Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Illumina sequencing of PCR products derived from TBLV-induced tumors in the presence and absence of Rem

ABSTRACT: Sequencing of portions (polymerase, envelope, and part of the 3’ LTR) of the TBLV retroviral genome were recovered by PCR amplification from tumors induced with or without Rem expression. PCR products from the mouse Gapdh gene were obtained as a control for acquisition of mutations during PCR and library preparation.

ORGANISM(S): Viruses

PROVIDER: GSE134189 | GEO | 2019/07/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Illumina sequencing of PCR products derived from TBLV-induced tumors in the presence and absence of Rem

Project description:Illumina sequencing of PCR products derived from TBLV-induced tumors in the presence and absence of Rem

| PRJNA554252 | ENA

REM-CR

Project description:REM-CR

| PRJEB73320 | ENA

rem-1 analysis in C. elegans

Project description:small RNA libraries from total RNA isolated from young adult animals Wild-type and rem-1 mutant animals were used for RNA isolation. Regular libraries were made using adaptor ligations at both ends. In addition, librraies were made from oxidised and TAP treated RNA.

2012-10-30 | E-GEOD-31783 | biostudies-arrayexpress

An Excitatory Circuit in Perioculomotor Midbrain for Non-REM Sleep Control

Project description:The perioculomotor (pIII) region of the midbrain was postulated as a sleep-regulating center in the 1890s but largely neglected in subsequent studies. Using activity-dependent labeling and gene-expression profiling, we identified pIII neurons that promote non-REM (NREM) sleep.

2019-05-01 | GSE124681 | GEO

Screening of reference genes by qRT-PCR in Chelonus formosanus

Project description:Chelonus formosanus is an important parasitic natural enemy of Lepidopteran insects and has great value in the biological control of insect pests. To screen the reference genes in the real-time fluorescence quantitative PCR (qRT-PCR) assay of Chelonus formosanus, six candidate reference genes were selected based on transcriptome data, including GAPDH, ACT, TU, TF, HSP, and RP. The expression stability of these six internal reference genes was determined by qRT-PCR in different tissues (head, chest, abdomen) and at different temperatures (11℃and 41℃), as well as with two insecticides (dinotefuran and chlorantraniliprole).

2024-12-14 | GSE283846 | GEO

Apobec-Mediated Retroviral Hypermutation In Vivo is Dependent on Mouse Strain [RNA-seq]

Project description:Retroviruses cause lifelong infections resulting from their ability to thwart innate immunity. The Apobec family of cytidine deaminases are part of the innate immune response that recognizes and mutates foreign nucleic acids, including those from multiple viruses. Multiple retroviral antagonists of Apobecs have been identified, including mouse mammary tumor virus (MMTV)-encoded Rem protein. Previous experiments have shown that Rem-null MMTV or closely related TBLV proviruses from BALB/c tumors accumulate G-to-A and C-to-T mutations typical of Apobecs compared to wild-type proviruses expressing Rem. The difference in mutations between Rem-expressing and non-expressing MMTV strains largely disappeared in mice lacking the Apobec family member, activation-induced cytidine deaminase (AID). These results suggested that Rem is an AID antagonist. In this study, we attempted to study AID-mediated mutations of TBLV proviruses lacking Rem expression obtained from tumors in C57BL/6 (B6) wild-type and AID-knockout backgrounds. Surprisingly, no differences in G-to-A mutations were observed in TBLV proviruses regardless of Rem expression, yet such mutations were significantly reduced in proviruses obtained from mA3/AID-double knockout mice relative to those from wild-type B6 or AID-knockout mice. Many cellular mRNAs involving the innate immune response, but not Apobecs, were elevated in the absence relative to the presence of Rem expression on the B6 AID-knockout background. These results revealed that Apobec-mediated mutagenesis is dependent on mouse strain and suggested a second means of Rem-dependent immune evasion.

2024-04-15 | GSE263655 | GEO

Apobec-Mediated Retroviral Hypermutation In Vivo is Dependent on Mouse Strain

2024-04-16 | GSE263741 | GEO

Strong Activation of Retroviral LTRs in HCC

Project description:<p>The ncRNA transcriptome of human hepatocellular carcinoma (HCC) is largely unexplored. We used CAGE to characterize transcription start sites across different etiologies of human HCCs with emphasis on ncRNAs. Here we report that retroviral LTR promoters, expressed in healthy tissues such as testis and placenta but not liver, are widely activated in HCC. Despite HCC heterogeneity, a subset of LTR-derived ncRNAs were more than 10-fold up-regulated in the vast majority of samples. HCCs with a high LTR activity mostly had a viral etiology, were less differentiated and showed higher risk of recurrence. CAGE enabled us to build a promoter map for HCC, which uncovers a new layer of complexity in HCC genomics.</p>

| phs000885 | dbGaP

PCR-Bias in multi-template PCR: validation data

Project description:PCR-Bias in multi-template PCR: validation data

| PRJEB77604 | ENA

Onco-exaptation of an Endogenous Retroviral LTR Drives IRF5 Expression in Hodgkin Lymphoma

Project description:The transcription factor interferon regulatory factor 5 (IRF5) is upregulated in Hodgkin lymphoma (HL) and a key regulator of the aberrant transcriptome characteristic of this disease. Here we show that IRF5 upregulation in HL is driven by transcriptional activation of a normally dormant endogenous retroviral LOR1a long terminal repeat (LTR) upstream of IRF5. Specifically, through screening of RNA-seq libraries, we detected LTR-IRF5 chimeric transcripts in multiple HL cell lines but not in normal B-cell controls. In HL, the LTR was in an open and hypomethylated epigenetic state and we further show the LTR is the site of transcriptional initiation. Among HL cell lines, usage of the LTR promoter strongly correlates with overall levels of IRF5 mRNA and protein, indicating that LTR transcriptional awakening is a major contributor to IRF5 upregulation in HL. Taken together, oncogenic IRF5 overexpression in HL is the result of a specific LTR transcriptional activation. We propose that such LTR derepression is a distinct mechanism of oncogene activation (“onco-exaptation”) and that such a mechanism warrants further investigation in molecular and cancer research.

| EGAS00001001205 | EGA

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