Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Targeting Succinate Receptor Effectively Inhibits Periodontitis

PROVIDER: PRJNA772167 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16455701_1.fastq.gz	Fastqsanger.gz
	SRR16455701_2.fastq.gz	Fastqsanger.gz
	SRR16455801_1.fastq.gz	Fastqsanger.gz
	SRR16455801_2.fastq.gz	Fastqsanger.gz
	SRR16455703_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 186

Similar Datasets

The deubiquitinase OTUD1 attenuates periodontal inflammation by restricting neutrophil protein transport

Project description:We report that OTUD1 acts as an immune regulator in periodontitis. OTUD1 inhibits neutrophils migration to inflammatory site via blocking surface protein presentation. Our data reveals that activation of OTUD1 may be a potential strategy for periodontitis treatment.

2024-10-31 | GSE216573 | GEO

Identification of the immune enhancement effect of CpG ODN on periodontitis genetic vaccine by RNA sequencing

Project description:Periodontitis is one of the main causes of tooth loss in adults. Early diagnosis and intervention can effectively control the progression of periodontitis. The research group constructed a periodontitis genetic vaccine in the early stage and improved the immunogenicity of the body by adding CpG oligonucleotide (CpG ODN). The purpose of this study was to analyse the potential mechanism by which CpG ODN adjuvants enhance the preventive effect of periodontitis genetic vaccines at the molecular level by transcriptome sequencing and to screen out key genes and signaling pathways for follow-up research.

2025-06-21 | GSE206597 | GEO

Myc-mediated SDHA Acetylation Triggers Epigenetic Regulation of Gene Expression and Tumorigenesis.

Project description:Trimethylated H3K4 (H3K4me3), which is often found surrounding the transcriptional start site of active genes, is strongly enriched in the promoter regions of Myc-targeted genes. Succinate, which inhibits JmjC domain-containing histone demethylases (JHDMs), can induce H3K4me3 level of the promoter regions. It's interesting to ask whether Myc can mediate H3K4me3 by regulating cellular succinate level. Here, We used ChIP-seq to study Myc modulates H3K4me3 by altering succinate levels, dimethyl succinate (DMS), a membrane-permeable succinate analog, was introduced to treat CA46 cells with high or depleted Myc expression. And we also performed RNA-seq assays in Myc expressed or depleted CA46 cells with or without DMS treatment.

2020-03-18 | GSE141227 | GEO

RNA-sequencing of FACS-sorted hematopoietic stem and progenitor cells (LSK) from bone marrow of WT and Sucnr1 knock-out mice

Project description:Succinate is a metabolic signal that links hypoxia to IL-1β and cell responses in myeloid cells through intracellular mechanisms, but also autocrine/paracrine processes through succinate receptor 1 (Sucnr1). Succinate and its receptor have been scarcely studied in the context of hematopoiesis under health or disease. We investigated the in vivo role and molecular mechanisms of succinate and Sucnr1 in normal and malignant hematopoiesis, using an in vivo knock-out (KO) of Sucnr1.

2025-12-02 | GSE215255 | GEO

Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

Project description:Drug resistance is vital for the poor prognosis of acute myeloid leukemia (AML) patients, but the underlying mechanism remains poorly understood. Given the unique microenvironment of bone marrow, we reasoned that drug resistance of AML might rely on distinct microenvironment-associated metabolic processes. Here, we identified SDH deficiency and over-cumulative succinate as typical features in AML, with a marked function in causing the resistance of AML cells to a wide range of anti-cancer therapies. Mechanistically, succinate promoted the accumulation of oncogenic proteins in a manner that precedes transcriptional activation. This function was mediated by succinate-triggered upregulation of UBC12 phosphorylation, which impaired its E2 function in cullins neddylation. Notably, decreasing succinate levels by fludarabine could effectively restore the drug sensitivity of SDH-deficient AML PDX. Together, we uncover a novel function of succinate in driving drug resistance by regulating p-UBC12/cullin activity, and indicate reshaping succinate metabolism as a promising treatment for SDH-deficient AML.

2024-08-27 | GSE247623 | GEO

Myc-mediated SDHA Acetylation Triggers Epigenetic Regulation of Gene Expression and Tumorigenesis

Project description:Trimethylated H3K4 (H3K4me3), which is often found surrounding the transcriptional start site of active genes, is strongly enriched in the promoter regions of Myc-targeted genes. Succinate, which inhibits JmjC domain-containing histone demethylases (JHDMs), can induce H3K4me3 level of the promoter regions. It's interesting to ask whether Myc can mediate H3K4me3 by inhibiting SDH activity and inducing cellular succinate level. Here, We used ChIP-seq to study Myc modulates H3K4me3 by altering succinate levels, dimethyl succinate (DMS), a membrane-permeable succinate analog, was introduced to treat P493-6 cells with high or depleted Myc expression. And we performed RNA-seq assays in Myc expressed or depleted P493-6 cells with or without DMS treatment. Besides, we also performed RNA-seq assays in Myc expressed or depleted P493-6 cells with or without 3-nitropropionic acid (3-NPA, SDH enzyme inhibitor) treatment.

2020-03-18 | GSE124255 | GEO

SDH deficiency-driven succinate accumulation dictates the drug resistance of AML through regulating p-UBC12/cullin activity

2024-08-28 | PXD047175 | Pride

SDH deficiency-driven succinate accumulation dictates the drug resistance of AML through regulating p-UBC12/cullin activity

2024-08-28 | PXD053722 | Pride

Extracellular Succinate Hyperpolarizes M2 Macrophages through SUCNR1/GPR91-Mediated Gq Signaling

Project description:Succinate functions both as a classical TCA cycle metabolite and as an extracellular metabolic stress signal sensed by the mainly Gi-coupled succinate receptor, SUCNR1. In the present study, we characterize and compare effects and signaling pathways activated by succinate and both classes of non-metabolite SUCNR1 agonists. By use of specific receptor and pathway inhibitors, rescue in G protein depleted cells and monitoring of receptor G protein activation by BRET we surprisingly identify Gq rather than Gi signaling, to be responsible for SUCNR1-mediated effects on basic transcriptional regulation. Importantly, in primary human M2 macrophages, where SUCNR1 is highly expressed, we demonstrate that physiological concentrations of extracellular succinate act through SUCNR1 activated Gq signaling to efficiently regulate transcription of immune function genes in a manner that hyperpolarizes their M2 versus M1 phenotype. Thus, sensing of stress-induced extracellular succinate by SUCNR1 is an important transcriptional regulator in human M2 macrophages through Gq signaling.

2021-04-30 | GSE173611 | GEO

ChIP-Seq analysis C57BL/6 thymocytes

Project description:In this study, we show that in addition to regulating DP thymocytes survival, RORgT also controls genes that regulate thymocyte migration, proliferation, and T cell receptor (TCR) selection. Strikingly, pharmacological inhibition of RORg skews TCR gene rearrangement, limits T cell repertoire diversity, and inhibits development of autoimmune encephalomyelitis. Thus, targeting RORgT not only inhibits Th17 cell development and function but also fundamentally alters thymic-emigrant recognition of self and foreign antigens.

2016-10-20 | GSE88916 | GEO

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