TRIM25 in the Regulation of the Antiviral Innate Immunity

Frontiers in Immunology

Adolfo García-Sastre¹  María Martín-Vicente⁴  Salvador Resino⁴  Isidoro Martínez⁴  Luz M. Medrano⁴ 

[1] Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY, United States;Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY, United States;Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY, United States;Unidad de Infección Viral e Inmunidad, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Madrid, Spain;

关键词: TRIM25;    innate immunity;    ubiquitination;    virus;    E3 ubiquitin ligase;   

DOI  :  10.3389/fimmu.2017.01187

来源: DOAJ

【 摘 要 】

TRIM25 is an E3 ubiquitin ligase enzyme that is involved in various cellular processes, including regulation of the innate immune response against viruses. TRIM25-mediated ubiquitination of the cytosolic pattern recognition receptor RIG-I is an essential step for initiation of the intracellular antiviral response and has been thoroughly documented. In recent years, however, additional roles of TRIM25 in early innate immunity are emerging, including negative regulation of RIG-I, activation of the melanoma differentiation-associated protein 5–mitochondrial antiviral signaling protein–TRAF6 antiviral axis and modulation of p53 levels and activity. In addition, the ability of TRIM25 to bind RNA may uncover new mechanisms by which this molecule regulates intracellular signaling and/or RNA virus replication.

【 授权许可】

Unknown