TRIM family proteins: retroviral restriction and antiviral defence

By S. Nisole, J. Stoye, A. Saïb. Nature Reviews Microbiology, 2005

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Structure, dynamics and functions of promyelocytic leukaemia nuclear bodies (2007, background): “First and foremost, PML is induced at the transcriptional level by type I and II interferons , which cause an increase in both the size and number of PML-NB”
Avoiding the void: cell-to-cell spread of human viruses (2008, background): “, the TRIM family of inter-species retroviral restriction factor”
TRIM proteins and cancer (2011, background): “In response to interferon-α (IFNα), IFNβ, IFNγ or p53, the expression level of PML is positively controlled, probably through signal transducer and activator of transcription (STAT) proteins and interferon response factors (IRFs”
Influenza A virus NS1 targets the ubiquitin ligase TRIM25 to evade recognition by RIG-I (2009, background): “In addition, tripartite motif (TRIM) proteins, containing an N-terminal RING domain with potential ubiquitin E3 ligase activity, represent a new class of antiviral molecules involved in innate immunity (Nisole et al., 2005; Ozato et al., 2008).”
TRIM family proteins and their emerging roles in innate immunity (2008, background): “TRIM proteins The most striking feature of TRIM superfamily proteins is the highly conserved order of domains in the RBCC moti”