{"title":"阻止BRCA1/ZBRK1抑制因子复合物与GOT2启动子结合可加速天冬氨酸的生物合成并促进细胞增殖","authors":"","doi":"10.1002/1878-0261.12784","DOIUrl":null,"url":null,"abstract":"Total RNAs of breast cancer cells and mouse embryonic fibroblasts MEF BRCA1 and MEF BRCA1 were extracted with TRIzol reagent (Invitrogen, Carlsbad, CA, USA). The cDNA was synthesized with the PrimeScript RT reagent Kit (Promega, Madison, WI, USA). Real-time PCR was carried out using an ABI 7500 real-time PCR system (Applied Biosystems, Foster City, CA, USA). The mRNA expression level of GOT2 and ASS1 was normalized to the endogenous expression of GAPDH. Primers were provided by Invitrogen as described below:","PeriodicalId":51134,"journal":{"name":"Molecular Oncology","volume":null,"pages":null},"PeriodicalIF":5.0000,"publicationDate":"2020-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/1878-0261.12784","citationCount":"0","resultStr":"{\"title\":\"Corrigendum to: Preventing BRCA1/ZBRK1 repressor complex binding to the GOT2 promoter results in accelerated aspartate biosynthesis and promotion of cell proliferation\",\"authors\":\"\",\"doi\":\"10.1002/1878-0261.12784\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Total RNAs of breast cancer cells and mouse embryonic fibroblasts MEF BRCA1 and MEF BRCA1 were extracted with TRIzol reagent (Invitrogen, Carlsbad, CA, USA). The cDNA was synthesized with the PrimeScript RT reagent Kit (Promega, Madison, WI, USA). Real-time PCR was carried out using an ABI 7500 real-time PCR system (Applied Biosystems, Foster City, CA, USA). The mRNA expression level of GOT2 and ASS1 was normalized to the endogenous expression of GAPDH. Primers were provided by Invitrogen as described below:\",\"PeriodicalId\":51134,\"journal\":{\"name\":\"Molecular Oncology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":5.0000,\"publicationDate\":\"2020-09-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1002/1878-0261.12784\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1002/1878-0261.12784\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/1878-0261.12784","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
用TRIzol试剂(Invitrogen, Carlsbad, CA, USA)提取乳腺癌细胞和小鼠胚胎成纤维细胞MEF BRCA1和MEF BRCA1的总rna。cDNA用PrimeScript RT reagent Kit (Promega, Madison, WI, USA)合成。实时PCR采用ABI 7500实时PCR系统(Applied Biosystems, Foster City, CA, USA)。将GOT2和ASS1 mRNA表达水平归一化为内源性GAPDH的表达。引物由Invitrogen公司提供,如下所述:
Corrigendum to: Preventing BRCA1/ZBRK1 repressor complex binding to the GOT2 promoter results in accelerated aspartate biosynthesis and promotion of cell proliferation
Total RNAs of breast cancer cells and mouse embryonic fibroblasts MEF BRCA1 and MEF BRCA1 were extracted with TRIzol reagent (Invitrogen, Carlsbad, CA, USA). The cDNA was synthesized with the PrimeScript RT reagent Kit (Promega, Madison, WI, USA). Real-time PCR was carried out using an ABI 7500 real-time PCR system (Applied Biosystems, Foster City, CA, USA). The mRNA expression level of GOT2 and ASS1 was normalized to the endogenous expression of GAPDH. Primers were provided by Invitrogen as described below:
期刊介绍:
Molecular Oncology highlights new discoveries, approaches, and technical developments, in basic, clinical and discovery-driven translational cancer research. It publishes research articles, reviews (by invitation only), and timely science policy articles.
The journal is now fully Open Access with all articles published over the past 10 years freely available.