Selected article for: "adaptor molecule and wild type"

Author: Rao, Xiaoquan; Zhao, Shi; Braunstein, Zachary; Mao, Hong; Razavi, Michael; Duan, Lihua; Wei, Yingying; Toomey, Amelia C.; Rajagopalan, Sanjay; Zhong, Jixin
Title: Oxidized LDL upregulates macrophage DPP4 expression via TLR4/TRIF/CD36 pathways
  • Document date: 2019_2_7
  • ID: 1n7xjjd5_31
    Snippet: MyD88 and TRIF are two main downstream molecules mediating TLR4 signaling. We then tested if TLR4-mediated DPP4 up-regulation is dependent on MyD88, a major adaptor molecule for TLR4 signaling. Bone marrow cells isolated from wild-type (WT) or Myd88 −/− mice were used for the induction of BMMs. The expressions of DPP4 on both WT and Myd88 −/− BMMs increased after treatment with 25 μg/mL oxLDL. However, deficiency of MyD88 did not diminis.....
    Document: MyD88 and TRIF are two main downstream molecules mediating TLR4 signaling. We then tested if TLR4-mediated DPP4 up-regulation is dependent on MyD88, a major adaptor molecule for TLR4 signaling. Bone marrow cells isolated from wild-type (WT) or Myd88 −/− mice were used for the induction of BMMs. The expressions of DPP4 on both WT and Myd88 −/− BMMs increased after treatment with 25 μg/mL oxLDL. However, deficiency of MyD88 did not diminish the upregulation of DPP4. In contrast, there was even a slight increase of DPP4 expression after oxLDL treatment in Myd88 −/− BMMs (Figs. 4a-4d) . We then used Trif −/− mice to examine the involvement of MyD88-independent pathways of TLR4 mediated DPP4 expression. Compared to WT BMMs, Trif −/− BMMs showed impaired upregulation of DPP4 following oxLDL treatment although it did not completely abolished oxLDL-induced DPP4 up-regulation (Figs. 5a-5c ).

    Search related documents:
    Co phrase search for related documents