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.

DLC1 is a direct target of activated YAP/TAZ that drives collective migration and sprouting angiogenesis.

J Cell Sci. 2020;

van der Stoel M, Schimmel L, Nawaz K, van Stalborch AM, de Haan A, Klaus-Bergmann A,, Valent ET, Koenis DS, van Nieuw Amerongen GP, de Vries CJ, de Waard V, Gloerich M, van Buul JD,, Huveneers S.

Products/Services Used	Details	Operation
Gene Synthesis	… The DLC1 promoter region (-418 to +319 bp from the transcriptional start site) containing the wild type TEAD motif (CATTCCA) or a mutated motif (AGACTAT) were purchased from GenScript and inserted at the 5' end of the luciferase gene between NheI and BglII restriction sites …	Get A Quote

摘要

Endothelial YAP/TAZ (YAP is also known as YAP1, and TAZ as WWTR1) signaling is crucial for sprouting angiogenesis and vascular homeostasis. However, the underlying molecular mechanisms that explain how YAP/TAZ control the vasculature remain unclear. This study reveals that the focal adhesion protein deleted-in-liver-cancer 1 (DLC1) is a direct transcriptional target of the activated YAP/TAZ-TEAD complex. We find that substrate stiffening and VEGF stimuli promote expression of DLC1 in endothelial cells. In turn, DLC1 expression levels are YAP and TAZ dependent, and constitutive activation of YAP is sufficient to drive DLC1 expression. DLC1 is needed to limit F-actin fiber formation, integrin-based focal adhesion... More