Genomes and Genes
Affiliation: University of Rochester
- Catalytic-independent inhibition of cIAP1-mediated RIP1 ubiquitination by EGLN3Jian Fu
Aab Cardiovascular Research Institute and Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA Electronic address
Cell Signal 28:72-80. 2016..This study provides novel insight into the mechanism underlying EGLN3 inhibition of NFκB signaling and sheds light on the regulation of RIP1 ubiquitination. ..
- EGLN3 inhibition of NF-κB is mediated by prolyl hydroxylase-independent inhibition of IκB kinase γ ubiquitinationJian Fu
Aab Cardiovascular Research Institute and Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York, USA
Mol Cell Biol 33:3050-61. 2013..This study provides novel insights into EGLN3 function and sheds new light on the regulation of IKKγ ubiquitination and NF-κB. ..
- EGLN3 prolyl hydroxylase regulates skeletal muscle differentiation and myogenin protein stabilityJian Fu
Cardiovascular Research Institute and Department of Medicine, Univeristy of Rochester Medical Center, Rochester, NY 14642, USA
J Biol Chem 282:12410-8. 2007..In addition, this report provides evidence for a novel pathway that regulates myogenin expression and skeletal muscle differentiation...
- Prolyl hydroxylase EGLN3 regulates skeletal myoblast differentiation through an NF-kappaB-dependent pathwayJian Fu
Department of Medicine, Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
J Biol Chem 285:8927-35. 2010..This study demonstrates a novel role for EGLN3 in the regulation of NF-kappaB and suggests that it is involved in mediating myogenic differentiation, which is HIF-independent...
- Smac3, a novel Smac/DIABLO splicing variant, attenuates the stability and apoptosis-inhibiting activity of X-linked inhibitor of apoptosis proteinJian Fu
Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
J Biol Chem 278:52660-72. 2003..Smac3-accelerated XIAP destabilization is, at least in part, attributed to its ability to enhance XIAP ubiquitination. Our study demonstrates that Smac3 is functionally additive to, but independent of, Smac/DIABLO...
- Chemopreventive agents induce programmed death-1-ligand 1 (PD-L1) surface expression in breast cancer cells and promote PD-L1-mediated T cell apoptosisPing Zhang
Center for Biomedical Research, University of Texas Health Center at Tyler, Tyler, TX 75708, USA
Mol Immunol 45:1470-6. 2008..Our studies reveal a potential link between chemotherapy and cancer immunoresistance...