Browse the search results

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.

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

Channel characteristics of the presequence translocation pore have a direct impact on protein import into the mitochondrial matrix.

Deletion of Alzheimer’s disease risk gene TREM2 augments sensitivity to the purinergic agonist ADP, leading to increased Ca²⁺ influx and reduced directional migration in human induced pluripotent stem cell-derived microglia.

RTN3 is upregulated upon RNA viral infection, in turn suppresses antiviral responses by impairing TRIM25-mediated RIG-I K63-linked polyubiquitination and decreases neutrophil populations and inflammatory infiltration, representing a novel inflammatory resolution.

Studying the impact of natural variation on a key immune gene highlights how focusing on a single wild-type sequence overlooks that rare variants cause the most disease.

Convergent screens targeting the levels of alpha-synuclein and tau identify TRIM28 as a driver of their stability, nuclear accumulation and subsequent toxicity.

The phagocytic receptor CED-1 is kept at the appropriate level by E3 ligase trim-21-mediated ubiquitination-proteasomal degradation for apoptotic cell clearance, which is independent of retromer-dependent recycling and lysosomal degradation.

Different aspects of thermal stimuli, such as speed and intensity, are detected by distinct TRP channel-based mechanisms, with TRPV1 and TRPM2 playing unique roles in warmth perception and thermal decision-making.

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