Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of Differential Expression Genes of Blood Leukocytes for Schizophrenia

ABSTRACT: Schizophrenia (SCZ) is a severe neurodevelopmental disorder with brain dysfunction. This study aimed to use bioinformatic analysis to identify candidate blood biomarkers for SCZ. Our study identified 1205 statistically significant DEGs, of which 623 genes were upregulated and 582 genes were downregulated. Functional enrichment analysis showed that DEGs were mainly enriched in cell chemotaxis, cell surface, and serine peptidase activity, as well as involved in Natural killer cell-mediated cytotoxicity. WGCNA identified 16 gene co-expression modules, and 5 modules were significantly correlated with SCZ (P < 0.05). There were 106 upregulated genes and 90 downregulated genes in the 5 modules. The top ten genes sorted by the Degree algorithm were RPS28, BRD4, FUS, PABPC1, PCBP1, PCBP2, RPL27A, RPS21, RAG1, and RPL27. RAG1 and the other 9 genes belonged to the turquoise and pink module respectively. Pathway enrichment analysis indicated that these 10 genes were mainly involved in processes such as Ribosome, cytoplasmic translation, RNA binding, and protein binding.

ORGANISM(S): Homo sapiens

PROVIDER: GSE263180 | GEO | 2024/06/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomic signatures of risk genes implicated in psychiatric disorders during neuronal differentiation

Project description:Susceptibility genes for Autism Spectrum Disorder (ASD), Fragile X Syndrome (FXS), monogenetic disorders with intellectual disabilities (ID) or schizophrenia (SCZ) converge on processes related to neuronal function and differentiation. Furthermore, ASD risk genes are enriched for FMRP (Fragile X Mental Retardation Protein) targets and for genes implicated in ID. In addition, a significant co-heritability was observed between ASD and SCZ. The genetic overlap between ASD, FXS, ID and SCZ together with the symptomatic differences gives rise to the question if pathomechanisms impair the same or different regulatory patterns activated during neuronal differentiation (ND). To test this idea, we performed transcriptome analysis of in-vitro differentiation of the neuroblastoma cell line model SH-SY5Y and identified genes that were differentially expressed, dynamically regulated, and coordinately expressed. The identified genetic modules activated during ND are enriched for genetic risk factors for these four disorders. Although risk genes for the disorders significantly overlap, we observed disorder specific enrichments: ASD or FXS implicated genes were likely to be positive regulators of ND whereas ID implicated genes were related to negative regulation. ASD and SCZ genes were specifically enriched among cholesterol and fatty acid associated modules. ID genes were overrepresented among cell cycle modules. In addition, we show that ASD genes are likely to be hub genes. We hypothesize that knowledge about genetic variants of an individual combined with network and pathway context of the related genes will allow differentiating between psychiatric disorders. 21 samples, consisting of 3 replicates harvested at 7 different time-points of RA+BDNF-induced neuronal differentiation

2016-06-01 | E-GEOD-69838 | biostudies-arrayexpress

Genome-wide gene expression profiling post PCCB knockdown in human forebrain organoids

Project description:We established PCCB knockdown human induced pluripotent stem cell (hiPSC) line using CRISPR interference (CRISPRi). The established PCCB knockdown and control hiPSCs were then used to generate human forebrain organoids (hFOs). On day 60 of organoid culture, PCCB knockdown and control hFOs were randomly selected for RNA-sequencing (RNA-seq). We found that differentially expressed genes (DEGs) affected by PCCB knockdown were enriched with GABAergic synapse, synaptic vesicle cycle, neurotransmitter transport, forebrain development, axon development, synaptic organization, and calcium signaling pathways. The DEGs were also significantly overlapped with schizophrenia (SCZ)-associated genes, including genes dysregulated in brains or organoids derived from SCZ patients, and genes reported in SCZ GWAS.

2023-05-02 | GSE226233 | GEO

Transcriptomic signatures of risk genes implicated in psychiatric disorders during neuronal differentiation

2016-06-01 | GSE69838 | GEO

Expression data from the human parietal cortex brain

Project description:Schizophrenia (SCZ) and bipolar disorder (BD) are highly heritable psychiatric disorders. Associated genetic and gene expression changes have been identified, but many have not been replicated and have unknown functions. We identified groups of genes whose expressions varied together, that is co-expression modules, then tested them for association with SCZ. Using weighted gene co-expression network analysis, we show that two modules were differentially expressed in patients versus controls. One, upregulated in cerebral cortex, was enriched with neuron differentiation and neuron development genes, as well as disease genome-wide association study genetic signals; the second, altered in cerebral cortex and cerebellum, was enriched with genes involved in neuron protection functions. The findings were preserved in five expression data sets, including sets from three brain regions, from a different microarray platform, and from BD patients. From those observations, we propose neuron differentiation and development pathways may be involved in etiologies of both SCZ and BD, and neuron protection function participates in pathological process of the diseases.

2012-12-31 | GSE35977 | GEO

Expression data from the human cerebellum brain

2012-12-31 | GSE35974 | GEO

Zbtb16 regulates social cognitive behaviors and neocortical development

Project description:Recent genomic studies suggest that a single gene is involved in multiple diseases, however it is unclear what mechanism destined for different diseases by a single gene. Mutations of ZBTB16 are associated with autism spectrum disorder (ASD) and schizophrenia (SCZ), but how ZBTB16 fates ASD or SCZ are unknown. Here we show the deletion of Zbtb16 in mice leads to both ASD- and SCZ-like behaviors such as social impairment, repetitive behaviors, risk-taking behaviors, and cognitive impairment. To elucidate the mechanism underlying the behavioral phenotypes, we carried out histological studies and observed impairments in thinning of neocortical layer 6 (L6) and a reduction of TBR1+ neurons in the prefrontal cortex (PFC) of Zbtb16 KO mice. Furthermore, we found increased dendritic spines and microglia as well as developmental defects in oligodendrocytes and neocortical myelination in the PFC of Zbtb16 KO mice. Using a genomics approach, we identified the Zbtb16-transcriptome that includes genes involved in both ASD and SCZ pathophysiology and neocortical maturation such as neurogenesis and myelination. Co-expression networks further identified Zbtb16-correlated modules that are unique to ASD or SCZ respectively. Our study provides insight into the differential role of the single gene ZBTB16 in ASD and SCZ.

2021-05-12 | GSE155424 | GEO

Sweet corn: low- vs. high-yielding hybrids

Project description:Transcriptional profiling of sweet corn plant density (crowding stress) tolerance influencing yield. Tolerance to crowding stress has played a crucial role in improving agronomic productivity in field corn; however, commercial sweet corn hybrids vary greatly in crowding stress tolerance. The experiment was conducted to 1) explore transcriptional changes among sweet corn hybrids with differential yield under crowding stress, 2) identify relationships between phenotypic responses and gene expression patterns, and 3) identify groups of genes associated with yield and crowding stress tolerance. Under conditions of crowding stress, three high-yielding and three low-yielding sweet corn hybrids were grouped for transcriptional and phenotypic analyses. Transcriptional analyses identified from 372 to 859 common differentially expressed genes (DEGs) for each hybrid. Large gene expression pattern variation among hybrids and only 26 common DEGs across all hybrid comparisons were identified, suggesting each hybrid has a unique response to crowding stress. Over-represented biological functions of DEGs also differed among hybrids. Strong correlation was observed between: 1) modules with up-regulation in high-yielding hybrids and yield traits, and 2) modules with up-regulation in low-yielding hybrids and plant/ear traits. Modules linked with yield traits may be important crowding stress response mechanisms influencing crop yield. Functional analysis of the modules and common DEGs identified candidate crowding stress tolerant processes in photosynthesis, glycolysis, cell wall, carbohydrate/nitrogen metabolic process, chromatin, and transcription regulation. Moreover, these biological functions were greatly inter-connected, indicating the importance of improving the mechanisms as a network. 3 high-and 3 low-yielding hybrids with 2-3 biological replications grown under high population density (crowding stress)

2016-01-05 | E-GEOD-73435 | biostudies-arrayexpress

Overexpression of poly(rC) binding protein 2 by alternative cleavage and polyadenylation promotes breast cancer progression via regulating UFD1 and NT5E

Project description:Alternative cleavage and polyadenylation (APA) is an important post-transcriptional regulatory mechanism, which could lead many diseases. PCBP2 plays critical roles in mRNA stabilization, translational enhancement and contributes to human cancer development and progression even though the molecular mechanism is not completely understood. Herein, we report that increased expression of PCBP2 is observed in human breast cancer tissues compared to benign or normal breast tissues, and high expression of PCBP2 is significantly associated with disease progression and poor outcome in patients with breast cancer. Knockdown of PCBP2 expression significantly decreased breast cancer cell proliferation, migration and invasion in vitro and in vivo. Molecularly, UFD1 and NT5E were identified as the downstream genes of PCBP2, which were scanned and verified based on RNA sequencing. Moreover, PCBP2 promotes oncogenic behaviors of breast cancer cells via upregulating the expression of UFD1 and NT5E by directly binding to their 3' untranslated regions (UTRs). Furthermore, we determine that the APA process is involved in regulating the overexpression PCBP2 in breast cancer cells. Therefore, our findings reveal that APA of PCBP2 3' UTR contributes to its overexpression and then promotes breast cancer progression by regulating the expression of UFD1 and NT5E.

2019-05-02 | GSE130564 | GEO

Olfactory neuroepithelial proteome in Schizophrenia & cannabis

Project description:In this study, we evaluated the common proteomic profile, as well as, the exclusively deregulated proteins in ON cells from healthy controls cannabis users (HC/c), SCZ patients non-cannabis users (SCZ/nc) and SCZ patients cannabis users (SCZ/c) as compared to healthy controls non-cannabis users (HC/nc). Moreover, we investigated quantitative and functional differences between HC/c and SCZ, and we characterized the distinct effect of cannabis in SCZ comparing SCZ/nc and SCZ/c.

2021-09-09 | PXD020739 | Pride

Human glioma cell line T98G: BAP-PCBP2 RIP vs. BAP-GFP RIP (Control)

Project description:RIP-Chip analysis of PCBP2 and identification of preferentially associated mRNAs. T98G cells were transfected transiently with BAP-tagged constructs. BAP-tagged proteins were biotinylated in vivo by the co-transfected hBirA enzyme. RNPs were recovered via precipitation with Steptavidin-sepharose beads. Finally, RNAs were purified and analyzed on microarrays. BAP-GFP as control was used in three independent sets of experiments. Two-condition experiment, BAP-PCBP2 vs. BAP-GFP cells. Biological replicates: 3 BAP-PCBP2 replicates, 3 BAP-GFP (Control) replicates

2013-07-24 | E-GEOD-44048 | 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