TRIM33 performs an essential function in B cell acute lymphoblastic leukemia through an association with a single cis element.

Higher-order assembly enables and links pathogen recognition and downstream steps in the TRIM5-mediated anti-HIV response.

TRIM23 plays a critical role in the switching from early to late adipogenic enhanceosomes by stabilizing the PPARγ protein.

Mutations in the TRIM5α retrovirus-binding interface frequently improve but rarely disrupt retroviral restriction.

Goblet cells secrete mucins—which are key components of mucus—in a process that is regulated by calcium ions, which enter the goblet cells via a mechanism involving a channel protein called TRPM5.

To protect mammals against retroviral infections, TRIM5 restriction factors recognize viral capsids by forming complementary hexagonal nets that can adapt to the patterns of capsid protein subunits on the viral capsid surface.

TRIM28 was found to be a versatile dual-function latency contributor by bridging both suppressive epigenetic modifications and RNAP II transcriptional-pausing, and can be a novel target to develop latency-reversing agents.

Repressing the conserved pro-differentiation let-7 microRNAs through limiting Ago2 levels is critical to maintaining pluripotency in stem cells.

HIV vaccine-induced binding and neutralizing antibody epitope specificities were mapped at high resolution directly from polyclonal sera, overcoming shortcomings in traditional serum mapping approaches and enabling highly detailed vaccine design.

TRIM37 prevents the formation of centriolar protein assemblies through an atypical de novo assembly pathway that would otherwise threaten genome integrity.