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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from L-02 and Hep3B cells

ABSTRACT: Constitutively expressed intracellular antiviral factors are responsible for the resistance of cells against alphavirus, especially for the inhibition of virus entry and early replication. We used microarrays to compare the gene expression profiles between resistant (L-02) and susceptible (Hep3B) cells and identified the antiviral genes that are defective in susceptible cells. RNA were extracted from normally cultured L-02 and Hep3B cells. cDNA and cRNA were produced and hybridized to Affymetrix microarrays.

ORGANISM(S): Homo sapiens

SUBMITTER: Yuan Lin

PROVIDER: E-GEOD-54342 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from L-02 and Hep3B cells

Project description:Constitutively expressed intracellular antiviral factors are responsible for the resistance of cells against alphavirus, especially for the inhibition of virus entry and early replication. We used microarrays to compare the gene expression profiles between resistant (L-02) and susceptible (Hep3B) cells and identified the antiviral genes that are defective in susceptible cells.

2014-01-23 | GSE54342 | GEO

Analysis of gene expression change between Ishikawa-02 SC and Ishikawa-02 shSOX2

Project description:We collected total RNA from both Ishikawa-02 SC and Ishikawa-02 shSOX2 and examined mRNA expression profile, comprehensively.

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ChIP sequencing following infection with CoV-02 Orf8 KO

Project description:ChIP sequencing performed on A549 cells following either Mock infection, infection with WT SARS-CoV-02, or infection with SARS-CoV-02 with Orf8 deletion

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ChIP sequencing following infection with CoV-02 Orf8 or ARKSAP KO

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Global transcriptional profile of Streptomyces avermitilis wild-type strain ATCC31267 and avermectin overproducing strain 76-02-e at different time points

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2013-05-24 | E-GEOD-47223 | biostudies-arrayexpress

Next-generation Sequencing contributes to Quantitative Analysis of Transcriptomes in circBNC2-KO L-02 cells

Project description:Purpose: We idenficied a circRNA, circBNC2, that was downregulated during hepatocytes injury. To study the function of circBNC2, we performed CRISPR-Cas9 to knock out circBNC2 in L-02 (a well recognized human hepatocytes) cells. Next-generation Sequencing was used to identified the differentially expressed mRNA between circBNC2-KO L-02 cells and wild-type L-02 cells.

2022-07-01 | GSE179620 | GEO

Altered expression of genes in WDR5 knockdown

Project description:WDR5 (WD repeat domain 5) plays an important role in the epigenetic regulation of gene transcription, involing in regulation of embryonic stem cell and cancer cell.Bladder cancer is one of the most common cancers that cause approximately 150,000 deaths per year worldwide.The goal of this study is to identify the target genes of WDR5 in bladder cancer.Our results inditcate that the genes regulated by WDR5 involved in a variety of biological functions, such as proliferation and anti-apoptosis. Bladder cancer cell line UM-UC-3 was transfected with the contol siRNA or two different WDR5 siRNA for 48h. The RNA of the transfected cells was extracted and hybridized on Affymetrix microarrays. We indentified the putative target genes of WDR5 in both WDR5 siRNA by comparing the diferent expressed genes among control, si-WDR5-2 and si-WDR5-3. We futher validated the data of microarray in UM-UC-3 and T24 by RT-qPCR and Western bloting.

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C1R.A*01:01, C1R.A*02:01, C1R.A*24:02 MHC class I immunopeptidome LC-MSMS

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2020-07-27 | PXD014754 | Pride

Substantial Influence of ERAP2 on the HLA-B*40:02 peptidome. Implications for HLA-B*27-negative ankylosing spondylitis.

Project description:HLA-B*40:02 is one of a few Major Histocompatibility Complex class I (MHC-I) molecules associated with ankylosing spondylitis (AS) independently of HLA-B*27. The endoplasmic reticulum aminopeptidase 2 (ERAP2), an enzyme that process MHC-I ligands and preferentially trims N-terminal basic residues, is also a risk factor for this disease. Like HLA-B*27 and other AS-associated MHC-I molecules, HLA-B*40:02 binds a relatively high percentage of peptides with ERAP2-susceptible residues. In this study the effects of ERAP2 depletion on the HLA-B*40:02 peptidome were analyzed. ERAP2 protein expression was knocked out by CRISPR in the transfectant cell line C1R-B*40:02 and the differences between the peptidomes from the wildtype and ERAP2-KO cells were determined by label-free quantitative comparisons. The qualitative changes dependent on ERAP2 affected about 5% of the peptidome, but quantitative changes in peptide amounts were much more substantial, reflecting a significant influence of this enzyme on the generation/destruction balance of HLA-B*40:02 ligands. As in HLA-B*27, a major effect was on the frequencies of N-terminal residues. In this position basic and small residues were increased in the absence of ERAP2 and aliphatic/aromatic residues were increased in the presence of the enzyme. Since most of the non-B*27 MHC-I molecules associated with AS risk also bind a relatively high percentage of peptides with N-terminal basic residues we hypothesize that the non-epistatic association of ERAP2 with AS might be related to the processing of peptides with these residues bound by AS-associated MHC-I molecules.

2019-09-25 | PXD014804 | Pride

Allele-specific alterations in the peptidome underlie the joint association of HLA-A*29:02 and Endoplasmic Reticulum Aminopeptidase 2 (ERAP2) with Birdshot Chorioretinopathy

Project description:Birdshot chorioretinopathy (BSCR) is a rare inflammatory eye disease very strongly associated with HLA-A*29:02, with >95% of patients carrying this allele. BSCR is also associated with endoplasmic reticulum aminopeptidase (ERAP)2, an enzyme involved in processing HLA class I ligands. We analyzed the relationship between both risk factors, to address the basis for their joint association with BSCR. Label-free quantitative mass spectrometry was used to characterize the effects of ERAP2 on the A*29:02-bound peptidome. An ERAP2-negative cell line was transduced with lentiviral constructs containing GFP or GFP-ERAP2, and the A*29:02 peptidomes from mock- and ERAP2-transduced cells were compared. A similar analysis was performed with two A*29:02-positive, ERAP1-concordant, cell lines differing in their expression or not of ERAP2. In both comparisons the presence of ERAP2 affected the following features of the A*29:02 peptidome: 1) Length, with increased amounts of peptides >9-mers, and 2) N-terminal residues, with less ERAP2-susceptible and more hydrophobic ones. The paradoxical effects on peptide length suggest that unproductive binding to ERAP2 might protect some peptides from over-trimming. The influence on N-terminal residues is consistent with a double effect of ERAP2: a direct one on peptide trimming and improved processing in concert with ERAP1. The alterations in the A*29:02 peptidome suggest that the association of ERAP2 with BSCR is through its effects on peptide processing. These differ from those on the ankylosing spondylitis-associated HLA-B*27. Thus, ERAP2 alters the peptidome of distinct HLA molecules as a function of their specific binding preferences, influencing different pathological outcomes in an allele-dependent way.

2018-05-17 | PXD007679 | Pride

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