile Huntington's disease and age-matched control individuals in BA6 cortex

Project description:Proteomics analyses of BA6 premotor cortex region in Juvenile Huntington's disease and age-matched control individuals

2023-04-12 | MSV000091703 | MassIVE

Proteomics analyses of Juvenile Huntington's disease and age-matched control individuals in the putamen

Project description:Proteomics analyses of Juvenile Huntington's disease and age-matched control individuals in the putamen

2023-04-11 | MSV000091676 | MassIVE

3′ sequencing from human Huntington's disease and control motor cortex and cerebellum.

Project description:Purpose: We applied polyA site sequencing (Passeq) to human Huntington's disease and control motor cortex and cerebellum to test if any genes change 3′UTR isoforms abundance. Methods: 3′ sequencing was performed on 6 motor cortices from grade 1 Huntington's patient brains, 4 motor cortices from grade 2 Huntington's patient brains, and 5 motor cortices from control brains. Cerebellum samples included 9 cerebella from grade 2-3 Huntington's patient brains, and 7 cerebella from control brains. To verify HTT isoforms in mice, sequencing was performed on 5 Q140 mouse striata and 3 wild-type mouse striata. Results: We report 11% of genes from Huntington's disease patient motor cortex exhibit a change in at least one of their 3′UTR isoforms, commensurate with the 11% of genes which show different total expression in HD motor cortex versus control. In contrast, gene isoform and expression changes are minimal (<5%) in Huntington's disease cerebellum versus controls. In the motor cortex, we show isoform and gene expression differs between between grade 1 and grade 2 brains. We identify a novel isoform of huntingtin mRNA which is conserved in wild-type and Huntington's model mice. Conclusions: This is the first study characterizing widespread alterations in 3′UTR isoform abundance in Huntington's disease. Alterations in isoform abundance may affect mRNA metabolism in Huntington's disease brains.

2017-09-21 | GSE96099 | GEO

3′ sequencing from human Huntington's disease and control motor cortex and cerebellum.

Project description:3′ sequencing from human Huntington's disease and control motor cortex and cerebellum.

| PRJNA378801 | ENA

sFANS RNAseq profiling of deep layer cortical cell types from human control and Huntington's Disease samples

Project description:The properties of the cell types that are most vulnerable in the Huntington's disease (HD) cortex have not been delineated. Here we have employed serial fluorescence activated nuclear sorting (sFANS) and deep molecular profiling to demonstrate that layer 5a pyramidal neurons are selectively vulnerable in primary motor cortex and other cortical areas.

2024-01-17 | GSE233408 | GEO

RNA-seq of micro RNAs (miRNAs) in Human prefrontal cortex to identify differentially expressed miRNAs between Huntington's Disease and control brain samples

Project description:To identify genome-wide differentially expressed microRNAs (miRNAs) between Huntington's disease (HD) and control Human pre-frontal cortex samples

2014-01-30 | E-MTAB-2206 | biostudies-arrayexpress

Juvenile fluoxetine evoked gene expression changes in the rat medial prefrontal cortex

Project description:To understand the consequences of chronic exposure to fluoxetine during juvenile life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood. To understand the consequences of chronic exposure to fluoxetine during juvenile life on global transcriptional changes withing the rat medial prefrontal cortex in adulthood.

2024-06-30 | GSE270731 | GEO

Parkinson Disease Frontal Cortex Transcriptomic analysis

Project description:We analyzed the transcriptome of the Frontal Cortex (FC) of Parkinson diseased (PD) individuals compared to age-matched controls.

2024-09-03 | GSE156928 | GEO

Huntington's disease brain-derived small RNAs recapitulate associated neuropathology in mice [human-miRNA]

Project description:Progressive motor alterations and selective death of striatal medium spiny neurons (MSNs) are key pathological hallmarks of Huntington's disease (HD), a neurodegenerative condition caused by a CAG trinucleotide repeat expansion in the coding region of the huntingtin (HTT) gene. Most research has focused on the pathogenic effects of the resultant protein product(s); however, growing evidence indicates that expanded CAG repeats within mutant HTT mRNA and derived small CAG repeat RNAs (sCAG) participate in HD pathophysiology. The individual contribution of protein versus RNA toxicity to HD pathophysiology remains largely uncharacterized and the role of other classes of small RNAs (sRNA) that are strongly perturbed in HD is uncertain. Here, have injected vehicle, CTL-sRNA (obtained from non-affected individuals) or HD-sRNA (obtained from patients with HD) from different brain areas (putamen, PT; cortex, CTX and cerebellum, CB) into the striatum of wild type (WT) mice and demonstrate that sRNA produced in the putamen and cortex of HD patients are sufficient to induce HD pathology in vivo. We have performed small RNA (sRNA) sequencing of the human samples used for injection. Here we describe the procedure to obtain and sequence human sRNA isolated from the different brain areas.

2021-02-16 | GSE165663 | GEO

Effect of Juvenile Environmental Tobacco Smoke Exposure on the Rat Frontal Cortex Neuroproteome

Project description:Exposure to secondhand tobacco smoke during early childhood has been linked with an increased risk for behavioral disorders, yet little is known regarding how brain development is impacted. Using an environmental tobacco smoke (ETS) passive inhalation model, this study assesses the neurodevelopmental impact of juvenile exposure during a critical period of frontal cortex development, specifically that of the rat orbital neocortex between postnatal days 8 and 22. Agnostic shotgun proteomics was employed to discern the biomolecular shift within this rapidly developing brain region that is responsible for higher-order behavioral control. The orbital cortex neuroproteome was assessed between ETS-exposed and room-air control animals employing a label-free shotgun approach with data-independent acquisition. Following protein roll-up, a total of X protein were found statistically altered in quantity out of Y total proteins identified. These results implicate a prominent shift within metabolic processes and synaptic organization related to excitatory and inhibitory neurotransmission. Findings derived from this dataset may further our understanding of how secondhand smoke exposure can perturb the orbital frontal cortex and result in developmental behavioral disorders.

2020-05-26 | PXD007690 | Pride

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