Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer

ABSTRACT: Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer

PROVIDER: PRJNA774805 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16578433_1.fastq.gz	Fastqsanger.gz
	SRR16578433_2.fastq.gz	Fastqsanger.gz
	SRR16578434_1.fastq.gz	Fastqsanger.gz
	SRR16578434_2.fastq.gz	Fastqsanger.gz
	SRR16578435_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 80

Similar Datasets

Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer [CUT&RUN]

Project description:Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer [CUT&RUN]

| PRJNA774787 | ENA

Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer [RNA-seq]

Project description:Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer [RNA-seq]

| PRJNA774807 | ENA

Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer [CUT&RUN]

Project description:Cancer cells exhibit rewired transcriptional regulatory networks that promote tumor growth and survival. However, the processes that configure these pathological networks remain poorly understood. Through a pan-cancer epigenomic analysis, we found that primate-specific endogenous retroviruses (ERVs) are an abundant source of enhancers that mediate transcriptional dysregulation in cancer. In colorectal cancer and other epithelial tumors, AP1 signaling drives aberrant activation of enhancers derived from the primate-specific ERV family LTR10. CRISPR studies revealed that LTR10 elements control colorectal cancer-specific gene expression at multiple loci associated with tumorigenesis. Within the human population, individual LTR10 elements show extensive structural variation due to repeat instability of an internal variable number tandem repeat (VNTR) region that affects AP1 binding. Our findings reveal that ERV-derived enhancers link oncogenic signaling to transcriptional dysregulation and shape the evolution of cancer-specific regulatory networks.

2021-10-31 | GSE186608 | GEO

Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer [RNA-seq]

2021-10-31 | GSE186618 | GEO

Endogenous retroviruses mediate IFN-independent protection against HSV-2 infection

Project description:Endogenous retroviruses mediate IFN-independent protection against HSV-2 infection

| PRJNA768446 | ENA

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia

Project description:Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia

| PRJNA563616 | ENA

Endogenous retroviruses mediate IFN-independent protection against HSV-2 infection

Project description:Endogenous retroviruses (ERVs) are genomic sequences that originated from retroviruses and are present in most eukaryotic genomes. Both beneficial and detrimental functions are attributed to ERVs, but whether ERVs contribute to antiviral immunity is not well studied. Here, we used herpes simplex virus type 2 (HSV-2) infection as a model and found that mice deficient in Toll-like receptor 7 (Tlr7-/-) that have high systemic levels of infectious ERVs are resistant to intravaginal HSV-2 infection, compared with wildtype C57BL/6 (B6) mice. We deleted the endogenous ecotropic murine leukemia virus (Emv2) locus on the Tlr7-/- background (Emv2-/-Tlr7-/-) and found that Emv2-/-Tlr7-/- mice lose protection against HSV-2 infection. Intravaginal application of purified ERVs prior to HSV-2 infection delays disease in both B6 and highly susceptible interferon-alpha receptor-deficient (Ifnar1-/-) mice. We did not observe enhanced type I interferon (IFN-I) signaling in the vaginal tissues from Tlr7-/- mice or B6 mice treated with purified ERVs, and instead found enrichment in genes associated with extracellular matrix organization. Together, our results revealed an IFN-independent modulation of the vaginal epithelium by ERVs that protects mice against vaginal HSV-2 infection and delays disease.

2021-10-06 | GSE185281 | GEO

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [ChIP-Seq]

Project description:Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [ChIP-Seq]

| PRJNA563608 | ENA

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [DNase-Seq]

Project description:Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [DNase-Seq]

| PRJNA563620 | ENA

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [RNA-Seq]

Project description:Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [RNA-Seq]

| PRJNA563622 | ENA