Fig. 7: IL-17RB played a key role in activating autophagy and K63-mediated ubiquitination of Beclin-1 induced by rIL-17B. | Oncogene

Fig. 7: IL-17RB played a key role in activating autophagy and K63-mediated ubiquitination of Beclin-1 induced by rIL-17B.

From: IL-17B/IL-17RB signaling cascade contributes to self-renewal and tumorigenesis of cancer stem cells by regulating Beclin-1 ubiquitination

Fig. 7

A TEM was used to detect autophagosome formation in rIL-17B- or PBS-treated MGC-803 cells infected with shControl or shIL-17RB lentiviral constructs. B The expression of LC3, P62, and GAPDH was assayed using western blotting in rIL-17B- or PBS-treated MGC-803 cells infected with shControl or shIL-17RB lentiviral constructs. C, D MGC-803 cells were transfected with the HA-Beclin-1 plasmid and subjected to IP by using an HA antibody or control IgG, followed by IB with ubiquitin/K63-linked ubiquitin, Beclin-1, IL-17RB, and GAPDH antibodies. E IP was used to analyze shIL-17RB or shControl MGC-803 cells that had been transfected with HA-Beclin-1 and the MYC-TRAF6 plasmid by using an HA antibody or control IgG, followed by IB with HA and MYC antibodies. F IP was used to analyze shIL-17RB or shControl MGC-803 cells treated with rIL-17B or PBS transfected with the HA-Beclin-1 plasmid by using an HA antibody or control IgG, followed by IB with K63-linked ubiquitin, Beclin-1, IL-17RB, and GAPDH antibodies. G IP was used to analyze shIL-17RB or shControl MGC-803 cells transfected with HA-Beclin-1 and the MYC-TRAF6 plasmid by using an HA antibody or control IgG with/without rIL-17B treatment, followed by IB with HA, MYC, and GAPDH antibodies.

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