资源 » 参考数据库 » 客户发表文献

至今，GenScript的服务及产品已被Cell, Nature, Science, PNAS等1300多家生物医药类杂志引用近万次，处于行业领先水平。NIH、哈佛、耶鲁、斯坦福、普林斯顿、杜克大学等约400家全球著名机构使用GenScript的基因合成、多肽服务、抗体服务和蛋白服务等成功地发表科研成果，再次证明GenScript 有能力帮助业内科学家Make research easy.

MicroRNA-552 deficiency mediates 5-fluorouracil resistance by targeting SMAD2 signaling in DNA-mismatch-repair-deficient colorectal cancer.

Cancer Chemother. Pharmacol.. 2019;

ZhaoPing，MaYu-Guang，ZhaoYang，LiuDi，DaiZhi-Jun，YanChang-You，GuanHai

Products/Services Used	Details	Operation
Mutagenesis Services	The putative binding site of miR-552 in the three prime untranslated region (3′-UTR) of SMAD2 gene, along with its mutated derivative, was cloned into pGL3 Luciferase Reporter Vector (Promega, Shanghai, China), with the aid of CloneEZ® Kit (GenScript, HongKong, China) and QuikChange II Site-Directed Mutagenesis Kit (Agilent, Beijing China).	Get A Quote

摘要

Although DNA-mismatch-repair-deficient (dMMR) status and aberrant expression of miRNAs are both critically implicated in the pathogenesis of resistance to 5-fluorouracil (5-FU) in colorectal cancer (CRC)， whether these two factors regulate tumor response to 5-FU in a coordinated manner remains unknown. This study is designed to elucidate whether changes in miR-552 expression levels correlate to 5-FU-based chemoresistance in CRC， and to further identify the putative targets of miR-552 using multiple approaches.