| Abstrakt: |
A recent study conducted by researchers at Tianjin Medical University Cancer Institute and Hospital has shed light on the mechanisms underlying HIV-1 latency. The study identified PRMT2 as a key suppressor of Tat activation, which contributes to proviral latency in multiple cell line latency models and in HIV-1-infected patient CD4+ T cells. The researchers found that PRMT2 methylates Tat arginine 52 (R52), reinforcing its nucleolar sequestration and preventing its incorporation into the Super Elongation Complex (SEC) droplets, thereby promoting proviral latency. These findings provide new insights into the subnuclear distribution and transactivating function of Tat, which could potentially be targeted for therapeutic interventions to eradicate latent viral reservoirs. [Extracted from the article] |
