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源自尿激酶受体的D2A-Ala肽对细胞增殖和侵袭的抑制作用的数据。

Data on the inhibition of cell proliferation and invasion by the D2A-Ala peptide derived from the urokinase receptor.

作者信息

Furlan Federico, Eden Gabriele, Archinti Marco, Arnaudova Ralitsa, Andreotti Giuseppina, Citro Valentina, Cubellis Maria Vittoria, Motta Andrea, Degryse Bernard

机构信息

Dept. of Molecular Biology and Functional Genomics, DIBIT, Università Vita-Salute San Raffaele, Via Olgettina 58, 20132 Milan, Italy.

IFOM, FIRC Institute of Molecular Oncology, Via Adamello 16, 20139 Milan, Italy.

出版信息

Data Brief. 2019 Jan 9;22:903-908. doi: 10.1016/j.dib.2019.01.009. eCollection 2019 Feb.

Abstract

The data presented in this article are connected to our research article entitled "D2A-Ala peptide derived from the urokinase receptor exerts anti-tumoural effects in vitro and in vivo" (Furlan et al., 2018). These data further extend our understanding of the inhibitory effects of D2A-Ala peptide. Dose-response curve using a wide range of concentrations of D2A-Ala shows that this peptide has no effects per se on proliferation of rat smooth muscle cells (RSMC). However, D2A-Ala dose-dependently inhibits epidermal growth factor (EGF)-induced RSMC proliferation. Kinetics lasting up to seven days revealed that D2A-Ala peptide completely blocked EGF-promoted RSMC proliferation. Moreover, D2A-Ala peptide inhibited invasion of HT 1080 cells towards RSMC.

摘要

本文所呈现的数据与我们发表的题为《源自尿激酶受体的D2A - Ala肽在体内外发挥抗肿瘤作用》(Furlan等人,2018年)的研究文章相关。这些数据进一步扩展了我们对D2A - Ala肽抑制作用的理解。使用多种浓度的D2A - Ala绘制的剂量反应曲线表明,该肽本身对大鼠平滑肌细胞(RSMC)的增殖没有影响。然而,D2A - Ala以剂量依赖的方式抑制表皮生长因子(EGF)诱导的RSMC增殖。长达七天的动力学研究表明,D2A - Ala肽完全阻断了EGF促进的RSMC增殖。此外,D2A - Ala肽抑制HT 1080细胞向RSMC的侵袭。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2971/6352295/ef896415c674/gr1.jpg

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