用户名: 密码: 验证码:
Transient expression of recombinant ACKR4 (CCRL1) gene, an atypical chemokine receptor in human embryonic kidney (HEK 293) cells
详细信息    查看全文
  • 作者:Bahareh Parsi ; Abolghasem Esmaeili ; Mohammad Hashemi…
  • 刊名:Molecular Biology Reports
  • 出版年:2016
  • 出版时间:July 2016
  • 年:2016
  • 卷:43
  • 期:7
  • 页码:583-589
  • 全文大小:1,538 KB
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Life Sciencesr>Animal Anatomy, Morphology and Histologyr>Animal Biochemistryr>
  • 出版者:Springer Netherlands
  • ISSN:1573-4978
  • 卷排序:43
文摘
ACKR4 also called CCX-CKR, CCRL1 as a member of atypical chemokine receptors, regulates the biological responses by clearance or transporting homeostatic chemokines such as CCL19, CCL21, CCL25, and CXCL13. Since these chemokines are involved in cancer development and metastasis, ACKR4 could have inhibition roles in cancer cell proliferation and invasion. Forming complexes with chemokine receptors by ACKR4 as in the case of hCXCR3 which lead to chemotaxis prevention is the other function of this protein is. However, as an atypical chemokine receptor, ACKR4 is less well-characterized compared to other members. Here, as the first step in understanding the molecular mechanisms of ACKR4 action, transfectants in HEK293T cell, was generated. In this study, ACKR4 coding sequence was cloned and human embryonic kidney 293T cells were used for recombinant production of ACKR4 protein. The liposome-mediated transfection with ACKR4 CDs, were detected in ACKR4 positive cells as early as 48 h post-transfection. The production of ACKR4 protein was confirmed using RT-PCR, dot blot, western blot, and flow cytometry. ACKR4 may represent a novel molecular target in cancer therapy, which might provide a chance for new therapeutic strategy. Therefore, the first step in the understanding of the molecular mechanisms of ACKR4 action is generation ACKR4-HEK293T recombinant cells.KeywordsACKR4CCX-CKRCCRL1Atypical chemokineTransfectionHEK293T

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700