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.
Two mutations in TRPM3 resulting in developmental and epileptic encephalopathies result in a gain-of-channel function, which may lie at the basis of epileptic activity and neurodevelopmental symptoms in the patients.
The dramatic extension of lifespan in Sirt6-deficient mice by Trp53 haploinsufficiency suggests that SIRT6 has distinct biological function from SIRT1 in regulating p53 activity and preventing cells from senescence/apoptosis.
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.
Purkinje cells feature molecular heterogeneity that introduces differentiation in physiological properties between zebrin-identified cerebellar modules and thereby underlies the differential control on sensorimotor integration.
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.
The 3Å structure and correlated functional analysis of the TRPM2 cation channel from Nematostella vectensis shed light on the molecular mechanisms of TRPM2 regulation by intra- and extracellular Ca2+, and of inactivation of human TRPM2.