Tomasz Wegierski

TL;DR: It is found that TRPV4, like TRPP2, is an essential component of the ciliary mechanosensor, and the concept that defective ciliary flow sensing constitutes the fundamental mechanism of cystogenesis is challenged.

TL;DR: It is shown that TRPP2, the ion channel mutated in autosomal dominant polycystic kidney disease (ADPKD), protects cells from apoptosis by lowering the Ca2+ concentration in the endoplasmic reticulum (ER) and provides a molecular mechanism for the increased apoptosis rates in ADPKD upon loss of TR PP2 channel function.

TL;DR: It is shown that SFKs mediate tyrosine phosphorylation of TRPV4 in different cell lines, indicating that tyrosines represent an important modulatory mechanism, which may underlie the recently described function of TRPs4 in inflammatory hyperalgesia.

TL;DR: It is shown that ubiquitination represents an important mechanism to control the presence of TRPV4 at the plasma membrane and that AIP4‐mediated regulation is a unique property of select TRP channels.

TL;DR: It is reported that OS-9, a ubiquitously expressed endoplasmic reticulum (ER)-associated protein, interacts with the cytosolic N-terminal tail of TRPV4 and appears to protect TRPv4 subunits from the precocious ubiquitination and ER-associated degradation.