Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression changes in B-ALL and DLBCL cells induced by EdC, a replication stress-inducing nucleoside analog prodrug.

ABSTRACT: RNA-sequencing analysis of B-ALL and DLBCL cell lines validate the replication stress-inducing mechanism of action (MOA) of EdC. Downregulation of genes involved in cell cycle progression and DNA biosynthesis support initial findings that EdC induces G1/S phase arrest, and upregulation of genes involved in DNA damage response (DDR) and the interferon alpha and gamma response support initial findings that EdC induces DNA damage and apoptosis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE248424 | GEO | 2023/12/08

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

EDC-3 and EDC-4 Regulate Embryonic mRNA Clearance and Biomolecular Condensate Specialization

Project description:Animal development is dictated by the selective and timely decay of mRNAs in developmental transitions, but the impact of mRNA decapping scaffold proteins in development is unknown. This study unveils the roles and interactions of the DCAP-2 decapping scaffolds EDC-3 and EDC-4 in the embryonic development of C. elegans. EDC-3 facilitates the timely removal of specific embryonic mRNAs, including cgh-1, car-1, and ifet-1 by reducing their expression, and preventing excessive accumulation of DCAP-2 condensates in somatic cells. We further uncover a novel role for EDC-3 in defining the boundaries between P-bodies, germ granules, and stress granules. Lastly, we show that EDC-4 counteracts EDC-3 and engenders the assembly of DCAP-2 with the GID (CTLH) complex, a ubiquitin ligase involved in maternal-to-zygotic transition (MZT). Our findings support a model wherein multiple RNA decay mechanisms temporally partake in the clearance of maternal and zygotic mRNAs throughout embryonic development.

2024-09-23 | GSE273136 | GEO

Gene expression changes in B-ALL and DLBCL cells induced by EdC, a replication stress-inducing nucleoside analog prodrug.

Project description:Gene expression changes in B-ALL and DLBCL cells induced by EdC, a replication stress-inducing nucleoside analog prodrug.

| PRJNA1043724 | ENA

EDC-3 and EDC-4 Regulate Embryonic mRNA Clearance and Biomolecular Condensate Specialization

Project description:EDC-3 and EDC-4 Regulate Embryonic mRNA Clearance and Biomolecular Condensate Specialization

| PRJNA1140226 | ENA

Vibrio cholerae strain:EDC-690

Project description:Vibrio cholerae strain:EDC-690 Genome sequencing and assembly

| PRJNA598238 | ENA

EDC-3 and EDC-4 Regulate Embryonic mRNA Clearance and Biomolecular Condensate Specialization

Project description:Animal development is dictated by the selective and timely decay of mRNAs in developmental transitions. The implication of mRNA decapping scaffold proteins in these processes was unknown. This study delineates the roles and interactions of the DCAP-2 decapping scaffolds EDC-3 and EDC-4 in the embryonic development of C. elegans. EDC-3 facilitates the timely removal of specific embryonic mRNAs, including ifet-1, car-1, and cgh-1, reducing their expression, and preventing excessive accumulation of DCAP-2 condensates in somatic cells. We further uncover a novel role for EDC-3 in defining the biochemical boundaries between P-bodies, P-granules, and stress granules. Lastly, we show that EDC-4 counteracts EDC-3 and mediates the assembly of DCAP-2 with the GID (CTLH) complex, a ubiquitin ligase involved in maternal-to-zygotic transition (MZT). Our findings refine a model wherein multiple RNA decay mechanisms temporally partake in the clearance of maternal and zygotic mRNAs throughout embryonic development.

2024-02-02 | MSV000093990 | MassIVE

Rna_seq analysis of muscle in click and EDC treated mouse

Project description:First, two groups of mice were subjected to hindlimb ischemic modeling. Then, peptide hydrogels synthesized by EDC reaction and click reaction were injected into the ischemic limbs of each group of mice, respectively. Several days later, RNA-seq analysis was performed on the ischemic limb muscles of both groups of mice.

2023-12-23 | GSE250423 | GEO

An Undesirable Side Effect of EDC-catalyzed Carboxyl Labeling Approach

Project description:Carbodiimide catalyzed carboxyl and amine conjugation (amidation) has been widely used to protect carboxyl groups. N-(3-dimethylaminopropyl)-N’-ethylcarbodiimide (EDC) is the most commonly used carbodiimide reagent in protein chemis-try due to its high efficiency and high solubility in aqueous media. It has also been applied in different proteomics studies including protein terminomics, protein glycosylation and crosslinking. Herein, we report that the EDC catalyzed amidation could cause a +155 Da side-modification at the tyrosine residue and severely hamper the identification of Tyr-containing peptides. We discovered the extremely low identification rate of Tyr-containing peptides in different published studies that employed EDC-catalyzed amidation. We carried out a systematic study and discovered a +155 Da side-modification occur-ring specifically on Tyr as the addition of EDC. Consideration of the side-modification in database search enabled the identification of 13 times more Tyr-containing peptides. Furthermore, we demonstrated that the treatment with carbonate-containing buffer could effectively reduce the side-product. Our study also implies that chemical reactions in proteomic studies should be carefully evaluated prior to their wide applications.

2020-12-10 | PXD020042 | Pride

Vibrio cholerae O1 str. EDC-020

Project description:Vibrio cholerae O1 str. EDC-020 Genome sequencing and assembly

| PRJNA76215 | ENA

Vibrio cholerae O1 str. EDC-022

Project description:Vibrio cholerae O1 str. EDC-022 Genome sequencing and assembly

| PRJNA76217 | ENA

Sapacitabine, the prodrug of CNDAC, is a nucleoside analog with a unique action mechanism of inducing DNA strand breaks.

Project description:Sapacitabine is an orally bioavailable prodrug of the nucleoside analog 2'-C-cyano-2'-deoxy-1-?-D-arabino-pentofuranosylcytosine (CNDAC). Both the prodrug and active metabolite are in clinical trials for hematologic malignancies and/or solid tumors. CNDAC has a unique mechanism of action: after incorporation into DNA, it induces single-strand breaks (SSBs) that are converted into double-strand breaks (DSBs) when cells go through a second S phase. In our previous studies, we demonstrated that CNDAC-induced SSBs can be repaired by the transcription-coupled nucleotide excision repair pathway, whereas lethal DSBs are mainly repaired through homologous recombination. In the current work, we used clonogenic assays to compare the DNA damage repair mechanism of CNDAC with two other deoxycytidine analogs: cytarabine, which is used in hematologic malignacies, and gemcitabine, which shows activity in solid tumors. Deficiency in two Rad51 paralogs, Rad51D and XRCC3, greatly sensitized cells to CNDAC, but not to cytarabine or gemcitabine, indicating that homologous recombination is not a major mechanism for repairing damage caused by the latter two analogs. This study further suggests clinical activity and application of sapacitabine that is distinct from that of cytarabine or gemcitabine.

| S-EPMC3777512 | biostudies-other

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data