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GPR35 mediates lysophosphatidic acid-signaling in bone marrow-derived macrophages at the transcriptional level

ABSTRACT: GPR35 mediates lysophosphatidic acid-signaling in bone marrow-derived macrophages at the transcriptional level

PROVIDER: PRJNA641170 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12071813_1.fastq.gz	Fastqsanger.gz
	SRR12071813_2.fastq.gz	Fastqsanger.gz
	SRR12071814_1.fastq.gz	Fastqsanger.gz
	SRR12071814_2.fastq.gz	Fastqsanger.gz
	SRR12071815_1.fastq.gz	Fastqsanger.gz

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GPR35 mediates lysophosphatidic acid-signaling in bone marrow-derived macrophages at the transcriptional level

Project description:Purpose: Our previous experiments showed that LPA activated inhibitory G-protein signaling in human GPR35-transfected cells. We wanted to test the LPA signaling in presence or absence of GPR35. Methods: We isolated RNA from bone-marrow derived macrophages (BMDMs) from WT or GPR35-deficient mice that were treated with LPA or LPS, and left untreated for control. Results: We have found that GPR35-deficiency alters the transcriptional profiles in response to LPA in BMDMs. On the other hand, LPS-treated WT and GPR35-deficient BMDMs showed similar transcriptional changes. Conclusion: GPR35-deficientcy alters the LPA but not LPS signaling.

2020-06-23 | GSE153012 | GEO

Influence of GPR35 deficiency on the ileal and macrophage transcriptome

Project description:Mutations in GPR35 (G protein coupled receptor 35) are linked to ulcerative colitis and primary sclerosing cholangitis. How GPR35, which interacts with the Na/K-ATPase to determine ion transport, influences the transcriptome of macrophages and the ileum is unknown. Here compare transcript expression in bone marrow-derived macrophages and isolated ileum from mice deficient in GPR35 (knockout) with wild type mice by bulk RNA sequencing.

2025-02-07 | GSE252926 | GEO

GPR35+ tumor-associated neutrophils promote tumor growth in hepatocellular carcinoma.

Project description:Bulk RNA-seq profiling of tumor-associated neutrophils from Hepa1-6 mouse hepatocellular carcinoma (HCC) models. Neutrophils were isolated from mice HCC tissues and classified as GPR35+ or GPR35- subsets (n=3 per group). Differential expression analysis revealed significant upregulation of MAPK signaling pathway and pathways associated with neutrophil migration and cytokines production in GPR35+ neutrophils. These data support the pro-tumorigenic role of GPR35+ neutrophils in HCC.

2026-04-05 | GSE305407 | GEO

Low input RNA sequencing of GPR35-positive and negative intestinal macrophages

Project description:Aim: We aimed to determine differences in transcriptional profiles of GPR35-positive and negative macrophages in the steady state intestine. Method: Corresponding subpopulations were sorted by FACS from intestinal lamina propria cells of unmanipulated wild-type C56BL/6 mice. RNA from 4 replicates of each group were sequenced and analyzed. Result: GPR35 positive macrophages are transcriptionally distinct from GPR35 negative macrophages overall with 2798 downregulated and 2773 upregulated genes, and regarding cytokine expression profile with higher Il1b, Tnf and Il10 mRNA expressions. Conclusion: Our study reports the first analysis on transcriptional charasteristics of intestinal macrophages depending on their GPR35 expression providing insights into the function of GPR35 in these cells.

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Spleen vs Lysophosphatidic Acid Treated B cell

Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with Lysophosphatidic Acid labeled with Cy5- time course with repeats Keywords: ordered

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GPR35 regulates anxiety susceptibility

Project description:GPR35 regulates colitis-associated anxiety susceptibility

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GPR35 promotes glycolysis, proliferation and oncogenic signalling by engaging with the sodium potassium pump

Project description:We used human embryonic kidney HEK293T cells transfected with human GPR35 cDNAs as baits that were engineered to express Strep or hemagglutinin (HA) tags at the C terminus to perform an unbiased proteomics survey for GPR35 interaction partners.

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Single-cell RNA-sequencing of proximal colon epithelial cells from Gpr35 knock-out mice

Project description:We performed a single-cell transcriptome analysis of proximal colon epithelial cells from 4 Gpr35 KO and 4 WT female littermates mice at a steady state.

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Agonist-induced phosphorylation of orthologues of the orphan receptor GPR35 as an activation biomarker

Project description:Mass spectrometry, mutagenesis and labelling with [32P] orthophosphate identified that each of the five hydroxy-amino acids in the intracellular C-terminal tail of human GPR35a became phosphorylated in response to agonist occupancy of the receptor and that, apart from Ser294, each of these contributed to the effectiveness of interaction of the receptor with arrestin-3. Key to such interactions was Ser303. Despite there being a greater number of hydroxy-amino acids in the C-terminal tail of both mouse and rat GPR35 the serine corresponding to residue 303 in human GPR35a also played a dominant role in arrestin-3 interactions for both rodent orthologues. Fully phospho-site deficient mutants of human GPR35a and mouse GPR35 failed to interact effectively with arrestin-3 and the human phospho-deficient variant was not internalized from the surface of cells in response to agonist treatment. Even in cells stably expressing species orthologues of GPR35 a substantial proportion of the expressed protein(s) was, however, immature. Phospho-site specific antisera targeting the region encompassing Ser303 in human (Ser301 in mouse) GPR35 identified only the mature forms of GPR35 and provided effective biomarkers of the activation status of the receptors both in immunoblotting and immunocytochemical studies. Such antisera may be useful tools to evaluate target engagement in drug discovery and target validation programmes.

2022-04-04 | PXD030548 | Pride

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Project description:Cirrhosis is a milieu that develops hepatocellular carcinoma (HCC), the second most lethal cancer worldwide. HCC prediction and prevention in cirrhosis are key unmet medical needs. Here we have established an HCC risk gene signature applicable to all major HCC etiologies: hepatitis B/C, alcohol, and non-alcoholic steatohepatitis. A transcriptome meta-analysis of >500 human cirrhotics revealed global regulatory gene modules driving HCC risk and lysophosphatidic acid pathway as a central chemoprevention target. Pharmacological inhibition of the pathway in vivo reduced tumors and reversed the gene signature, which was verified in organotypic ex vivo culture of patient-derived fibrotic liver tissues. These results demonstrate the utility of clinical organ transcriptome to enable a strategy, reverse-engineering precision cancer prevention.

2016-12-16 | GSE72960 | GEO

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