Soluble tumor necrosis factor (TNF) receptor-1 induces apoptosis via reverse TNF signaling and autocrine transforming growth factor-ß1 Georg H. Waetzig * ,§ , 1 , Philip Rosenstiel * , 1 , Alexander Arlt † , Andreas Till * , Karen Bräutigam * , Heiner Schäfer † , Stefan Rose-John ‡ , Dirk Seegert § , 2 and Stefan Schreiber * , 2 ,3 * Institute of Clinical Molecular Biology and † Laboratory of Molecular Gastroenterology and Hepatology, 1. Department of Medicine, Schleswig-Holstein University Medical Center, Kiel, Germany; ‡ Institute of Biochemistry, Christian-Albrechts-University, Kiel, Germany; and § Conaris Research Institute AG, Kiel, Germany 3 Correspondence: Institute of Clinical Molecular Biology, Schleswig-Holstein University Medical Center, Schittenhelmstrasse 12, Kiel 24105, Germany. E-mail: s.schreiber@mucosa.de <h3>SPECIFIC AIMS</h3> Transmembrane forms of the pivotal proinflammatory cytokine tumor necrosis factor-α (TNF-α) and its two receptors are cleaved by the cell membrane-anchored proteinase TNF-α converting enzyme (TACE), resulting in appreciable serum levels of soluble TNF-α and TNF-α receptors (sTNFR1 and -2). The aims of the present study were to 1) investigate whether sTNFR1 has any signaling functions beyond its known role of neutralizing and buffering TNF-α in the circulation and 2) characterize these novel signaling pathways in
/lp/fed-of-american-socs-for-experimental-biology/soluble-tumor-necrosis-factor-tnf-receptor-1-induces-apoptosis-via-Ujs3d2Tjus