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A National Translational Science Network of Precision-based Immunotherapy for Primary Liver Cancer (PLC)

ABSTRACT: A National Translational Science Network of Precision-based Immunotherapy for Primary Liver Cancer (PLC)

PROVIDER: PRJNA887182 | ENA |

REPOSITORIES: ENA

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A National Translational Science Network of Precision-based Immunotherapy for Primary Liver Cancer (PLC)

Project description:A National Translational Science Network of Precision-based Immunotherapy for Primary Liver Cancer (PLC)

| PRJNA887181 | ENA

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Inhibition of the PI-PLC by U73122

Project description:au13-01_pi-plc What are the genes that are regulated by basal PI-PLC? Arabidopsis thaliana cells in suspension (5-days old). Cultivated in environment (middle) Gamborg+2,4-D. Added inhibitors 4 hr before extraction of the RNAs. We try to determine the role of phospholipases C ( PI-PLC) in the control of the basal expression of the genes of suspension of Arabidopsis thaliana. A first experience in which we used the edelfosine as inhibitor allowed us to identify numerous genes the basal expression of which is altered by this inhibition. We want to confirm these results with another inhibitor. 4 dye-swap - treated vs untreated comparison - treatment variations

2013-09-01 | E-GEOD-46941 | biostudies-arrayexpress

Inhibition of the PI-PLC by U73122

2013-09-01 | GSE46941 | GEO

PLC/PRF/5 cells ChIP on CHIP

Project description:PLC/PRF/5 cells were harvested for chromatin immunoprecipitation followed by CHIP analysis performed on Aligent platform.

2017-07-10 | GSE100968 | GEO

Department of Food Science and Biotechnology, Kangwon National University

Project description:Department of Food Science and Biotechnology, Kangwon National University Genome sequencing and assembly

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RRBS of PCK1 knockout in PLC/PRF/5

Project description:RRBS analysis of Parental and PCK1 knockout groups of PLC/PRF/5 cells.

2023-07-06 | GSE221725 | GEO

PLC-γ1 Can Regulate T-Cell Activation by Positive and Negative Feedback via Lck

Project description:Phospholipase C gamma 1 (PLC-γ1) occupies a critically important position in the T cell signaling pathway. While its functions as a regulator of both Ca2+ signaling and PKC-family kinases are well characterized, PLC-γ1’s role in the regulation of early T cell receptor signaling events is incomplete. Activation of the T cell receptor leads to the formation of a signalosome complex between SLP-76, LAT, PLC-γ1, Itk, and Vav1. Recent studies have revealed the existence of both positive and negative feedback pathways from components of the signalosome complex to the apical kinase in the pathway, Lck. To determine the role, if any, of PLC-γ1 in these feedback networks, we performed a quantitative phosphoproteomic analysis of the PLC-γ1-deficient T cells. These data revealed a previously unappreciated role for PLC-γ1 in the positive regulation of Zap-70 and T cell receptor tyrosine phosphorylation. Conversely, PLC-γ1 negatively regulated the phosphorylation of signalosome associated proteins including previously established Lck substrate phosphorylation sites within this complex. While the positive and negative regulatory phosphorylation sites on Lck were largely unchanged, Tyr192 phosphorylation was elevated in Jgamma1. The data supports a model wherein Lck’s targeting, but not its kinase activity is altered by PLC-γ1, possibly through Lck Tyr192 phosphorylation.

2017-06-28 | PXD005165 | Pride

Ileal Crohn’s disease exhibits reduced activity of phospholipase C-β3 (PLC-β3)-dependent Wnt/b-catenin signaling pathway [microarray]

Project description:Crohn’s disease is a chronic, debilitating inflammatory bowel disease. Here we report a critical role for phospholipase C-β3 (PLC-β3) in intestinal homeostasis. In PLC-β3- deficient mice, exposure to oral dextran sodium sulfate induced lethality and severe inflammation in the small intestine. The lethality was due to PLC-β3 deficiency in multiple non-hematopoietic cell types. PLC-β3 deficiency resulted in reduced Wnt/β-catenin signaling, which is essential for homeostasis and regeneration of the intestinal epithelium. PLC-β3 regulated the Wnt/β-catenin pathway in small intestinal epithelial cells (IECs) at transcriptional, epigenetic, and potentially protein-protein interaction levels. PLC-β3- deficient IECs were unable to respond to stimulation by R-spondin 1, an enhancer of Wnt/β-catenin signaling. Reduced expression of PLC-β3 and its signature genes was found in biopsies of ileal Crohn’s disease patients. PLC-β regulation of Wnt signaling was evolutionally conserved in Drosophila. Our data indicate that reduction of PLC-β3- mediated Wnt/β-catenin signaling contributes to the pathogenesis of ileal Crohn’s disease.

2024-10-06 | GSE244937 | GEO

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