a new beta cell model: the derivation of a human pancreatic beta cell line has been a long and difficult task. now, philippe ravassard and colleagues have successfully created a functional beta cell line. they used a step-by-step method, first transducing human fetal pancreas with an immortalizing factor to prevent senescence, then grafting them into severe combined immunodeficiency (scid) mice, which allowed proliferation and differentiation into beta cells. a second round of transduction with a different immortalizing factor and passaging through scid mice enabled the authors to amplify the beta cells and subsequently culture them. ravassard et al. analyzed one of their cell lines and found it expressed characteristic beta cell markers and did not show significant expression of markers associated with other types of pancreatic cells. moreover, the beta cells could secrete insulin in response to glucose stimulation and ameliorated chemically induced diabetes in a mouse model, demonstrating functionality. thus, the derivation of this new beta cell line represents an important technical step forward. grasping mutant cftr: the delta f508 mutation in the cystic fibrosis transmembrane conductance regulator (cftr) is the most common disease-causing mutation in people with cystic fibrosis. this mutation prevents the cftr protein from reaching the cell surface. a new study shows that the activation of an unconventional secretion pathway mediated by golgi reassembly stacking proteins (grasps) allows the transport of both this mutant and wild-type cftr to the plasma membrane. the misfolded delta f508 cftr usually remains a core-glycosylated immature form in the endoplasmic reticulum (er) and cannot be secreted through the golgi-mediated exocytic pathway. heon yung gee and colleagues showed that this protein reached the membrane after blocking er-to-golgi trafficking in vitro. this transport route was mediated by inositol-requiring protein 1 (ire-1), which activates the unfolded protein response (upr). using knockout and overexpression strategies in cultured cells, the authors found that grasps were required for this unconventional transport route. interestingly, grasp upregulation rescued the mutant cftr without inducing the er stress-mediated upr, but ire-1 was still needed for the phosphorylation and activity of grasp. in mice harboring the delta f508 cftr mutation, transgenic expression of grasp rescued the apical expression of the misfolded cftr and increased survival. hijacking an antibody: genetic mutations often drive viral escape from antibody-mediated neutralization. a new study describes an alternative form of resistance where human cytomegalovirus (cmv) incorporates the antibody and uses it to subsequently infect new cells. the human monoclonal igg msl-192 recognizes the viral glycoprotein h (gh) and blocks infection of fibroblasts with cmv in vitroa new beta cell model: the derivation of a human pancreatic beta cell line has been a long and difficult task. now, philippe ravassard and colleagues have successfully created a functional beta cell line. they used a step-by-step method, first transducing human fetal pancreas with an immortalizing factor to prevent senescence, then grafting them into severe combined immunodeficiency (scid) mice, which allowed proliferation and differentiation into beta cells. a second round of transduction with a different immortalizing factor and passaging through scid mice enabled the authors to amplify the beta cells and subsequently culture them. ravassard et al. analyzed one of their cell lines and found it expressed characteristic beta cell markers and did not show significant expression of markers associated with other types of pancreatic cells. moreover, the beta cells could secrete insulin in response to glucose stimulation and ameliorated chemically induced diabetes in a mouse model, demonstrating functionality. thus, the derivation of this new beta cell line represents an important technical step forward. grasping mutant cftr: the delta f508 mutation in the cystic fibrosis transmembrane conductance regulator (cftr) is the most common disease-causing mutation in people with cystic fibrosis. this mutation prevents the cftr protein from reaching the cell surface. a new study shows that the activation of an unconventional secretion pathway mediated by golgi reassembly stacking proteins (grasps) allows the transport of both this mutant and wild-type cftr to the plasma membrane. the misfolded delta f508 cftr usually remains a core-glycosylated immature form in the endoplasmic reticulum (er) and cannot be secreted through the golgi-mediated exocytic pathway. heon yung gee and colleagues showed that this protein reached the membrane after blocking er-to-golgi trafficking in vitro. this transport route was mediated by inositol-requiring protein 1 (ire-1), which activates the unfolded protein response (upr). using knockout and overexpression strategies in cultured cells, the authors found that grasps were required for this unconventional transport route. interestingly, grasp upregulation rescued the mutant cftr without inducing the er stress-mediated upr, but ire-1 was still needed for the phosphorylation and activity of grasp. in mice harboring the delta f508 cftr mutation, transgenic expression of grasp rescued the apical expression of the misfolded cftr and increased survival. hijacking an antibody: genetic mutations often drive viral escape from antibody-mediated neutralization. a new study describes an alternative form of resistance where human cytomegalovirus (cmv) incorporates the antibody and uses it to subsequently infect new cells. the human monoclonal igg msl-192 recognizes the viral glycoprotein h (gh) and blocks infection of fibroblasts with cmv in vitro