Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

H.sapiens - Cerebral cortex, SC (Pingetal,scidata.2020)

ABSTRACT: abundance based on Spectral counting, Interaction consistency score: 18.6, Coverage: 54

ORGANISM(S): 9606

SUBMITTER: Christian von Mering

PROVIDER: 521722927 | PAXDB | 2020

REPOSITORIES: PAXDB

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	bioprojects-abundance-files-v4.0.zip	Other

Items per page:

1 - 1 of 1

Publications

Global quantitative analysis of the human brain proteome and phosphoproteome in Alzheimer's disease.

Ping Lingyan L Kundinger Sean R SR Duong Duc M DM Yin Luming L Gearing Marla M Lah James J JJ Levey Allan I AI Seyfried Nicholas T NT

Scientific data 20200928 1

Alzheimer's disease (AD) is characterized by an early, asymptomatic phase (AsymAD) in which individuals exhibit amyloid-beta (Aβ) plaque accumulation in the absence of clinically detectable cognitive decline. Here we report an unbiased multiplex quantitative proteomic and phosphoproteomic analysis using tandem mass tag (TMT) isobaric labeling of human post-mortem cortex (n = 27) across pathology-free controls, AsymAD and symptomatic AD individuals. With off-line high-pH fractionation and liquid ...[more]

PMID: 32985496

Similar Datasets

Transcriptomics Responses to Hypoxia and Ketamine in Ovine Fetal Cerebral Cortex

Project description:Transient hypoxia in pregnancy stimulates a physiological reflex response that redistributes blood flow and defends oxygen delivery to the fetal brain. The chemoreceptor reflex that is responsible for this physiological response is dependent on glutamatergic neurotransmission which, in times of vigorous activity, could produce cell death secondary to calcium uptake. We designed the present experiment to test the hypotheses that transient hypoxia produces damage of the cerebral cortex and that ketamine, an antagonist of NMDA receptors, reduces the damage. Late-gestation, chronically catheterized fetal sheep were subjected to a 30 min period of ventilatory hypoxia that decreased fetal PaO2 from 17Â±1 to 10Â±1 mm Hg, or normoxia (PaO2 17Â±1 mm Hg), with or without pretreatment (10 min before hypoxia/normoxia) with ketamine (3 mg/kg, iv). One day (24 h) after hypoxia/normoxia, fetal cerebral cortex was removed and mRNA extracted for transcriptomics and systems biology analysis. Hypoxia stimulated a transcriptomics response consistent with a reduction in cellular metabolism and an increase in inflammation. Ketamine pretreatment reduced both of these responses. The inflammation response modeled with transcriptomic system biology was validated by immunohistochemistry and showed increased abundance of microglia/macrophages after hypoxia in the cerebral cortical tissue that ketamine significantly reduced. We conclude that transient hypoxia produces inflammation of the fetal cerebral cortex and that ketamine, in a standard clinical dose, reduces the inflammation response. 4 groups: hypoxia, hypoxia plus ketamine, normoxia, normoxia plus ketamine. Hypoxia produced by low PO2 in maternal inspired gas for 30 min, followed by normoxia recovery for 23.5 hours. Control fetuses maintained at normoxia for 30 min, followed by another 23.5 h of normoxia. Fetal frontal cerebral cortex collected for mRNA at end of 23.5 h recovery period.

2016-04-06 | E-GEOD-76110 | biostudies-arrayexpress

Thiele2013 - Cerebral cortex glial cells

Project description: Not available

| MODEL1310110064 | biostudies-other

Thiele2013 - Cerebral cortex neuronal cells

Project description: Not available

| MODEL1310110033 | biostudies-other

Lack of cerebral bmaa in human cerebral cortex.

Project description: Not available

| S-EPMC2677491 | biostudies-literature

Interactions between Yeast Proteins and Rsp5 Ubiquitin Ligase

Project description:To identify substrates of the ubiquitinating E3 enzyme Rsp5 we applied purified Rsp5 to duplicate protein arrays. The Rsp proteins were expressed as fusion proteins to GST. We used as a control Ubr1, a RING domain containing E3 ligase We analyzed Rsp5 from S.cerevisiae on duplicate arrays, with four control chips, two without Rsp5 and two with Ubr1.

2008-12-30 | E-GEOD-14218 | biostudies-arrayexpress

LC-MS/MS for harmaline-treated mice cerebellar cortex

Project description:Harmaline-induced tremor mice model has been well-recognized as a mature pharmacological model for ET, but his model has always been used to test drugs, the exact underlying mechanism of this mouse model has never been fully understood. This project is to provide a novel inspection for ET targeted treatment by revealing the protein signals for harmaline-induced mice model.

2026-01-05 | PXD055985 | Pride

Global optimization of cerebral cortex layout.

Project description: Not available

| S-EPMC327154 | biostudies-literature

RP58 controls neuron and astrocyte differentiation by downregulating the expression of Id1-4 genes in the developing cortex

Project description:Appropriate number of neurons and glial cells is generated from neural stem cells (NSCs) by the regulation of cell cycle exit and subsequent differentiation. Although the regulatory mechanism remains obscure, Id (inhibitor of differentiation) proteins are known to contribute critically to NSC proliferation by controlling cell cycle. Here we report that a transcriptional factor, RP58, negatively regulates all 4 Id genes (Id1-Id4) in developing cerebral cortex. Consistently, Rp58 knockout (KO) mice demonstrated enhanced astrogenesis accompanied with an excess of NSCs. These phenotypes were mimicked by the overexpression of all Id genes in wild-type cortical progenitors. Furthermore, Rp58 KO phenotypes were rescued by the knockdown of all Id genes in mutant cortical progenitors but not by the knockdown of each single Id gene. Finally, we determined p57 as an effector gene of RP58-Id-mediated cell fate control. These findings establish RP58 as a novel key regulator that controls the self-renewal and differentiation of NSCs and restriction of astrogenesis by repressing all Id genes during corticogenesis. Sample RNAs were obtained from E16.5 Rp58 KO mouse cerebral cortex or control cortex. Two independent total RNA samples from each mouse strain were mixed and purified using the RNeasy Mini Kit (Qiagen). Oligonucleotide microarray analysis was performed using Panorama Micro Array gene expression chips, each containing approx 22000 probe sets (Sigma-Aldrich) according to the manufacturer's instructions.

2014-12-08 | E-GEOD-34327 | biostudies-arrayexpress

Expression data from mouse cerebral cortex

Project description:Differential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains We used Affymetrix microarray to explore the global gene expression patterns of mouse cerebral cortex of different mouse strains at two developmental stages Cerebral cortex from two mouse strains [C57BL/6J(B6) and C3H/J (C3H)] at post-natal day 1 (p1) and post-natal 11 weeks (11 wk) were harvested for microarray experiments

2013-10-21 | E-GEOD-46443 | biostudies-arrayexpress

Salivary cytokine alterations in HIV infection

Project description:This SuperSeries is composed of the following subset Series: GSE24037: Salivary cytokine alterations in HIV infection part 1 GSE24064: Salivary cytokine alterations in HIV infection part 2 Refer to individual Series

2011-09-08 | E-GEOD-24411 | biostudies-arrayexpress