HIV latency reversing agents act through Tat post translational modifications

RARRES3 regulates signal transduction through post-translational protein modifications

We recently reported that retinoic acid receptor responder 3 (RARRES3)-mediated protein deacylation resulted in significant inhibition of the transformed properties of breast cancer cells. This finding suggests a key role of RARRES3 in the regulation of growth signaling and metastasis in cancer cells and as a potential therapeutic target for cancer therapy.

Post-translational modifications of tubulin

Microtubules are the largest filamentous components of the eukaryotic cytoskeleton. In spite of their extraordinary level of structural conservation, microtubules fulfill a vast range of different functions in cells. How this functional diversity is achieved remains an open question; however, recent advances point towards post-translational modifications (PTMs) of tubulin as a potent mechanism ...

Chemical-biology Approach to Delineate the Mechanism of Action of Hiv-1 Latency Reversing Agents

Trade-off between synergy and efficacy in combinations of HIV-1 latency-reversing agents

Eradicating HIV-1 infection is difficult because of the reservoir of latently infected cells that gets established soon after infection, remains hidden from antiretroviral drugs and host immune responses, and retains the capacity to reignite infection following the cessation of treatment. Drugs called latency-reversing agents (LRAs) are being developed to reactivate latently infected cells and ...

Shocking HIV out of hiding: where are we with clinical trials of latency reversing agents?

PURPOSE OF REVIEW To provide an overview of the initial experiences with the use of latency-reversing agents (LRAs) in clinical trials in HIV and to discuss and contrast results arising from these studies. RECENT FINDINGS Although the clinical administration of histone deacetylase inhibitors (HDACis) and disulfiram to HIV-infected individuals on antiretroviral therapy significantly increased ...