Ontology highlight
ABSTRACT:
PROVIDER: PRJNA650395 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12374618_1.fastq.gz | Fastqsanger.gz | |||
| SRR12374618_2.fastq.gz | Fastqsanger.gz | |||
| SRR12374619_1.fastq.gz | Fastqsanger.gz | |||
| SRR12374619_2.fastq.gz | Fastqsanger.gz | |||
| SRR12374620_1.fastq.gz | Fastqsanger.gz |
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Project description:RATIONALE: The Epstein Barr virus can cause cancer and lymphoproliferative disorders. Ganciclovir is an antiviral drug that acts against the Epstein Barr virus. Arginine butyrate may make virus cells more sensitive to ganciclovir. Combining ganciclovir and arginine butyrate may kill more Epstein Barr virus cells and tumor cells.
PURPOSE: Phase I trial to study the effectiveness of arginine butyrate plus ganciclovir in treating patients who have cancer or lymphoproliferative disorders that are associated with the Epstein Barr virus.
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Project description:Gene expression analysis in Epstein-Barr virus negative DLBCL samples obtained from patients with Richter syndrome, lymphocytes from CLL patients and epstein-Barr virus positive DLBCL cell lines derived after CLL tumors xenotransplantation
2020-08-29 | GSE103265 | GEO
Project description:In homologous recombination deficient cells, polymerase theta (Pol θ)-mediated end-joining (TMEJ) repairs replicative DNA breaks during mitosis through interactions with RHINO and TOPBP1. V(D)J recombination and class switch recombination (CSR) rely on DNA breakage in G1-phase B lymphocytes and repair by non-homologous end-joining (NHEJ). In this study, we assayed CSR in primary B cells deficient in XRCC4, SHLD1, and Pol θ. We found that B cells deficient in both XRCC4 and Pol θ, or SHLD1 and Pol θ, exhibit an increased rate of IgH breaks, while retaining CSR levels similar to those of B cells deficient in XRCC4 or SHLD1. We show that in XRCC4- or SHLD1-deficient B cells, Pol θ promotes the formation of aberrant recombination products characterized by exacerbated double-strand break (DSB) end resection, inversion and microhomology, and that these end-joining events occur independently of RHINO. Furthermore, we find that TMEJ of RAG-generated DSBs is also independent of RHINO and concomitant to S/G2 entry. Based on these results, we propose that in the absence of NHEJ, TMEJ repairs persistent G1-phase DSBs in S/G2, rather than in mitosis.
2025-08-26 | GSE306291 | GEO
Project description:Ubiquitination is a crucial post-translational modification required for the proper repair of DNA double-strand breaks (DSBs) induced by ionising radiation (IR). DSBs are mainly repaired through homologous recombination (HR) when template DNA is present and non-homologous end joining (NHEJ) in its absence. Additionally, microhomology-mediated end joining (MMEJ) and single strand annealing (SSA) provide back-up DSBs repair pathways. However, the mechanisms controlling their use remain poorly understood. By employing a high-resolution CRISPR screen of the ubiquitin system after IR, we systematically uncover genes required for cell survival and elucidate a critical role of the E3 ubiquitin ligase SCFcyclin F in cell cycle dependent DSB repair. We show that SCFcyclin F -mediated EXO1 degradation prevents DNA end resection in mitosis, allowing MMEJ to take place. Moreover, we identify a conserved cyclin F recognition motif, distinct from the one used by other cyclins, with broad implications in cyclin specificity for cell cycle control.
2024-10-17 | PXD051841 | Pride
Project description:Comparsion of cellular gene expression between a control B lymphoma cell-line (BJAB pz2) stably transfected with an empty vector and a BJAB cell-line stably expressing Epstein-Barr virus EBNA 3C (BJAB E3C-4). These cell lines are described in Wang, F., C. Gregory, C. Sample, M. Rowe, D. Liebowitz, R. Murray, A. Rickinson, and E. Kieff. 1990. Epstein-Barr virus latent membrane protein (LMP1) and nuclear proteins 2 and 3C are effectors of phenotypic changes in B lymphocytes: EBNA-2 and LMP1 cooperatively induce CD23. J Virol 64:2309-2318)
2012-03-13 | E-MEXP-3585 | biostudies-arrayexpress
Project description:Two DNA repair pathways, non-homologous end joining (NHEJ) and alternative end joining (A-EJ), are involved in V(D)J recombination and chromosome translocation. Previous studies reported distinct repair mechanisms for chromosome translocation, with NHEJ predominantly involved in human and A-EJ in mice. NHEJ depends on DNA-PKcs, a critical partner in synapsis formation and downstream component activation. While DNA-PKcs inhibition promotes chromosome translocations harboring microhomologies in mice, its synonymous effect in human is not known. We find partial DNA-PKcs inhibition in human cell lines leads to increased genome-wide translocations composed mostly of direct joints, indicating the continued involvement of dampened NHEJ in these processes. In contrast, complete DNA-PKcs inhibition and genetic inhibition DNA-PKcs kinase domain substantially increased microhomology-mediated end joining (MMEJ), thus bridging the two different translocation mechanisms between human and mice. Similar to a previous study on Ku70 deletion, DNA-PKcs deletion in G1/G0-phase mouse pro-B cell lines, impair the recombination of RAG1/2-mediated DNA double-strand breaks (DSBs). This DNA-PKcs-deficient repair mechanism exhibited reduced V(D)J recombination efficiency, increased end resection, decreased polymerase-mediated insertions, loss of recombination fidelity and generated relatively higher rates of chromosome translocation as a consequence of dysregulated coding and signal end joining. Our study underscores DNA-PKcs in suppressing illegitimate chromosome rearrangement in both species.
2023-12-30 | GSE249453 | GEO
Project description:To generate antibodies with different effector functions, B cells undergo Immunoglobulin class switch recombination (CSR). The ligation step of CSR is usually mediated by the classical non-homologous end-joining (cNHEJ) pathway. In cNHEJ-deficient cells, a remarkable ~25% CSR can be achieved by the alternative end-joining (A-EJ) pathway that preferentially uses microhomology (MH) at the junctions. While A-EJ mediated repair of endonuclease generated breaks requires DNA end-resection, we show that CtIP-mediated DNA end-resection is dispensable for A-EJ-mediated CSR using cNHEJ-deficient B cells. High-throughput sequencing analyses revealed that loss of ATM/ATR phosphorylation of CtIP at T855 or ATM kinase inhibition suppress resection without altering the MH-pattern of the A-EJ-mediated switch junctions. Moreover, we found that ATM kinase promotes Alt-EJ mediated CSR by suppressing inter-chromosomal translocations independent of end-resection. Finally, temperol analyses reveal that MHs are enriched in early internal deletions even in cNHEJ-proficient B cells. Thus, we propose that repetitive IgH switch regions represent favoriate substrates for MH-mediated end-joining contributing to the robustness and resection-indepndence of A-EJ-mediated CSR.
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Project description:Epstein-Barr virus has been reported to regulate cellular microRNA expression in B cells. In the present study, we investigated the differential microRNAs modulated by Epstein-Barr virus in Naspharyngeal Carcinoma, using CapitalBio corporation's mammalian miRNA arrays. Three cellular models were used in this study: the human naspharyngeal carcinoma cell line TW03 as a blank control; TW03 transfected with Epstein-Barr virus encoded LMP1; TW03 transfected with Epstein-Barr virus encoded LMP2A
2011-01-13 | E-GEOD-26596 | biostudies-arrayexpress