Dataset Information

REXO5 Promotes Genomic Integrity Through Regulating R-loop Using Its Exonuclease Activity.

ABSTRACT: Chronic myeloid leukemia (CML), caused by BCR::ABL1 fusion gene, is known to regulate disease progression by altering the expression of genes. However, the molecular mechanisms underlying these changes are largely unknown. In this study, we identified RNA Exonuclease 5 (REXO5) as a novel gene with elevated mRNA expression levels in chronic myeloid leukemia (CML) patients. Additionally, using the REXO5 knockout (KO) K562 cell lines, we revealed a novel role for REXO5 in the DNA damage response (DDR). Compared to wild-type (WT) cells, REXO5 KO cells showed an accumulation of R-loops and increased DNA damage. We demonstrated that REXO5 translocates to sites of DNA damage through its RNA recognition motif (RRM) and selectively binds to R loops. Interestingly, we identified that REXO5 regulates R-loop levels by degrading mRNA within R-loop using its exonuclease domain. REXO5 KO showed ATR-CHK1 activation. Collectively, we demonstrated that REXO5 plays a key role in the physiological control of R-loops using its exonuclease domain. These findings may provide novel insights into how REXO5 expression contribute to CML pathogenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE268456 | GEO | 2024/06/08

REPOSITORIES: GEO

ACCESS DATA

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Project description:Moore2004 - Chronic Myeloid Leukemic cells and T-lymphocytes interaction A mathematical model for the interaction of between cancer cells and immune system, involving CML cancer cells, naive and effector T-lymphocytes. This model is described in the article: A mathematical model for chronic myelogenous leukemia (CML) and T cell interaction. Moore H, Li NK. J. Theor. Biol. 2004 Apr; 227(4): 513-523 Abstract: In this paper, we propose and analyse a mathematical model for chronic myelogenous leukemia (CML), a cancer of the blood. We model the interaction between naive T cells, effector T cells, and CML cancer cells in the body, using a system of ordinary differential equations which gives rates of change of the three cell populations. One of the difficulties in modeling CML is the scarcity of experimental data which can be used to estimate parameters values. To compensate for the resulting uncertainties, we use Latin hypercube sampling (LHS) on large ranges of possible parameter values in our analysis. A major goal of this work is the determination of parameters which play a critical role in remission or clearance of the cancer in the model. Our analysis examines 12 parameters, and identifies two of these, the growth and death rates of CML, as critical to the outcome of the system. Our results indicate that the most promising research avenues for treatments of CML should be those that affect these two significant parameters (CML growth and death rates), while altering the other parameters should have little effect on the outcome. This model is hosted on BioModels Database and identified by: BIOMD0000000662. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Dataset Information

REXO5 Promotes Genomic Integrity Through Regulating R-loop Using Its Exonuclease Activity.

Dataset's files

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets