Cyclic and ruled Lagrangian surfaces in complex Euclidean space

We study those Lagrangian surfaces in complex Euclidean space which are foliated by circles or by straight lines. The former, which we call cyclic, come in three types, each one being described by means of, respectively, a planar curve, a Legendrian curve of the 3-sphere or a Legendrian curve of the anti de Sitter 3-space. We also describe ruled Lagrangian surfaces. Finally we characterize those cyclic and ruled Lagrangian surfaces which are solutions to the self-similar equation of the Mean Curvature Flow. Finally, we give a partial result in the case of Hamiltonian stationary cyclic surfaces

Intersections of quadrics, moment-angle manifolds, and Hamiltonian-minimal Lagrangian embeddings

We study the topology of Hamiltonian-minimal Lagrangian submanifolds N in C^m constructed from intersections of real quadrics in a work of the first author. This construction is linked via an embedding criterion to the well-known Delzant construction of Hamiltonian toric manifolds. We establish the following topological properties of N: every N embeds as a submanifold in the corresponding moment-angle manifold Z, and every N is the total space of two different fibrations, one over the torus T^{m-n} with fibre a real moment-angle manifold R, and another over a quotient of R by a finite group with fibre a torus. These properties are used to produce new examples of Hamiltonian-minimal Lagrangian submanifolds with quite complicated topology.Comment: 14 pages, published version (minor changes

Role of Interaction and Nucleoside Diphosphate Kinase B in Regulation of the Cystic Fibrosis Transmembrane Conductance Regulator Function by cAMP-Dependent Protein Kinase A

Cystic fibrosis results from mutations in the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-dependent protein kinase A (PKA) and ATP-regulated chloride channel. Here, we demonstrate that nucleoside diphosphate kinase B (NDPK-B, NM23-H2) forms a functional complex with CFTR. In airway epithelia forskolin/IBMX significantly increases NDPK-B co-localisation with CFTR whereas PKA inhibitors attenuate complex formation. Furthermore, an NDPK-B derived peptide (but not its NDPK-A equivalent) disrupts the NDPK-B/CFTR complex in vitro (19-mers comprising amino acids 36-54 from NDPK-B or NDPK-A). Overlay (Far-Western) and Surface Plasmon Resonance (SPR) analysis both demonstrate that NDPK-B binds CFTR within its first nucleotide binding domain (NBD1, CFTR amino acids 351-727). Analysis of chloride currents reflective of CFTR or outwardly rectifying chloride channels (ORCC, DIDS-sensitive) showed that the 19-mer NDPK-B peptide (but not its NDPK-A equivalent) reduced both chloride conductances. Additionally, the NDPK-B (but not NDPK-A) peptide also attenuated acetylcholine-induced intestinal short circuit currents. In silico analysis of the NBD1/NDPK-B complex reveals an extended interaction surface between the two proteins. This binding zone is also target of the 19-mer NDPK-B peptide, thus confirming its capability to disrupt NDPK-B/CFTR complex. We propose that NDPK-B forms part of the complex that controls chloride currents in epithelia