https://www.selleckchem.com/products/nsc16168.html Macroautophagy/autophagy is an intracellular process involved in the breakdown of macromolecules and organelles. Recent studies have shown that PKD2/PC2/TRPP2 (polycystin 2, transient receptor potential cation channel), a nonselective cation channel permeable to Ca2+ that belongs to the family of transient receptor potential channels, is required for autophagy in multiple cell types by a mechanism that remains unclear. Here, we report that PKD2 forms a protein complex with BECN1 (beclin 1), a key protein required for the formation of autophagic vacuoles, by acting as a scaffold that interacts with several co-modulators via its coiled-coil domain (CCD). Our data identified a physical and functional interaction between PKD2 and BECN1, which depends on one out of two CCD domains (CC1), located in the carboxy-terminal tail of PKD2. In addition, depletion of intracellular Ca2+ with BAPTA-AM not only blunted starvation-induced autophagy but also disrupted the PKD2-BECN1 complex. Consistently, PKD2 overexpression tr/LC3 microtubule associated protein 1 light chain 3; MTORC1 mechanistic target of rapamycin kinase complex 1; NBR1 NBR1 autophagy cargo receptor; PIK3C3/VPS34 phosphatidylinositol 3-kinase catalytic subunit type 3; PKD2/PC2 polycystin 2, transient receptor potential cation channel; RTN4/NOGO reticulon 4; RUBCN/RUBICON rubicon autophagy regulator; SQSTM1/p62 sequestosome 1; UVRAG UV radiation resistance associated; WIPI2 WD repeat domain, phosphoinositide interacting 2.Purpose An elevation in blood pressure (BP) during exercise is the normal physiological response, however an abnormally exaggerated rise in BP, in terms of hypertensive response to exercise (HRE), is seen as a prognostic factor for end-organ damage and mortality. HRE is more common in hypertensive (HT) patients and data are lacking on the effect of antihypertensive medication on HRE. In this study, we evaluated patients who underwent treadmill exer