AC6 is the major adenylate cyclase forming a diarrheagenic protein complex with cystic fibrosis transmembrane conductance regulator in cholera.

The World Health Organization(WHO) has reported a worldwide surge in cases of cholera caused by the intestinal pathogen , and, combined, such surges have claimed several million lives, mostly in early childhood. Elevated cAMP production in intestinal epithelial cells challenged with cholera toxin (CTX) results in diarrhea due to chloride transport by a cAMP-activated channel, the cystic fibrosis transmembrane conductance regulator (CFTR). However, the identity of the main cAMP-producing proteins that regulate CFTR in the intestine and may be relevant for secretory diarrhea is unclear.

Personalized medicine in CF: from modulator development to therapy for cystic fibrosis patients with rare CFTR mutations.

Cystic fibrosis (CF) is the most common life-shortening genetic disease affecting ~1 in 3,500 of the Caucasian population. CF is caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. To date, more than 2,000 CFTR mutations have been identified, which produce a wide range of phenotypes.

Guanylate cyclase 2C agonism corrects CFTR mutants.

Cystic fibrosis (CF) is a genetic disorder in which epithelium-generated fluid flow from the lung, intestine, and pancreas is impaired due to mutations disrupting CF transmembrane conductance regulator (CFTR) channel function. CF manifestations of the pancreas and lung are present in the vast majority of CF patients, and 15% of CF infants are born with obstructed gut or meconium ileus. However, constipation is a significantly underreported outcome of CF disease, affecting 47% of the CF patients, and management becomes critical in the wake of increasing life span of CF patients.

Cytoskeletal architecture and cell motility remain unperturbed in mouse embryonic fibroblasts from Plk3 knockout mice.

Polo-like kinase 3 (Plk3) is best known for its involvement in cell cycle checkpoint regulation following exposure to cytotoxicants or induction of DNA damage. Yet, Plk3 has also been implicated in roles beyond those of cellular responses to DNA damage. Here, we have investigated the proposition, suggested by the Plk literature, that Plk3 regulates cytoskeletal architecture and cell functions mediated by the cytoskeleton.

Rapid Prototyping of Heterotypic Cell-Cell Contacts.

Disparities in cellular behaviour between cultures of a single cell type and heterogeneous co-cultures require constructing spatially-defined arrays of multiple cell types. Such arrays are critical for investigating cellular properties as they exist in vivo. Current methods rely upon covalent surface modification or external physical micromanipulation to control cellular organization on a limited range of substrates.

Micropatterning different cell types with microarray amplification of natural directional persistence.

In vivo, different cell types assemble in specific patterns to form functional tissues. Reproducing this process in vitro by designing scaffold materials to direct cells precisely to the right locations at the right time is important for the next generation of biomaterials. Here, using microarray amplification of natural directional persistence (MANDIP), simultaneous assembly of fibroblasts and endothelial cells is demonstrated by directing their long-range migration.

A stable, label-free optical interferometric biosensor based on TiO2 nanotube arrays.

Optical interferometry of a thin film array of titanium dioxide (TiO2) nanotubes allows the label-free sensing of rabbit immunoglobulin G (IgG). A protein A capture probe is used, which is immobilized on the inner pore walls of the nanotubes by electrostatic adsorption. Control experiments using IgG from chicken (which does not bind to protein A) confirms the specificity of the protein A-modified TiO2 nanotube array sensor.