期刊：
Bioscience, Biotechnology, and Biochemistry,2006年70(9):2035-2041 ISSN：0916-8451
通讯作者：
Luo, Jin-Xian
作者机构：
[Luo, Jin-Xian] Sun Yat Sen Univ, Minist Educ, Key Lab Genet Engn, Dept Biochem, Guangzhou 510275, Peoples R China.;Hengyang Normal Univ, Dept Life Sci, Hengyang 421001, Peoples R China.
通讯机构：
[Luo, Jin-Xian] S;Sun Yat Sen Univ, Minist Educ, Key Lab Genet Engn, Dept Biochem, Guangzhou 510275, Peoples R China.
关键词：
phage display;small peptide;screening;human CC chemokine receptor (CCR) 5;CHO cells
摘要：
Human CC chemokine receptor (CCR) 5 is a G protein-coupled receptor involved in a broad range of human diseases that mediates HIV-1 viral entry into cells. Certain small molecule receptor antagonists to CCR5 have been useful in therapy for these diseases. In this study, CCR5-expressing CHO cells (CHO/CCR5 cells) were used to select CCR5-binding peptides from a phage-displayed 12-mers peptide library. All of the 30 clones selected from the library showed specific binding to CHO/CCR5 cells by enzyme linked immunosorbent assay (ELISA). Seventeen out of the 30 clones shared the amino acid motif AFDWTFVPSLIL. The motif-containing phages and synthetic peptide AFDWTFVPSLIL blocked the binding of mAb 2D7 to CHO/CCR5 cells and competitively inhibited the ability of chemokine regulated on activation normal T cell expressed and secreted (RANTES) binding to CHO/CCR5 cells. Furthermore, the peptide AFDWTFVPSLIL also inhibited RANTES induced increase in the intracellular Ca2+ level in CHO/CCR5 cells. These results suggest that the peptide AFDWTFVPSLIL was specific for CCR5 and that it might become a CCR5 antagonist.
摘要：
By ELISA and fluorescence quantitative PCR （ FQ - PCR）, the destructive effect of chitson -I2 against the HBsAg and HBV DNA were investigated. The results showed Chitson -I2 solution of 1. 56250 g/L（5 min） 和0.78125 g/L（ 10 min） could destruct antigenicity of serum HBsAg. Chitson - I2 solution of 6.25000 g/L（5 min）和3. 12500 g/L（ 15 min） had a good destructive effect on HBV DNA. Suggesting Chitson- 12 solution had a good destructive effect on Hepatitis B vires in vitro.
摘要：
目的探讨CCR5亲和短肽对单核细胞趋化活性的影响。方法采用流式细胞仪观察短肽对单抗2D7与单核细胞结合的影响；Quantikine Human RANTES试剂盒检测短肽与RANTES对单核细胞的竞争性结合作用；体外趋化性实验观察短肽对单核细胞的趋化作用；大鼠体内实验观察短肽对动脉粥样硬化形成的影响。结果短肽能抑制2D7与单核细胞的结合；也能竞争性抑制RANTES与单核细胞的结合，其IC50约为5．6mg/L（3．98μmol／L）。在体外，短肽对单核细胞没有趋化性（P=0．074），且能抑制RANTES对单核细胞的趋化作用，短肽＋RANTES组的穿膜细胞数（23±10）显著少于RANTES组（62±13）。体内实验结果表明，短肽能降低单核细胞在大鼠主动脉弓部位的聚集（P〈0．05）。结论短肽对单核细胞具有很强的亲和作用，且短肽能抑制单核细胞对RANTES的趋化性，因而可降低或延缓动脉粥样硬化进程。
