2,427
Views
22
CrossRef citations to date
0
Altmetric
Autophagic Punctum

DDR1 (discoidin domain receptor tyrosine kinase 1) drives glioblastoma therapy resistance by modulating autophagy

ORCID Icon & ORCID Icon
Pages 1487-1488 | Received 10 Apr 2019, Accepted 07 May 2019, Published online: 23 May 2019

Figures & data

Figure 1. Inhibition of DDR1 modulates radiosensitization through autophagy. Schematic representation of DDR1 function in GBM cells upon radiochemotherapy. Under basal conditions, DDR1 associates with YWHA/14–3-3-BECN1-AKT1 protein complex, mediates pro-survival DDR1 signaling and radiochemoresistance. Upon DDR1 inhibition, the YWHA/14–3-3-BECN1-AKT1 protein complex dissociates from DDR1. BECN1 interacts with PIK3C3/VPS34 and ATG14 and induces autophagic cell death forradiochemosensitization. P, phosphorylation.

Figure 1. Inhibition of DDR1 modulates radiosensitization through autophagy. Schematic representation of DDR1 function in GBM cells upon radiochemotherapy. Under basal conditions, DDR1 associates with YWHA/14–3-3-BECN1-AKT1 protein complex, mediates pro-survival DDR1 signaling and radiochemoresistance. Upon DDR1 inhibition, the YWHA/14–3-3-BECN1-AKT1 protein complex dissociates from DDR1. BECN1 interacts with PIK3C3/VPS34 and ATG14 and induces autophagic cell death forradiochemosensitization. P, phosphorylation.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.