Crosstalk of autophagy and inflammatory signaling pathways during acute intestinal inflammation (C03)

This project is based on the hypothesis that autophagy factor ATG16L1 represents a direct substrate for IKK¿ in intestinal epithelial cells (IECs) and might control the inflammatory response in acute ulcerative coli-tis. We will employ primary organoid systems derived from mice with defined genetic alterations to describe the exact mode of interaction between IKK¿ and ATG16L1. Moreover, as IKK¿ seems to have contrasting functions in myeloid cells and IECs, we will define the divergent mechanisms that control caspase-1 activity in myeloid cells.

DFG Programme Collaborative Research Centres

Subproject of SFB 1177:  Molecular and Functional Characterization of Selective Autophagy

Applicant Institution Goethe-Universität Frankfurt am Main

Co-Applicant Institution Georg-Speyer-Haus
Institut für Tumorbiologie und experimentelle Therapie

Project Head Professor Dr. Florian R. Greten