The Role of the Microtubule Cytoskeleton in Neurodevelopmental Disorders

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Building the Neuronal Microtubule Cytoskeleton

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Dynamic microtubules regulate dendritic spine morphology and synaptic plasticity

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Human TUBB3 Mutations Perturb Microtubule Dynamics, Kinesin Interactions, and Axon Guidance

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Mutations in TUBG1, DYNC1H1, KIF5C and KIF2A cause malformations of cortical development and microcephaly

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Mutations in α-Tubulin Cause Abnormal Neuronal Migration in Mice and Lissencephaly in Humans

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Axon Branching Requires Interactions between Dynamic Microtubules and Actin Filaments

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Mutations in the β-tubulin gene TUBB2B result in asymmetrical polymicrogyria

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Ndel1 Operates in a Common Pathway with LIS1 and Cytoplasmic Dynein to Regulate Cortical Neuronal Positioning

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Molecular mechanisms of dendrite stability

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LIS1 and XLIS (DCX) mutations cause most classical lissencephaly, but different patterns of malformation

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KIF5C, a Novel Neuronal Kinesin Enriched in Motor Neurons

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Doublecortin Is Required in Mice for Lamination of the Hippocampus But Not the Neocortex

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The wide spectrum of tubulinopathies: what are the key features for the diagnosis?

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Microtubules provide directional cues for polarized axonal transport through interaction with kinesin motor head

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Mixed microtubules steer dynein-driven cargo transport into dendrites

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Differentiation between oppositely oriented microtubules controls polarized neuronal transport

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Axon Extension Occurs Independently of Centrosomal Microtubule Nucleation

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Genetic Interactions between Doublecortin and Doublecortin-like Kinase in Neuronal Migration and Axon Outgrowth

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A Change in the Selective Translocation of the Kinesin-1 Motor Domain Marks the Initial Specification of the Axon

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The Microtubule-severing Proteins Spastin and Katanin Participate Differently in the Formation of Axonal Branches

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Mutations in Microcephalin Cause Aberrant Regulation of Chromosome Condensation

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Doublecortin Is the Major Gene Causing X-Linked Subcortical Laminar Heterotopia (SCLH)

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Which way to go? Cytoskeletal organization and polarized transport in neurons

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Large spectrum of lissencephaly and pachygyria phenotypes resulting from de novo missense mutations in tubulin alpha 1A (TUBA1A)

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MCPH1 regulates the neuroprogenitor division mode by coupling the centrosomal cycle with mitotic entry through the Chk1–Cdc25 pathway

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Mechanism of Microtubule Stabilization by Doublecortin

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LIS1, CLIP-170's Key to the Dynein/Dynactin Pathway

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MARK/PAR1 kinase is a regulator of microtubule-dependent transport in axons

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Mutations in STIL, Encoding a Pericentriolar and Centrosomal Protein, Cause Primary Microcephaly

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Microtubule Minus-End Binding Protein CAMSAP2 Controls Axon Specification and Dendrite Development

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Increased LIS1 expression affects human and mouse brain development

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Microtubules in Dendritic Spine Development

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Activity-Dependent Neuroprotective Protein Snippet NAP Reduces Tau Hyperphosphorylation and Enhances Learning in a Novel Transgenic Mouse Model

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Doublecortin Microtubule Affinity Is Regulated by a Balance of Kinase and Phosphatase Activity at the Leading Edge of Migrating Neurons

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The microcephaly ASPM gene is expressed in proliferating tissues and encodes for a mitotic spindle protein

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Tubulin-related cortical dysgeneses: microtubule dysfunction underlying neuronal migration defects

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Dendrites In Vitro and In Vivo Contain Microtubules of Opposite Polarity and Axon Formation Correlates with Uniform Plus-End-Out Microtubule Orientation

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STIL is required for centriole duplication in human cells

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Multiple Dose-Dependent Effects of Lis1 on Cerebral Cortical Development

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Axonal Transport RatesIn VivoAre Unaffected by Tau Deletion or Overexpression in Mice

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MAP2 defines a pre-axonal filtering Zone to regulate KIF1- versus KIF5-Dependent cargo transport in sensory neurons

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Initial Neurite Outgrowth in Drosophila Neurons Is Driven by Kinesin-Powered Microtubule Sliding

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Single-molecule tracking of tau reveals fast kiss-and-hop interaction with microtubules in living neurons

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Synaptic Regulation of Microtubule Dynamics in Dendritic Spines by Calcium, F-Actin, and Drebrin

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