Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Non-canonical immune response to inhibition of DNA methylation via stabilization of dsRNAs from endogenous retroviruses

ABSTRACT: Non-canonical immune response to inhibition of DNA methylation via stabilization of dsRNAs from endogenous retroviruses

PROVIDER: PRJNA638824 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11996357_1.fastq.gz	Fastqsanger.gz
	SRR11996357_2.fastq.gz	Fastqsanger.gz
	SRR11996358_1.fastq.gz	Fastqsanger.gz
	SRR11996358_2.fastq.gz	Fastqsanger.gz
	SRR11996359_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 22

Similar Datasets

Non-canonical immune response to inhibition of DNA methylation via stabilization of dsRNAs from endogenous retroviruses

Project description:5-Aza-2'-deoxycytidine, also known as decitabine, is a DNA hypomethylating agent (HMA) used to treat acute myeloid leukemia (AML) and pre-leukemic disorder myelodysplastic syndrome (MDS). Decitabine activates the transcription of endogenous retroviruses (ERV), which can induce immune response by acting as cellular double-stranded RNAs. Here, we employ an image-based screening system to identify dsRNA-binding factors that mediate the downstream effect of ERV induction. We find that STAUFEN1 (STAU1) knockdown decreases the interferon signature and rescues decitabine-mediated cell death. Our subsequent analyses reveal that STAU1 directly binds to ERV RNAs and stabilizes the RNAs together with a long noncoding RNA, TINCR. Analysis of a clinical patient cohort further supports that MDS and AML patients with low STAU1 and TINCR expressions exhibited poor response to the HMA therapy. Our study reveals that decitabine-mediated cell death is a consequence of complex interactions among different dsRNA binding proteins for access to their common dsRNA targets.

2021-04-14 | GSE152258 | GEO

Hijacking of transcriptional condensates by endogenous retroviruses

Project description:Hijacking of transcriptional condensates by endogenous retroviruses

| PRJNA669013 | ENA

H3.3 deposition at endogenous retroviruses in embryonic stem cells

Project description:We report DAXX-dependent deposition of histone H3.3 at at endogenous retroviruses in embryonic stem cells.

2015-07-16 | GSE70966 | GEO

Endogenous retroviruses promote prion-like spreading of proteopathic seeds

Project description:Prion-like spreading of protein misfolding is characteristic for neurodegenerative diseases, but the exact mechanisms of intercellular protein aggregate dissemination remain unresolved. Evidence accumulates that endogenous retroviruses, remnants of viral germline infections that are normally epigenetically silenced, become upregulated in neurodegenerative diseases such as amyotrophic lateral sclerosis and tauopathies. Here we uncover that activation of endogenous retroviruses affects prion-like spreading of proteopathic seeds. To identify changes in the proteome of donor cells that might contribute to protein aggregate spreading, we performed mass spectrometry analyses of total cell lysates and donor EV fractions using N2a cells expressing HA epitope-tagged Sup35 NM prion protein at early (P07) and late passages (P16) post cryopreservation. Among the proteins increased in donor cells and EVs upon prolonged culture, we identified mouse endogenous MLV retrovirus proteins to be highly increased.

2023-10-18 | PXD043201 | Pride

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment II

Project description:Telomerase plays a pivotal role in tumorigenesis by both telomere-dependent and telomere-independent activities, although the underlying mechanisms are not completely understood. Using single-sample gene set enrichment analysis (ssGSEA) across 9,264 tumour samples, we observed that expression of telomerase reverse transcriptase (TERT) is closely associated with immune-suppressive signatures. We demonstrated that TERT can activate a subclass of endogenous retroviruses (ERVs) to form double-stranded RNAs (dsRNAs), which were sensed by the RIG-1/MDA5-MAVS signalling pathway and triggered interferon signalling in cancer cells. Furthermore, we showed that TERT-induced ERVs/interferon signalling stimulated the expression of chemokines, including CXCL10, which induced suppressed T cell infiltration with increased percentage of CD4+ and FOXP3+ cells. These data reveal an unanticipated role for telomerase as a transcriptional activator of ERVs and provide strong evidence that TERT-mediated ERVs/interferon signalling contributes to immune suppression in tumours.

2022-02-22 | GSE169713 | GEO

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment I

2022-02-22 | GSE169711 | GEO

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment III

2022-02-22 | GSE169714 | GEO

TRIM28 silences endogenous retroviruses in neural progenitor cells

Project description:Here we show that in neural progenitor cells (NPCs) TRIM28 silences transcription of two groups of endogenous retroviruses (ERVs): IAP1 and MMERVK10C. Derepression of ERVs in Trim28-deficient NPCs was associated with a loss of H3K9me3 and resulted in transcriptional upregulation and reverse transcription. These findings demonstrate a unique dynamic transcriptional regulation of ERVs in NPCs. Analysis of upregulation of ERVs in Trim28-deficient NPCs

2015-01-07 | E-GEOD-45930 | biostudies-arrayexpress

TRIM28 silences endogenous retroviruses in neural progenitor cells

2015-01-07 | GSE45930 | GEO

Endogenous retroviruses are associated with hippocampus-based memory impairment

Project description:Endogenous retroviruses are associated with hippocampus-based memory impairment

| PRJNA573055 | ENA