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)

Cysticercosis is caused by the metacestode form of Taenia solium-Cysticercus cellulosae and it causes great economic losses and threatens the people's health. There are some problems on how to control cysticercosis, in order to resolve the key problem that the native antigen to diagnose and prevent cysticercosis is very limited and is not satisfied, Pichia pastoris Expression System was used to express recombinant P2 protein. The interested P2 gene was got by digesting the pGEM - P2 vector using restriction endonuclease, then it was inserted into the secretory pPIC9K Pichia pastoris expression vector and transformed into E. coli. Positive recombinant plasmids were selected sequenced and named pPIC9K-P2 and it was linearized by Sal I and Bgl II, then the linear DNA transfored into Pichia pastoris GS115 by electroporation. The recombinant expression vector pPIC9K - P2 integrated into GS115 via homologous recombination between the transforming DNA and regions of homology within the genome. The transformants were screened for multicopy recombinants using G418 and were distinguished for Mut phenotypes by MD and MM. Two different phenotypes were generated-HIS+ MUT+ (Methanol utilization plus) and HIS+ MUT(S) (Methanol utilization slow). PCR analysis of the multicopy recombinants indicated that the P2 gene was integrated within the genome of pichia Pastoris. The multicopy recombinants were named GS115/pPIC9K - P2HIS+ MUT+ and GS115/pPIC9K-P2HIS+ MUT(S), both HIS+ MUT+ and HIS+ MUT(S) were induced with methanol. The results of SDS-PAGE and Western blot demonstrated that the culture supernatant of the induced Pichia pastoris contained P2 protein which was accumulated up to 33 % of total proteins in the culture supernant and its molecular weight is 12.6kD. The results of the clinical study indicated that the expression P2 protein could be used to diagnose human cysticercosis and swine cysticercosis as diagnosis antigen.
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PMID:[Expression of phosphoprotein P2 of Cysticercus cellulosae in Pichia pastoris and its application]. 1596 58

A stop codon defect in methylmalonyl-CoA mutase (resulting in a truncated unstable protein) accounts for up to 14% of mutations identified as causes of Methylmalonic aciduria. There are currently limited treatment regimes for patients with this inherited condition. We aimed to investigate the use of stop codon read-through drugs in a genomic reporter assay cell line with a defect in the mutase gene. A single C-T base change was introduced into exon 6 of the human MUT sequence in the BAC clone RP11-463L20 resulting in an arginine residue being replaced with a TGA stop codon. An enhanced green fluorescent protein reporter gene was introduced in-frame with exon 13 of the MUT gene. The construct was transfected into HeLa cells to produce the genomic reporter assay cell line. To test the suppression of nonsense mutations, cells were incubated in the presence of different compounds for a period of 72 h then analysed by flow cytometry. Treatment of the cells with gentamicin resulted in a 1.6-fold increase in reporter protein, whilst G418 treatment resulted in no change, however the two drugs together acted synergistically to increase the production of methylmalonyl-CoA mutase 2.0-fold (confirmed by mRNA, flow cytometry and enzyme activity). Zidovudine, adefovir and cisplatin were also found to have some activity in the stop codon read-through genomic reporter assay. These results encourage further testing of compounds as well as follow up animal studies. This is the first study to demonstrate the use of stop codon read-through drugs for the potential treatment of Methylmalonic aciduria.
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PMID:Stop codon read-through of a methylmalonic aciduria mutation. 1942 50