The parkin-coregulated gene product PACRG promotes TNF signaling by stabilizing LUBAC

Author:

Meschede Jens1ORCID,Šadić Maria2ORCID,Furthmann Nikolas1ORCID,Miedema Tim1ORCID,Sehr Dominik A.1,Müller-Rischart A. Kathrin2,Bader Verian1ORCID,Berlemann Lena A.1ORCID,Pilsl Anna2,Schlierf Anita2,Barkovits Katalin3ORCID,Kachholz Barbara1,Rittinger Katrin4ORCID,Ikeda Fumiyo5ORCID,Marcus Katrin3,Schaefer Liliana6ORCID,Tatzelt Jörg27ORCID,Winklhofer Konstanze F.12ORCID

Affiliation:

1. Molecular Cell Biology, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, 44801 Bochum, Germany.

2. Neurobiochemistry, Adolf Butenandt Institute, Ludwig Maximilians University, 80336 Munich, Germany.

3. Medizinisches Proteom-Center, Ruhr University Bochum, 44801 Bochum, Germany.

4. The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.

5. Institute of Molecular Biotechnology (IMBA), 1030 Vienna, Austria.

6. Pharmacenter Frankfurt/ZAFES, Institute for General Pharmacology and Toxicology, Goethe University, 60590 Frankfurt am Main, Germany.

7. Biochemistry of Neurodegenerative Diseases, Institute of Biochemistry and Pathobiochemistry, Ruhr University Bochum, 44801 Bochum, Germany.

Abstract

PACRG can functionally substitute for the LUBAC adaptor subunit SHARPIN to stimulate NF-κB signaling.

Funder

Michael J. Fox Foundation for Parkinson’s Research

Deutsche Forschungsgemeinschaft

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

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