Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TET deficiency promotes oncogenesis and DNA damage in B cells by increasing the levels of G-quadruplexes and R-loops [G4-seq]

ABSTRACT: TET deficiency promotes oncogenesis and DNA damage in B cells by increasing the levels of G-quadruplexes and R-loops [G4-seq]

PROVIDER: PRJNA678336 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13057611_1.fastq.gz	Fastqsanger.gz
	SRR13057611_2.fastq.gz	Fastqsanger.gz
	SRR13057612_1.fastq.gz	Fastqsanger.gz
	SRR13057612_2.fastq.gz	Fastqsanger.gz
	SRR13057613_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

TET deficiency promotes oncogenesis and DNA damage in B cells by increasing the levels of G-quadruplexes and R-loops [G4-seq]

Project description:Enzymes of the TET family are methylcytosine dioxygenases that undergo frequent mutational or functional inactivation in both hematological and solid cancers. Recent studies have identified recurrent loss-of-function mutations in TET proteins in human patients with Diffuse Large B-Cell Lymphoma (DLBCL). Here we investigate the role of TET proteins in the pathogenesis of DLBCL by deleting the Tet2 and Tet3 genes in mature B cells in mice. Tet deletion perturbs mature B-cell homeostasis and causes spontaneous development of Germinal Center-derived B cell lymphomas. We show that an increase in G-quadruplexes and R-loops a common feature of TET deficiency in B cells as well as other hematopoietic cells. Genome-wide analyses revealed that G-quadruplexes and R-loops accumulated primarily near transcription start sites in TET-deficient B cells, and their accumulation correlated with increased DNA double-strand breaks. Moreover, CRISPR-mediated depletion of nucleases and helicases that regulate G-quadruplexes and R-loops led to decreased viability of TET-deficient but not control primary B cells. Our studies elucidate a molecular mechanism by which TET loss-of-function might predispose to development of B cell-derived and other malignancies, and highlight novel therapeutic avenues that could be further explored.

2021-10-28 | GSE161452 | GEO

TET deficiency promotes oncogenesis and DNA damage in B cells by increasing the levels of G-quadruplexes and R-loops [HTGTS]

2021-10-28 | GSE161461 | GEO