Chromogranin B and other members of the granin protein family form condensates that recruit clients like proinsulin. The condensation in the lumen of -Golgi network (TGN) is critical for the biogenesis of secretory granules. Here, we describe a protocol to purify the tagged version of chromogranin B close to its native form at the TGN, which can then be utilized for microscopy-based assays to monitor condensate formation in vitro and client partitioning depending on the material properties of chromogranin B assemblies.
View Article and Find Full Text PDFThe brain has a highly selective semipermeable blood barrier, termed the blood-brain barrier (BBB), which prevents the delivery of therapeutic macromolecular agents to the brain. The integration of MR-guided low-intensity pulsed focused ultrasound (FUS) with microbubble pre-injection is a promising technique for non-invasive and non-toxic BBB modulation. MRI can offer superior soft-tissue contrast and various quantitative assessments, such as vascular permeability, perfusion, and the spatial-temporal distribution of MRI contrast agents.
View Article and Find Full Text PDFCa influx into the -Golgi Network (TGN) promotes secretory cargo sorting by the Ca-ATPase SPCA1 and the luminal Ca binding protein Cab45. Cab45 oligomerizes upon local Ca influx, and Cab45 oligomers sequester and separate soluble secretory cargo from the bulk flow of proteins in the TGN. However, how this Ca flux into the lumen of the TGN is achieved remains mysterious, as the cytosol has a nanomolar steady-state Ca concentration.
View Article and Find Full Text PDFA receptor protein called TGN46 has an important role in sorting secretory proteins into vesicles going to different destinations inside cells.
View Article and Find Full Text PDFHerpes simplex virus 1 is an important human pathogen that has been intensively studied for many decades. Nevertheless, the molecular mechanisms regulating its establishment, maintenance, and reactivation from latency are poorly understood. Here, we show that HSV-1-encoded miR-H2 is post-transcriptionally edited in latently infected human tissues.
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