Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

APMS analysis of endogenous mGlu2 receptor interactome in mice prefrontal cortex

ABSTRACT: Metabotropic glutamate receptor 2 (mGlu2) attracts particular attention as a possible target for a new class of antipsychotics. However, the signaling pathways transducing the effects of mGlu2 in the brain remain poorly characterized. Here, we addressed this issue by identifying native mGlu2 interactome in mouse prefrontal cortex. Nanobody-based affinity purification and mass spectrometry identified 149 candidate mGlu2 partners.

INSTRUMENT(S): Q Exactive HF-X

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Prefrontal Cortex

SUBMITTER: Franck Vandermoere

LAB HEAD: Franck Vandermoere

PROVIDER: PXD038192 | Pride | 2024-01-29

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Maxquant_band_1.zip	Other
	Maxquant_band_2.zip	Other
	Maxquant_band_3.zip	Other
	Maxquant_band_4.zip	Other
	Maxquant_band_5.zip	Other

Items per page:

1 - 5 of 26

Similar Datasets

Phosphoproteomics analysis of anti-cancer effects of ginsenoside Rg3 in human breast cancer cells

Project description:The breast cancer incidence has been increasing in China, with the earlier age of onset compared with Western countries. Traditional Chinese medicine has been provided as one of the major source of anti-cancer drugs. Ginseng is one of the most common traditional medicines in China. Ginsenosides, the saponins in the plant Panax (ginseng) are the major active components responsible for their chemopreventive effects from cancer. However, the mechanisms by which ginsenosides exert their anti-cancer effect remain elusive. By combining TMT-based quantitation with TiO2-based phosphopeptide enrichment, we performed a quantitative analysis of the changes of the phosphoproteomes in ginsenoside Rg3-treated breast cancer MDA-MB-231 cells. We were able to quantitate 5,140 phosphorylation sites on 2,041 phosphoproteins. Our data show that the phosphorylation status of 13 sites was changed in MDA-MB-231 cells upon Rg3 treatment. The perturbed phosphoproteins are CPSF7, EEF2, HIRIP3, MAGED2, MPRIP, MYCBP2, PAWR, PPP1R12A, RANBP2, SEPT9, TMPO, and UFL1. These proteins are involved in various biological processes, including protein synthesis, cell division, and inhibition of NF-κB signaling. Our study revealed that Rg3 exerts its anti-cancer effects through a combination of different signaling pathways.

2018-01-08 | PXD003092 | Pride

Quantitative Phosphoproteomics Reveals Genistein as a Modulator of Cell Cycle and DNA Damage Response Pathways

Project description:Around one sixth of breast cancer cases are classified as triple-negative breast cancer (TNBC), named after the absence of the expression of estrogen receptors (ER), progesterone receptors (PR), and human epidermal growth factor receptor 2 (HER2); however, patients with TNBC suffer from poor clinical outcome and shortage of targeted therapy. Genistein, an estrogenic soy isoflavone, shows anti-cancer effects in TNBC cells such as inducing G2/M cell cycle arrest and apoptosis. However, the underlying mechanism of its anti-cancer effects is poorly understood and its elucidation can help the development of novel therapeutic strategies for TNBC. In this study, by combining isobaric tag-based TMT labeling with titanium dioxide-based phosphopeptide enrichment, we quantitated 5,445 phosphorylation sites on 2,008 phosphoproteins in a TNBC cell line, MDA-MB-231, upon genistein treatment. Our analysis revealed 332 genistein-regulated phosphorylation sites on 226 proteins. Our data show that genistein can regulate several biological processes during the cell cycle, including DNA replication, cohesin complex cleavage, and kinetochore formation. In the meantime, genistein can also activate DNA damage response, including activation of ATR and BRCA1 complex. Overall, for the first time, our study present the evidence that genistein could inhibit TNBC cell growth by regulating the cell cycle and DNA damage response. Our findings help elucidate the mechanisms through which genistein exerts its anti-cancer effects in TNBC cells.

2016-01-26 | PXD002735 | Pride

CTRP6 promotes macrophage inflammatory response and its deficiency attenuates LPS-induced inflammation

Project description:Macrophages play critical roles in inflammation and tissue homeostasis, and their functions are regulated by various autocrine, paracrine, and endocrine factors. We have previously shown that CTRP6, a secreted protein of the C1q family, targets both adipocytes and macrophages to promote obesity-linked inflammation in adipose tissue. However, the gene programs and signaling pathways directly regulated by CTRP6 in macrophage remain unknown. Here, we combine transcriptomic and phosphoproteomic analyses to show that CTRP6 activates inflammatory gene programs and signaling pathways in bone marrow-derived macrophages (BMDMs). Treatment of BMDMs with CTRP6 upregulates proinflammatory, and suppresses the anti-inflammatory, gene expression. We show that CTRP6 activates p44/42-MAPK, p38-MAPK, and NF-κB signalings to promote inflammatory cytokine secretion from BMDMs, and that pharmacologic inhibition of these signaling pathways largely abolish the effects of CTRP6. Pretreatment of BMDMs with CTRP6 further augments LPS-induced inflammatory signaling and cytokine secretion from BMDMs. Consistent with the metabolic phenotype of proinflammatory M1-like macrophages, CTRP6 treatment induces a shift toward aerobic glycolysis and lactate production, reduces oxidative metabolism, and elevates mitochondrial ROS production in BMDMs. We use a Ctrp6 knockout mouse model to further confirm the physiologic relevance of our in vitro findings. BMDMs from CTRP6-deficient mice are less inflammatory at baseline and show a marked suppression of LPS-induced inflammatory gene expression and cytokine secretion. Loss of CTRP6 in mice also dampens LPS-induced inflammation and hypothermia. Collectively, we provide mechanistic evidence that CTRP6 regulates macrophage function, and neutralizing CTRP6 activity may have beneficial effects in reducing inflammation.

2024-01-26 | PXD042268 | Pride

MG1655 flagellar regulator ChIP-seq (FlhD, FlhC, FliA)

Project description:We mapped the genome-wide binding of the flagellar regulators FlhD, FlhC, and FliA in FLAG-tagged derivatives of E. coli K-12 MG1655 using ChIP coupled with deep sequencing (ChIP-seq). We identify new binding sites for each factor.

2014-04-10 | E-MTAB-2457 | biostudies-arrayexpress

Mining gastric cancer cellular quantitative proteomics data to analyse the proteome change upon CAMKK2 inhibition

Project description:Gastric cancer is a global health concern. Molecular alterations in various signaling pathways have been implicated in the development and late-stage progression/metastasis of gastric cancer. Reports have suggested that Wnt signaling pathway might contribute to gastric carcinogenesis by stimulating migration and invasion of gastric cancer cells. This study aimed at analysing the proteome change upon CAMKK2 inhibition in gastric cancer cells using LC-MS/MS based quantitative proteomic approach. A TMT based quantitative approach was used to identify the significantly altered proteins upon CAMKK2 inhibition. Gene Ontology (GO) analysis and pathway analysis was done for the significantly altered proteins and was later validated by immunoblotting.

2021-04-13 | PXD023423 | Pride

Genome-Scale Mapping of Escherichia coli σ54 Reveals Widespread, Conserved Intragenic Binding

Project description:We investigated the genome-wide binding sites for sigma54 and RNA polymerase in wild-type Escherichia coli MG1655.

2015-08-06 | E-MTAB-3697 | biostudies-arrayexpress

Dissecting psa locus regulation in Yersinia pestis

Project description:We looked at H-NS bound sites in wild type Yersinia pestis and in a mutant strain in which the psaE gene was deleted.

2021-06-01 | E-MTAB-10694 | biostudies-arrayexpress

Salmonella 14028s AraC ChIP-Seq

Project description:We mapped the genome-wide binding of C-terminally FLAG-tagged AraC in S. enterica subsp. enterica serovar Typhimurium strain 14028s using ChIP coupled with deep sequencing (ChIP-seq). We identified five putative target loci for AraC: upstream of araB/araC, araE, araJ, STM14_0178, and within sseD.

2013-10-09 | E-MTAB-1915 | biostudies-arrayexpress

ChIP-seq of sigma 70 in wild-type and hns mutant Escherichia coli K-12 MG1655

Project description:We mapped the genome-wide binding of sigma 70 in E. coli K-12 MG1655 and an hns mutant that is otherwise isogenic using ChIP coupled with deep sequencing (ChIP-seq). We show that intragenic binding of sigma 70 is increased in the hns mutant.

2013-12-15 | E-MTAB-2148 | biostudies-arrayexpress

Sigma38 binding sites in E. Coli

Project description:ChIP-seq to identify sigma38 binding sites in wild-type and delta ssrS (6S RNA knockout) strains of E. Coli K-12 MG1655, during stationary phase ChIP-seq using antibody against sigma38 in wild-type and ssrS deletion strain. Two replicates for wild type and one replicate for ssrS deletion.

2016-06-10 | E-GEOD-74836 | biostudies-arrayexpress