Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT01586 (G418)
 2,237 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sequence of a Saccharomyces cerevisiae cDNA encoding a novel 61-kDa protein serine/threonine phosphatase, termed PPQ1, is presented. The protein consists of two distinct domains: the carboxy-terminal phosphatase domain is approximately 60% identical to either PP1 or the carboxy-terminal domains of PPZ1 and PPZ2, while the amino-terminal region is rich in serine and asparagine. Deletion of the gene encoding PPQ1 reduces cell growth on several carbon sources, and lowers cell density in the stationary phase. Cells in which PPQ1 gene has been deleted show altered morphology from wild-type cells in the stationary phase in the absence of an essential amino acid and a reduced rate of protein synthesis in the exponential phase. They are hypersensitive to the protein synthesis inhibitors, cycloheximide and G418, implicating PPQ1 in the regulation of translation.
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PMID:PPQ, a novel protein phosphatase containing a Ser + Asn-rich amino-terminal domain, is involved in the regulation of protein synthesis. 826 60

In this research, hemagglutinating virus of Japan envelope (HVJ-E) was used to reprogram somatic cells by fusion with mouse embryonic stem (ES) cells. Neomycin-resistant mouse embryonic fibroblasts (MEFs) were used as somatic cells. Nanog-overexpressing puromycin-resistant EB3 cells were used as mouse ES cells. These two cells were fused by exposing to HVJ-E and the generated fusion cells were selected by puromycin and G418 to get the stable fusion cell line. The fusion cells form colonies in feeder-free culture system. Microsatellite analysis of the fusion cells showed that they possessed genes from both ES cells and fibroblasts. The fusion cells were tetraploid, had alkali phosphatase activity, and expressed stem cell marker genes such as Pou5f1, Nanog, and Sox2, but not the fibroblast cell marker genes such as Col1a1 and Col1a2. The pluripotency of fusion cells was confirmed by their expression of marker genes for all the three germ layers after differentiation induction, and by their ability to form teratoma which contained all the three primary layers. Our results show that HVJ-E can be used as a fusion reagent for reprogramming of somatic cells.
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PMID:Reprogramming of somatic cells induced by fusion of embryonic stem cells using hemagglutinating virus of Japan envelope (HVJ-E). 2033 50

Lung cancer is the leading cause of cancer-related death worldwide, mainly due to its highly metastatic properties. Previously, we reported an inverse correlation between Rho-kinase inhibitor and the progression of the lung cancer cells. The purpose of this study was to investigate the effects of RhoA on the proliferation, adhesion, invasion, and migration of SPCA1 lung carcinoma cells and to explore the underlying molecular mechanisms. RNA interference was used to downregulate RhoA expression in these cells. Through G418 screening, we generated SPCA1 lung cancer cell lines with stable RhoA silencing. We then observed the cell behaviour, and used matrix metalloproteinase (MMP) activity and western blot assays to evaluate the underlying molecular mechanisms. The proliferation, adhesion, migration, and invasion of SPCA1 lung cancer cells were decreased after knockdown of RhoA. At the molecular level, the total amounts of active MMP2 and MMP9 were decreased by about 17.21% (P<0.05) and 45.32% (P<0.01), respectively. Myosin phosphatase targeting subunit 1 phosphorylation (P-MYPT1) was reduced by 36.16% (P<0.05). Taken together, our findings show that the knockdown of RhoA prevents proliferation and metastasis in SPCA1 lung cancer cells. Changes in MMP2, MMP9, and P-MYPT1 levels and activity might be some of the molecular mechanisms underlying these effects.
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PMID:Loss of RhoA expression prevents proliferation and metastasis of SPCA1 lung cancer cells in vitro. 2566 83