Genes (47)
Species: human : 36 mouse : 11 | |
Mouse | GLS2 | 27165 | glutaminase 2 (liver, mitochondrial) | The influence of progressive tumor growth on phosphate-activated glutaminase (PAG) expression in splenocytes from mice bearing Ehrlich ascites carcinoma cells was investigated. Changes in phosphate-activated glutaminase activities determined in intact cells and isolated mitochondria have been followed during mouse Ehrlich ascites carcinoma development. The pH dependence of the phosphate-activated glutaminase isolated from Ehrlich tumour cells suggests a functional role for two prototropic groups with apparent pKa of 9.3 and 7.7 at the active site of the protein; these pKa values are compatible with cysteine and histidine residues, respectively. Changes in the relative mRNA levels of phosphate-activated glutaminase (PAG) and glutamine synthetase (GS) in the liver and kidney of mice bearing a highly malignant strain of Ehrlich ascites tumor cells were determined at different days after tumor transplantation. | Mouse | CACYBP | 27101 | calcyclin binding protein | A protein target of mouse calcyclin, p30, which we call calcyclin-binding protein (CacyBP), was identified in mouse brain and Ehrlich ascites tumor (EAT) cells. | Mouse | PLA2G6 | 8398 | phospholipase A2, group VI (cytosolic, calcium-independent) | The cytotoxic activity of F3 and F4 against Ehrlich ascites carcinoma cells might be due to the presence of a cytotoxin rather than to the direct cytolytic effect of the PLA2 because the non-lethal F4 is free from PLA2. | Mouse | TIMP1 | 7076 | TIMP metallopeptidase inhibitor 1 | Furthermore, TIMP-1 treatment did not affect the levels of matrix metalloproteinase (MMP)-2 and MMP-9 mRNA in the Ehrlich tumor cells in vitro, although these expressions in the tumor were markedly suppressed in the TIMP-Tg-mice, compared to the Cont-mice at the end of the experiment. | Mouse | SRM | 6723 | spermidine synthase | The antitumor effect of dicyclohexylammonium sulfate (DCHA), a potent inhibitor of spermidine synthase, was tested on mice inoculated with Ehrlich ascites carcinoma, Ehrlich solid carcinoma and solid sarcoma-180. | Mouse | SLC9A1 | 6548 | solute carrier family 9, subfamily A (NHE1, cation proton antiporter 1), member 1 | The Na+/H+ exchanger isoforms NHE1, NHE2, and NHE3 were all found to be expressed in Ehrlich ascites tumor cells, as evaluated by Western blotting and confocal microscopy. | Mouse | SLC2A3 | 6515 | solute carrier family 2 (facilitated glucose transporter), member 3 | We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but not GLUT2, GLUT4, or GLUT5. | Mouse | MPST | 4357 | mercaptopyruvate sulfurtransferase | 1. The activity of cysteine aminotransferase (CAT), 3-mercaptopyruvate sulfurtransferase (MPST) and rhodanese is much lower in Ehrlich ascites tumor cells (EATC) than in mouse liver. | Mouse | MPI | 4351 | mannose phosphate isomerase | In contrast, Ehrlich ascites tumor cells obtained from the peritoneum of BALB/c mice had low MPI activity (half of the HKM activity and, therefore, a ratio of 2). | Mouse | GLS | 2744 | glutaminase | Our results suggest that inhibition of glutaminase expression using anti-sense technology induces phenotypic changes in Ehrlich ascites tumor cells that allow the development of an effective anti-tumor immune response, which makes the cells unable to develop in vivo tumors. Ehrlich ascites tumor cells expressing anti-sense glutaminase mRNA lose their capacity to evade the mouse immune system. Using anti-sense technology, an Ehrlich ascites tumor cell line (0.28AS-2) with reduced glutaminase activity has been obtained. | Mouse | FH | 2271 | fumarate hydratase | Ehrlich ascites carcinoma induced significant changes in liver fumarase (activation) and aconitase (inhibition). Changes induced by Ehrlich ascites carcinoma in hepatic fumarase and aconitase activities. | Human | TUBA1C | 84790 | tubulin, alpha 1c | Preparations of cycled tubulin from Ehrlich ascites tumor cells contain several accessory proteins; once or twice cycled microtubule preparations are usually composed of fibers 10 nm in diameter, but lack vimentin. Tubulin was phosphorylated mainly at tyrosine residues by membranes from mouse liver and Ehrlich ascites tumor with ATP in the presence of MnCl2, ZnCl2, NaVO3, and Nonidet P-40 in an epidermal growth factor (EGF)- and insulin-independent manner. Catecholamine-induced stimulation of adenylate cyclase in parallel with a change in tubulin assembly in Ehrlich ascites tumor cells. In vitro formation of different tubulin polymers from purified tubulin of Ehrlich ascites tumor cells. The results demonstrate that the in vitro assembly of tubulin from Ehrlich ascites tumor cells does not require high molecular weight proteins or gamma-like factor(s) as has been proposed for the neurotubulin system. In vitro assembly of tubulin from nonneural cells (Ehrlich ascites tumor cells). In vivo TriEL also caused MT depolymerization in interphase and mitotic PtK-1 and Ehrlich ascites tumor (EAT) cells as monitored by indirect immuno-fluorescent staining of tubulin and electron microscopy. | Human | CACYBP | 27101 | calcyclin binding protein | Co-immunoprecipitation of CacyBP/SIP with S100B from brain and with S100A6 from Ehrlich ascites tumor cells suggests that these interactions are physiologically relevant and that the ubiquitinylation complex involving CacyBP/SIP might be regulated by S100 proteins. | Human | VAT1 | 10493 | vesicle amine transport 1 | Mammalian protein homologous to VAT-1 of Torpedo californica: isolation from Ehrlich ascites tumor cells, biochemical characterization, and organization of its gene. This VAT-1 homolog was isolated from a murine breast cancer cell line (Ehrlich ascites tumor) and identified by sequencing of cleavage peptides. The isolated VAT-1 homolog protein displays an ATPase activity and exists in two isoforms with isoelectric points of 5.7 and 5.8. cDNA was prepared from Ehrlich ascites tumor cells, and the murine VAT-1 homolog sequence was amplified by polymerase chain reaction and partially sequenced. | Human | EIF2S2 | 8894 | eukaryotic translation initiation factor 2, subunit 2 beta, 38kDa | Purification and characterization of eukaryotic initiation factor (eIF)-2 alpha kinases from Ehrlich ascites tumor cells. With complexes formed by using a partially purified preparation of eIF-2 from Ehrlich ascites tumor cells, it is possible to reverse the 40S subunit induced inhibition by creating conditions which eliminate free GDP from the system. Translation of exogenous mRNAs in micrococcal nuclease-treated extracts from Ehrlich ascites tumor cells is greatly stimulated by the addition of crude initiation factors or initiation factors eIF-2B and eIF-2 containing eIF-2B. Previously, we have shown that phosphorylation of the eukaryotic initiation factor eIF-2 alpha increases under several physiological stresses in which protein synthesis is inhibited in Ehrlich ascites tumor cells. | Human | EIF2B4 | 8890 | eukaryotic translation initiation factor 2B, subunit 4 delta, 67kDa | Translation of exogenous mRNAs in micrococcal nuclease-treated extracts from Ehrlich ascites tumor cells is greatly stimulated by the addition of crude initiation factors or initiation factors eIF-2B and eIF-2 containing eIF-2B. | Human | TKT | 7086 | transketolase | Thiamine pyrophosphate (TPP) content, activities of thiamine pyrophosphokinase (TPKase), thiamine pyrophosphatase, transketolase (TK), pyruvate (PDG) and oxoglutarate dehydrogenases (OGDG) were measured in the liver and cells of Ehrlich ascites carcinoma (EAC) on the 5th, 10th and 15th day after transplantation of the tumor to mice fed a thiamine-deficient diet. | Human | SSTR1 | 6751 | somatostatin receptor 1 | It is suggested that the LTD4-induced activation of K and Cl transporting systems in Ehrlich ascites tumor cells is mediated via a G-protein coupled receptor and that LTD4 might exert its effect through another lipoxygenase product. | Human | SIGLEC1 | 6614 | sialic acid binding Ig-like lectin 1, sialoadhesin | The aim of this study was to assess whether Ehrlich tumor (ET) - a murine mammary carcinoma - growth may modify the sialoadhesin expression by bone marrow macrophages and/or sialoadhesin-inducing activity in ET-bearing sera. | Human | SLC12A1 | 6557 | solute carrier family 12 (sodium/potassium/chloride transporter), member 1 | The Na-K-2Cl cotransporter is in a permanently activated state in cytoplasts from Ehrlich ascites tumor cells. | Human | SLC9A3 | 6550 | solute carrier family 9, subfamily A (NHE3, cation proton antiporter 3), member 3 | The Na+/H+ exchanger isoforms NHE1, NHE2, and NHE3 were all found to be expressed in Ehrlich ascites tumor cells, as evaluated by Western blotting and confocal microscopy. | Human | SLC2A5 | 6518 | solute carrier family 2 (facilitated glucose/fructose transporter), member 5 | We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but not GLUT2, GLUT4, or GLUT5. | Human | SLC2A2 | 6514 | solute carrier family 2 (facilitated glucose transporter), member 2 | We found that Ehrlich ascites tumor cells possess only glucose transporter 1 (GLUT1) and GLUT3 but not GLUT2, GLUT4, or GLUT5. | Human | RPS6 | 6194 | ribosomal protein S6 | After mengovirus infection of Ehrlich ascites tumor cells, an increased incorporation of radioactive phosphate into ribosomal protein S6 was detected. Phosphorylation of ribosomal protein S6 in the Ehrlich ascites tumor cell. Enhanced phosphorylation of ribosomal protein s6 and other cytoplasmic proteins after mengovirus infection of Ehrlich ascites tumor cells. | Human | PRIM1 | 5557 | primase, DNA, polypeptide 1 (49kDa) | The effect of a single-stranded DNA-binding protein (SSB-protein) form Ehrlich ascites tumour cells (EAT) on the activity of homologous purified DNA-polymerases alpha and beta, DNA-replicase, primase and DNA-polymerases from phage T4 and Bacillus stearothermophillus was studied. |
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