Welcome to the first ever installment of Research Roundup. So that you can quickly find the science most relevant to you, we’ll be curating some of the best bits of research around membrane proteins.
Okay, here’s what we’ve got for you.
TRPV1 activation and internalization is part of the LPS-induced inflammation in human iPSC-derived cardiomyocytes
hiPSC-derived cardiomyocytes express the TRPV1 channel within the plasma membrane, TRPV1 mediates the LPS-induced inflammation, and stimulation with LPS leads to TRPV1 internalization. Also, research here seems to show a prolonged disturbance of TRPV-associated current that is induced by exposure to LPS as well as the inflammatory cytokine interleukin-6.
Cohesin-protein Shugoshin-1 controls cardiac automaticity via HCN4 pacemaker channel
A mutation in Shugoshin-1 causes the Chronic Atrial and Intestinal Dysrhythmia (CAID) Syndrome, but the underlying mechanisms are unknown. Here, the authors show that Shugoshin-1 controls cardiac pacemaker activity by interacting with HCN4 to enhance its cell-surface expression, and that the CAID-Syndrome mutation disrupts cardiac pacemaking by interfering with this important non-canonical interaction.
α-Synuclein–induced Kv4 channelopathy in mouse vagal motoneurons drives nonmotor parkinsonian symptoms
In our mutant mouse model, the induction of an α-synucleinopathy in dorsal motor nucleus of the vagus (DMV) motoneurons caused shrinkage and dysregulated surface densities of Kv4 channels, which, in turn, reduced firing rates. The research teams show that this functional remodeling of intact DMV neurons leads to impaired pacemaker function in vitro and in vivo, which, in turn, reduces gastrointestinal motility, a common early symptom of prodromal Parkinson’s disease.
Phrixotoxin-2 (STP-710) for blocking Kv4 channels.