A. G. Hendricks

Huntingtin polyglutamine expansions misdirect axonal transport by perturbing motor and adaptor recruitment

This study shows that HTT polyQ expansions disrupt motor and adaptor recruitment to vesicles, causing transport defects and altered responses to neuroinflammatory stress.

Measurements of neurite extension and nucleokinesis in an iPSC-derived model system following microtubule perturbation

The paper develops methods to measure neurite extension and nucleokinesis in iPSC-derived neurons and shows that microtubule-targeting drugs significantly affect these processes.

Doublecortin restricts neuronal branching by regulating tubulin polyglutamylation

This study shows DCX regulates neuronal branching by promoting tubulin polyglutamylation, with loss of DCX leading to reduced polyglutamylation and increased neurite branching.

Optogenetic control of kinesins -1, -2, -3, and dynein reveals their specific roles in vesicular transport

This study uses optogenetic inhibitors to investigate the roles of kinesins-1, -2, -3, and dynein in vesicular transport, revealing their specific contributions to endosome and lysosome motility.

The sets of kinesins and dynein transporting endocytic cargoes determine the effect of tau on their motility

The paper investigates how different motor protein sets on endocytic cargoes influence their motility and response to tau, finding that tau inhibits retrograde transport of early phagosomes more than late phagosomes.

Huntingtin S421 phosphorylation increases kinesin and dynein engagement on early endosomes and lysosomes

This study shows that phosphorylation of huntingtin at S421 increases kinesin and dynein engagement on early endosomes and lysosomes, leading to longer and more processive organelle movement.

Tau differentially regulates the transport of early endosomes and lysosomes

This study shows that tau differentially regulates the transport of early endosomes and lysosomes by inhibiting kinesin motors, with lysosomes being more affected than early endosomes.

The Pathogenic R5L Mutation Disrupts Formation of Tau Complexes on the Microtubule by Altering Local N-Terminal Structure

This paper investigates the R5L mutation in Tau, showing it does not reduce microtubule-binding affinity but alters N-terminal structure, impairing Tau complex formation on microtubules.

The mechanochemical origins of the microtubule sliding motility within the kinesin-5 domain organization

This study investigates how the structural features of kinesin-5, specifically tail-motor domain interactions and minifilament length, influence microtubule sliding motility and spindle organization.

Proteins with prion-like domains can form viscoelastic condensates that enable membrane remodeling and endocytosis

The paper shows that prion-like domain-containing endocytic coat proteins form viscoelastic condensates that enable actin-independent membrane remodeling and endocytosis in yeast.

Dynamic crosslinking of the actin cytoskeleton governs the cytoplasm's transition to fluid-like behavior

This study investigates how dynamic actin crosslinking affects the viscoelastic properties of the cytoplasm, showing that a mutation in ACTN4 alters its response to tension.

MAP7 recruits kinesin-1 to microtubules to direct organelle transport

This study shows that MAP7 recruits kinesin-1 to microtubules, enhancing plus-end-directed organelle transport by increasing kinesin binding and motor engagement.

Tau directs intracellular trafficking by regulating the forces exerted by kinesin and dynein teams

This study shows tau modulates intracellular transport by biasing bidirectional motility toward the microtubule minus-end through motor-specific regulation of kinesin and dynein forces.