Imaging of choledochal cysts.

Choledochal cysts are rare cystic dilatations of the intrahepatic and/or extrahepatic biliary tree, which may be mistaken for other cystic lesions if their characteristic features are not recognized. The etiology is unknown, and likely multifactorial, and it is uncertain whether they are congenital or acquired. Multiple imaging modalities can be used to diagnose choledochal cysts, including ultrasound, computed tomography, magnetic resonance (MR) cholangiopancreatography (MRCP), endoscopic retrograde cholangiopancreatography, and percutaneous transhepatic cholangiography. MRCP has replaced the more invasive techniques as the gold standard of diagnosis. In addition, MRCP is helpful in detecting an abnormal pancreaticobiliary junction, which is seen in the majority of choledochal cysts. Reaching a correct diagnosis is essential, given the associated risk of complications, including cholangitis, biliary strictures, stones, and malignancy, and accurately assessing the location and length of involvement is important for surgical planning. This review aims to familiarize radiologists with the different types of choledochal cysts and their imaging features according to the Todani classification.

The role of monoubiquitination in endocytic degradation of human ether-a-go-go-related gene (hERG) channels under low K+ conditions.

A reduction in extracellular K(+) concentration ([K(+)](o)) causes cardiac arrhythmias and triggers internalization of the cardiac rapidly activating delayed rectifier potassium channel (I(Kr)) encoded by the human ether-a-go-go-related gene (hERG). We investigated the role of ubiquitin (Ub) in endocytic degradation of hERG channels stably expressed in HEK cells. Under low K(+) conditions, UbKO, a lysine-less mutant Ub that only supports monoubiquitination, preferentially interacted and selectively enhanced degradation of the mature hERG channels. Overexpression of Vps24 protein, also known as charged multivesicular body protein 3, significantly accelerated degradation of mature hERG channels, whereas knockdown of Vps24 impeded this process. Moreover, the lysosomal inhibitor bafilomycin A1 inhibited degradation of the internalized mature hERG channels. Thus, monoubiquitination directs mature hERG channels to degrade through the multivesicular body/lysosome pathway. Interestingly, the protease inhibitor lactacystin inhibited the low K(+)-induced hERG endocytosis and concomitantly led to an accumulation of monoubiquitinated mature hERG channels, suggesting that deubiquitination is also required for the endocytic degradation. Consistently, overexpression of the endosomal deubiquitinating enzyme signal transducing adaptor molecule-binding protein significantly accelerated whereas knockdown of endogenous signal transducing adaptor molecule-binding protein impeded degradation of the mature hERG channels under low K(+) conditions. Thus, monoubiquitin dynamically mediates endocytic degradation of mature hERG channels under low K(+) conditions.