Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-22334E-GEOD-22336
PROVIDER: PRJNA129245 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE22334: Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression GSE22336: UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing Refer to individual Series
2010-08-01 | E-GEOD-22337 | biostudies-arrayexpress
Project description:UDP-GlcNAc 2-epimerase/ManNAc kinase (GNE) is an inducer of apoptotic processes in Capan-1 pancreatic carcinoma cells: GNE silencing
2025-01-24 | E-GEOD-22336 | ExpressionAtlas
Project description:Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus. Pancreatic cancer cells Capan-1. Three GNE-silencing samples and three control samples.
2010-08-01 | E-GEOD-22336 | biostudies-arrayexpress
Project description:Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus. Pancreatic cancer cells Capan-1. Three p16-transfectants and three mock-transfectants.
2010-08-01 | E-GEOD-22334 | biostudies-arrayexpress
Project description:Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression
| PRJNA129243 | ENA
Project description:The hexosamine pathway (HP) is a key anabolic pathway whose product uridine 5’-diphospho-N-acetyl-D-glucosamine (UDP-GlcNAc) is an essential precursor for all glycosylation processes in mammals. It modulates the ER stress response, is implicated in cancer and diabetes, and HP activation extends lifespan in Caenorhabditis elegans. The highly conserved glutamine fructose-6-phosphate amidotransferase 1 (GFAT 1) is the first and rate-limiting HP enzyme. GFAT 1 activity is modulated through UDP-GlcNAc feedback inhibition and by kinase signaling, including Ser205 phosphorylation by protein kinase A (PKA). The consequence and molecular mechanism of GFAT 1 PKA phosphorylation, however, remains poorly understood. Here, we identify the GFAT 1 R203H substitution that elevates UDP-GlcNAc levels in C. elegans, leading to ER stress resistance. In human GFAT-1, the R203H substitution interfered with UDP-GlcNAc inhibition and with PKA-mediated Ser205 phosphorylation. Of note, Ser205 phosphorylation had two discernible effects: It lowered baseline GFAT 1 activity while abolishing UDP-GlcNAc feedback inhibition. Thus, GFAT-1 phosphorylation by PKA uncoupled the feedback loop of the HP and depending on UDP-GlcNAc availability, phosphorylation by PKA lowers or enhances GFAT 1 activity in vivo. Mechanistically, our data indicate that the relative positioning of the two GFAT 1 domains might be affected by phosphorylation and we propose a model how Ser205 phosphorylation modulates the activity and feedback inhibition of GFAT 1.
2020-07-23 | PXD020451 | Pride
Project description:Induction of apoptotic processes in Capan-1 pancreatic carcinoma cells by restoration of p16INK4a expression
2025-01-24 | E-GEOD-22334 | ExpressionAtlas
Project description:GNE myopathy, a recessive autosomal disease caused by mutations in Glucosamine-(UDP-N-Acetyl)-2-Epimerase/N-Acetylmannosamine Kinase (GNE), is characterized by deficient sialic acid (SA) production and the formation of rimmed vacuoles. Similar to other autophagic vacuolar myopathies, defective autophagy has been identified as a causative factor in GNE myopathy. However, the molecular mechanism underlying this defective autophagy has not been fully determined. Through transcriptome analysis of two GNE myoblast models derived from human pluripotent stem cells (hPSCs), several gene sets associated with autophagy were identified as pathogenic gene signatures of GNE myopathy. This prediction, along with subsequent biochemical validation using GNE knockout in C2C12 myoblasts (KO cells), revealed that high production of extracellular matrix promoted focal adhesion and subsequent activation of the AKT-mTORC axis, leading to inhibitory phosphorylation of ULK1 and impeding autophagy initiation in KO cells. Notably, transcriptome-based drug screening for candidates that inversely correlate with the pathogenic gene signature identified copanlisib, an FDA-approved PI3K inhibitor, as a potential therapeutic candidate for GNE myopathy. As predicted, copanlisib enhanced autophagy by inhibiting mTOR-dependent ULK1 phosphorylation. These results suggest that copanlisib could be a feasible therapeutic option for patients with GNE myopathy.
2026-05-15 | GSE278862 | GEO
Project description:Heparan sulfate (HS), a long linear polysaccharide, is implicated in various steps of tumorigenesis, including angiogenesis. We successfully interfered with HS biosynthesis using a peracetylated 4-deoxy analog of the HS constituent GlcNAc and studied the compoundM-bM-^@M-^Ys metabolic fate and its effect on angiogenesis. The 4-deoxy analog was activated intracellularly into UDP-4-deoxy-GlcNAc and HS expression was inhibited up to ~96% (IC50 = 16 M-BM-5M). HS chain size was reduced, without detectable incorporation of the 4-deoxy analog, likely due to reduced levels of UDP-GlcNAc and/or inhibition of glycosyltransferase activity. Comprehensive gene expression analysis revealed reduced expression of genes regulated by HS binding growth factors as FGF-2 and VEGF. Cellular binding and signaling of these angiogenic factors was inhibited. Micro-injection in zebrafish embryos strongly reduced HS biosynthesis, and angiogenesis was inhibited in both zebrafish and chicken model systems. All these data identify 4-deoxy-GlcNAc as a potent inhibitor of HS synthesis which hampers pro-angiogenic signaling and neo-vessel formation. 9 samples were analyzed: 3 biological replicates from untreated SKOV3 cells, 3 biological replicates from SKOV3 cells treated with peracetylated GlcNAc, 3 biological replicates from SKOV3 cells treated with peracetylated 4-deoxy-GlcNAc
2013-08-23 | E-GEOD-48284 | biostudies-arrayexpress