Galaxy银河|澳门官网·登录入口

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.

Mutant P53 Gain-Of-Function Induces Epithelial-Mesenchymal Transition Through Modulation Of The Mir-130B-Zeb1 Axis.

Oncogene.. 2012-07; 
Dong P, Karaayvaz M, Jia N, Kaneuchi M, Hamada J, Watari H, Sudo S, Ju J, Sakuragi N. Department of Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, Japan.
Products/Services Used Details Operation

摘要

The tumor suppressor gene p53 has been implicated in the regulation of epithelial-mesenchymal transition (EMT) and tumor metastasis by regulating microRNA (miRNA) expression. Here, we report that mutant p53 exerts oncogenic functions and promotes EMT in endometrial cancer (EC) by directly binding to the promoter of miR-130b (a negative regulator of ZEB1) and inhibiting its transcription. We transduced p53 mutants into p53-null EC cells, profiled the miRNA expression by miRNA microarray and identified miR-130b as a potential target of mutant p53. Ectopic expression of p53 mutants repressed the expression of miR-130b and triggered ZEB1-dependent EMT and cancer cell invasion. Loss of an endogenous p53 mutation inc... More

关键词

EMT; cancer; gain-of-function; miRNA; p53 mutation
XML 地图