关于由源自β2肾上腺素能受体（β2AR）和趋化因子受体4（CXCR4）的氨基酸序列的肽模拟物诱导的人类中性粒细胞活化的数据。
Data on human neutrophil activation induced by pepducins with amino acid sequences derived from β2AR and CXCR4.
作者信息
Holdfeldt André, Winther Malene, Gabl Michael, Dahlgren Claes, Forsman Huamei
机构信息
Department of Rheumatology and Inflammation Research, University of Gothenburg, Gothenburg, Sweden.
出版信息
Data Brief. 2016 Jun 1;8:411-4. doi: 10.1016/j.dib.2016.05.065. eCollection 2016 Sep.
The data described here is related to the research article titled (Gabl et al., 2016) [1]. Pepducins with peptide sequence derived from one of the intracellular domains of a given G-protein coupled receptor (GPCR) can either activate or inhibit cell functions. Here we include data on human neutrophil function induced by pepducins derived from β2AR (ICL3-8) and CXCR4 (ATI-2341), respectively. ICL3-8 exerts neither direct activating effect on the NADPH-oxidase as measured by superoxide release nor inhibitory effect on FPR signaling. ATI-2341 dose-dependently triggers neutrophil activation and these cells were subsequently desensitized in their response to FPR2 specific agonists F2Pal10 and WKYMVM. Moreover, the ATI-2341 response is inhibited by PBP10 and the peptidomimetic Pam-(Lys-betaNSpe)6-NH2 (both are FPR2 specific inhibitors), but not to the FPR1 specific inhibitor cyclosporine H.
此处描述的数据与题为（加布尔等人，2016年）[1]的研究文章相关。具有源自特定G蛋白偶联受体（GPCR）细胞内结构域之一的肽序列的肽模拟物可以激活或抑制细胞功能。在这里，我们纳入了分别由源自β2肾上腺素能受体（ICL3 - 8）和CXC趋化因子受体4（ATI - 2341）的肽模拟物诱导的人类中性粒细胞功能的数据。通过超氧化物释放测量，ICL3 - 8对NADPH氧化酶既没有直接激活作用，对甲酰甲硫氨酸-亮氨酸-苯丙氨酸（FPR）信号也没有抑制作用。ATI - 2341剂量依赖性地触发中性粒细胞活化，并且这些细胞随后对FPR2特异性激动剂F2Pal10和WKYMVM的反应脱敏。此外，ATI - 2341的反应受到PBP10和肽模拟物Pam -（Lys - betaNSpe）6 - NH2（两者都是FPR2特异性抑制剂）的抑制，但不受FPR1特异性抑制剂环孢菌素H的抑制。
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