Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BRAT1 Links Integrator and Defective RNA Processing with Neurodegeneration

ABSTRACT: We have identified differentially expressed genes and defects in processing of UsnRNAs in BRAT1-deficient and BRAT1-mutated patient cells by RNA-sequencing and BRAT1 as a structural and functional component of Integrator, linking defects in this critical endonuclease complex with hereditary neurodegenerative disease. Due to the sensitive nature of the data, raw data files have not been uploaded.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Homo sapiens

SUBMITTER: Jan Kubovčiak

PROVIDER: E-MTAB-10750 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNAseq analysis of IKKbeta knockdown EDC4 knockdown irradiated and untreated

Project description:U2OS cells expressing DOX inducible pTRIPZ shRNA against IKKbeta or EDC4 were irradiated or left untreated. RNA stability was determined as through actinomycin D chase experiment.

2018-10-29 | E-MTAB-7199 | biostudies-arrayexpress

RNA-seq of H2afj-ko and isogenic WT C57/Bl6-N mouse embryonic fibroblasts in proliferation and after etoposide-induced senescence.

Project description:Determine the effect of knocking out the H2afj gene on the transcriptome of MEFs induced into senescence with etoposide. MEFs were produced from individual H2A.J-ko or isogenic WT C57BL/6-N embryos. 3 different female WT and H2A.J-ko MEFs were used for the transcriptome analyses. MEFs were cultivated in DMEM + Gluta-Max (Gibco 31966) + 10%FBS + pen/strep in a 5% carbon dioxyde and 5% oxygen incubator. MEFs were passed twice before inducing senescence by treatment with 2.5 µM etoposide for 6 days (with media changed after 3 days), followed by 3 days incubation in fresh medium without etoposide.

2020-11-02 | E-MTAB-9704 | biostudies-arrayexpress

Transcription profiling of mouse myoblasts from postnatal day 2 WT and Foxj3 KO

Project description:Myoblasts harvested from a postnatal day 2 WT and Foxj3 KO litter. We used Affymetrix microarrays to identify dysregulated transcripts in Foxj3 mutant myoblasts. Experiment Overall Design: Myoblasts were passaged 3 times prior to harvest

2008-06-11 | E-GEOD-10628 | biostudies-arrayexpress

Expression data of BRPF3 depletion from the human osteosarcoma U2OS cell line

Project description:The Bromo-domain and PHD-finger protein, BRPF3, forms a complex with HBO1 and regulates the initiation of DNA replication. BRPF3-dependent histone H3K14 enriched in chromatin surrounding a fraction of replication origins may play an important role in origin firing. We used microarrays to evaluate whether replication defect due to the lack of BRPF3 is associated with transcriptional changes of replication genes. Human osteosarcoma U2OS cells depleted for BRPF3 were used for RNA extraction and hybridization on Affymetrix microarrays. Cells were treated with either scamble siRNA (Control_1_B1) or siRNA against BPRF3 (BRPF3_B1) for 48 hours. Two samples in a biological replica set were prepared in exactly the same way and labeled as Control_1_B2 and BRPF3_B2 respectively.

2016-01-12 | E-GEOD-65065 | biostudies-arrayexpress

RNA-seq of SUPT1, LOUCY, JURKAT and DND41 after treatment with 5-azacytidine and Vitamin C

Project description:TET2 is a know tumorsuppressor gene involved in the demethylation of DNA. TET2 catalyses the conversion of 5-methyl cytosine (5-mC) to 5-hydroximethyl cytosine (5-hmC), an important step in the removal of methylation from the DNA. In T-All mutations in TET2 are rare, however we have found that it is often silenced by DNA Methylation. 5-Azacytidine (5-AZA) is a an effective demethylating agent used as a cancer treatment and has been showed to be able to reactivate methylated genes. Similarly, Vitamin C is an important co-factor for TET2 and has been shown to have synergistic effects with 5-Azacytidine. By treating the TET2 methylated T-ALL cell lines Loucy and DND41 and comparing to TET2 expressing T-ALL cells lines such as SUP-T1 and Jurkat we aimed to explore if 5-AZA could reactivate TET2 in T-ALL, what effects this would have on tumorgenicity and whether Vitamin C had any synergy with these effects in T-ALL. As part of this effort we treated the cell lines SUP-T1, Jurkat, Loucy and DND41 with 5-AZA and Vitamin C and performed Total RNA-seq to explore the effects of 5-AZA and Vitamin C on the expression of genes and non-coding elements such as retrotransponsons.

2021-08-04 | E-MTAB-10512 | biostudies-arrayexpress

A TARBP2-dependent miRNA expression profile determines cancer stem cell properties and provides new candidate therapeutic reagents in Ewing's sarcoma

Project description:This SuperSeries is composed of the following subset Series: GSE30513: MicroRNA expression profiling of Ewing sarcoma cancer stem cells GSE31144: MicroRNA expression profiling of Ewing sarcoma cell lines upon TARBP2 depletion GSE31145: MicroRNA expression profiling of Ewing sarcoma spheres vs. adherent cells Refer to individual Series

2012-06-19 | E-GEOD-31146 | biostudies-arrayexpress

Breast Cancer Cell Secretome Analysis to Decipher miRNA Tumor Biology and Discover Potential Biomarkers

Project description:MicroRNA (miRNA/miR) miR526b and miR655 overexpressed tumor cell-free secretions promote breast cancer phenotypes in the tumor microenvironment (TME). However, the mechanisms of miRNA regulating TME have never been investigated. With mass spectrometry analysis of MCF7-miRNA-overexpressed versus miRNA-low MCF7-Mock tumor cell secretomes, we identified 34 novel secretory proteins coded by eight genes YWHAB, TXNDC12, MYL6B, SFN, FN1, PSMB6, PRDX4, and PEA15 those are differentially regulated. We used bioinformatic tools and systems biology approaches to identify these markers’ role in breast cancer. Gene ontology analysis showed that the top functions are related to apoptosis, oxidative stress, membrane transport, and motility, supporting miRNA-induced phenotypes. These secretory markers expression is high in breast tumors, and a strong positive correlation exists between upregulated markers’ mRNA expressions with miRNA cluster expression in luminal A breast tumors. Gene expression of secretome markers is higher in tumor tissues compared to normal samples, and immunohistochemistry data supported gene expression data. Moreover, both up and downregulated marker expressions are associated with breast cancer patient survival. miRNA regulates these marker protein expressions by targeting transcription factors of these genes. Premature miRNA (pri-miR526b and pri-miR655) are established breast cancer blood biomarkers. Here we report novel secretory markers upregulated by miR526b and miR655 (YWHAB, MYL6B, PSMB6, and PEA15) are significantly upregulated in breast cancer patients’ plasma, and are potential breast cancer biomarkers.

2023-05-10 | PXD031771 | Pride

Transcription profiling of human normal melanocytes and melamoma cell lines reveal defective cell cycle checkpoint functions in melanoma are associated with altered patterns of gene expression

Project description:Defects in DNA damage responses may underlie genetic instability and malignant progression in melanoma. Cultures of normal human melanocytes (NHMs) and melanoma lines were analyzed to determine whether global patterns of gene expression could predict the efficacy of DNA damage cell cycle checkpoints that arrest growth and suppress genetic instability. NHMs displayed effective G1 and G2 checkpoint responses to ionizing radiation-induced DNA damage. A majority of melanoma cell lines (11/16) displayed significant quantitative defects in one or both checkpoints. Melanomas with B-RAF mutations as a class displayed a significant defect in DNA damage G2 checkpoint function. In contrast the epithelial-like subtype of melanomas with wildtype N-RAS and B-RAF alleles displayed an effective G2 checkpoint but a significant defect in G1 checkpoint function. RNA expression profiling revealed that melanoma lines with defects in the DNA damage G1 checkpoint displayed reduced expression of p53 transcriptional targets, such as CDKN1A and DDB2, and enhanced expression of proliferation-associated genes, such as CDC7 and GEMININ. A Bayesian analysis tool was more accurate than significance analysis of microarrays for predicting checkpoint function using a leave-one-out method. The results suggest that defects in DNA damage checkpoints may be recognized in melanomas through analysis of gene expression. Experiment Overall Design: Normal human melanocyte and melanoma cell lines w/wo mutations in B-raf or N-ras were treated with 1.5 Gy IR irridiartion for G1 and G2 checkpoint determination. RNA was isolated from exponentially growing cultures and applied for microarray hybridizaton with Agilent 44 K (G4112A) array.

2008-06-15 | E-GEOD-7469 | biostudies-arrayexpress

RNA-seq of primary human fibroblasts after X-ray induced senescence

Project description:Determining by RNA-seq the extent of inflammatory gene expression induced in primary human fibroblasts after inducing senescence by X-irradiation.

2024-10-03 | E-MTAB-14201 | biostudies-arrayexpress

RNA-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR)

Project description:We aim at understanding how ionizing radiations (IR) increase the risk of developing myeloid leukemia. We recently showed that IR leads to the derepression of retroelements. Retroelements are major contributors of gene regulatory networks. However, the impact of retroelements derepression on the HSC transcriptome and function remains to be addressed. We hypothesized that retroelements derepression is involved in HSC transcriptomic alterations. To answer this question, we performed RNA-seq experiments in hematopoietic stem cells sorted from mice one month after they were irradiated and compared them to controls hematopoietic stem cells sorted from non-irradiated mice.

2022-06-24 | E-MTAB-11866 | 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