Vann Bennett

Tyrosine phosphorylation at a site highly conserved in the L1 family of cell adhesion molecules abolishes ankyrin binding and increases lateral mobility of neurofascin.

Clustering of voltage-sensitive sodium channels on axons is independent of direct Schwann cell contact in the dystrophic mouse.

Morphogenesis of the node of Ranvier: co-clusters of ankyrin and ankyrin-binding integral proteins define early developmental intermediates.

The phosphorylation state of the FIGQY tyrosine of neurofascin determines ankyrin-binding activity and patterns of cell segregation.

Adducin is an in vivo substrate for protein kinase C: phosphorylation in the MARCKS-related domain inhibits activity in promoting spectrin-actin complexes and occurs in many cells, including dendritic spines of neurons.

Restriction of 480/270-kD ankyrin G to axon proximal segments requires multiple ankyrin G-specific domains.

AnkyrinG is required for clustering of voltage-gated Na channels at axon initial segments and for normal action potential firing.

Nervous system defects of AnkyrinB (-/-) mice suggest functional overlap between the cell adhesion molecule L1 and 440-kD AnkyrinB in premyelinated axons.

Phosphorylation of adducin by Rho-kinase plays a crucial role in cell motility.

Ankyrin-B is required for intracellular sorting of structurally diverse Ca2+ homeostasis proteins.

Caenorhabditis elegans beta-G spectrin is dispensable for establishment of epithelial polarity, but essential for muscular and neuronal function.

Ankyrins and cellular targeting of diverse membrane proteins to physiological sites.

Spectrin and ankyrin-based pathways: metazoan inventions for integrating cells into tissues.

LAD-1, the Caenorhabditis elegans L1CAM homologue, participates in embryonic and gonadal morphogenesis and is a substrate for fibroblast growth factor receptor pathway-dependent phosphotyrosine-based signaling.

Ankyrin-G coordinates assembly of the spectrin-based membrane skeleton, voltage-gated sodium channels, and L1 CAMs at Purkinje neuron initial segments.

The ankyrin-B C-terminal domain determines activity of ankyrin-B/G chimeras in rescue of abnormal inositol 1,4,5-trisphosphate and ryanodine receptor distribution in ankyrin-B (-/-) neonatal cardiomyocytes.

Developing nodes of Ranvier are defined by ankyrin-G clustering and are independent of paranodal axoglial adhesion.

Ankyrins.

A new activity of doublecortin in recognition of the phospho-FIGQY tyrosine in the cytoplasmic domain of neurofascin.

Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death.

Alpha-adducin dissociates from F-actin and spectrin during platelet activation.

Kv3.1b is a novel component of CNS nodes.

L1-dependent neuritogenesis involves ankyrinB that mediates L1-CAM coupling with retrograde actin flow.

Inositol 1,4,5-trisphosphate receptor localization and stability in neonatal cardiomyocytes requires interaction with ankyrin-B.

Lateral membrane biogenesis in human bronchial epithelial cells requires 190-kDa ankyrin-G.

Isoform specificity among ankyrins. An amphipathic alpha-helix in the divergent regulatory domain of ankyrin-b interacts with the molecular co-chaperone Hdj1/Hsp40.

A cardiac arrhythmia syndrome caused by loss of ankyrin-B function.

Ankyrin-B targets beta2-spectrin to an intracellular compartment in neonatal cardiomyocytes.

Nav1.5 E1053K mutation causing Brugada syndrome blocks binding to ankyrin-G and expression of Nav1.5 on the surface of cardiomyocytes.

Ankyrin-B coordinates the Na/K ATPase, Na/Ca exchanger, and InsP3 receptor in a cardiac T-tubule/SR microdomain.

Isoform specificity of ankyrin-B: a site in the divergent C-terminal domain is required for intramolecular association.

Nanospring behaviour of ankyrin repeats.

Ankyrin-G and beta2-spectrin collaborate in biogenesis of lateral membrane of human bronchial epithelial cells.

Ankyrin-G is a molecular partner of E-cadherin in epithelial cells and early embryos.

Ankyrin-B syndrome: enhanced cardiac function balanced by risk of cardiac death and premature senescence.

Adducin promotes micrometer-scale organization of beta2-spectrin in lateral membranes of bronchial epithelial cells.

Organizing the fluid membrane bilayer: diseases linked to spectrin and ankyrin.

Being there: cellular targeting of voltage-gated sodium channels in the heart.

Ankyrin-B is required for coordinated expression of beta-2-spectrin, the Na/K-ATPase and the Na/Ca exchanger in the inner segment of rod photoreceptors.

Localization and structure of the ankyrin-binding site on beta2-spectrin.

An ankyrin-based mechanism for functional organization of dystrophin and dystroglycan.

Ankyrin-G promotes cyclic nucleotide-gated channel transport to rod photoreceptor sensory cilia.

Ankyrin-based patterning of membrane microdomains: new insights into a novel class of cardiovascular diseases.

AnkyrinG is required to maintain axo-dendritic polarity in vivo.

Cholinergic augmentation of insulin release requires ankyrin-B.

Membrane domains based on ankyrin and spectrin associated with cell-cell interactions.

Fast and forceful refolding of stretched alpha-helical solenoid proteins.

Full reconstruction of a vectorial protein folding pathway by atomic force microscopy and molecular dynamics simulations.

Ankyrin-B interactions with spectrin and dynactin-4 are required for dystrophin-based protection of skeletal muscle from exercise injury.

Ank3-dependent SVZ niche assembly is required for the continued production of new neurons.

Nanomechanics of streptavidin hubs for molecular materials.

Mechanical anisotropy of ankyrin repeats.

Mutation of conserved histidines alters tertiary structure and nanomechanics of consensus ankyrin repeats.

Cysteine 70 of ankyrin-G is S-palmitoylated and is required for function of ankyrin-G in membrane domain assembly.

E-cadherin polarity is determined by a multifunction motif mediating lateral membrane retention through ankyrin-G and apical-lateral transcytosis through clathrin.

A single divergent exon inhibits ankyrin-B association with the plasma membrane.

Spectrin- and ankyrin-based membrane domains and the evolution of vertebrates.

Ankyrin-G palmitoylation and βII-spectrin binding to phosphoinositide lipids drive lateral membrane assembly.

Ankyrin-G coordinates intercalated disc signaling platform to regulate cardiac excitability in vivo.

Glial ankyrins facilitate paranodal axoglial junction assembly.

A hierarchy of ankyrin-spectrin complexes clusters sodium channels at nodes of Ranvier.

Structural basis of diverse membrane target recognitions by ankyrins.

A PIK3C3-ankyrin-B-dynactin pathway promotes axonal growth and multiorganelle transport.

Developmental mechanism of the periodic membrane skeleton in axons.

Giant ankyrin-G: a critical innovation in vertebrate evolution of fast and integrated neuronal signaling.

Giant ankyrin-G stabilizes somatodendritic GABAergic synapses through opposing endocytosis of GABAA receptors.

Evolution in action: giant ankyrins awake.

Ankyrin-B metabolic syndrome combines age-dependent adiposity with pancreatic β cell insufficiency.

Dynamic spectrin/ankyrin-G microdomains promote lateral membrane assembly by opposing endocytosis.

Ankyrin-B directs membrane tethering of periaxin and is required for maintenance of lens fiber cell hexagonal shape and mechanics.

Ankyrin-G Inhibits Endocytosis of Cadherin Dimers.

An Adaptable Spectrin/Ankyrin-Based Mechanism for Long-Range Organization of Plasma Membranes in Vertebrate Tissues.

Common human ANK2 variant confers in vivo arrhythmia phenotypes.

Ankyrin-B is a PI3P effector that promotes polarized α5β1-integrin recycling via recruiting RabGAP1L to early endosomes.

Cell-autonomous adiposity through increased cell surface GLUT4 due to ankyrin-B deficiency.

Ankyrin-G regulated epithelial phenotype is required for mouse lens morphogenesis and growth.

βII-spectrin promotes mouse brain connectivity through stabilizing axonal plasma membranes and enabling axonal organelle transport.

autism mutation targeting giant ankyrin-B promotes axon branching and ectopic connectivity.

Neurodevelopmental mutation of giant ankyrin-G disrupts a core mechanism for axon initial segment assembly.