Mice deficient in the TRPM6 channel suffer from impaired prenatal development, shortened lifespan, growth deficit and disturbed energy balance due to a defect in epithelial Mg2+ uptake, thus highlighting a pivotal role of TRPM6 in organismal Mg2+ homeostasis.
Pro-nociceptive and pro-inflammatory TRPM3 (transient receptor potential melastatin 3) channels, expressed in somatosensory neurons, are inhibited by activation of Gαi-coupled receptors, such as µ-opioid receptors, in vitro and in vivo.
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.
Disease-associated mutants of the TRPM3 ion channel are overactive, and they are inhibited by the antiepileptic medication primidone, offering a potential therapeutic intervention to treat this channelopathy.
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.