Lu Rao

The P3018S disease variant reveals how dynein's trailing motor sets ensemble velocity.

The paper investigates how the P3018S mutation in dynein affects its function, revealing that the trailing motor in multi-dynein assemblies dictates ensemble velocity.

Pathogenic KIF1A R350 Variants Disrupt A Conserved Kinesin-Tubulin Salt Bridge

The paper identifies a conserved salt bridge between KIF1A R350 and -tubulin E415, whose disruption in pathogenic variants correlates with altered motor function.

Enhanced axonal transport in large vertebrates: KIF5A adaptations in giraffes and pythons

This study identifies amino acid substitutions in KIF5A from giraffes and pythons that enhance axonal transport speed, revealing convergent evolutionary adaptations for long-distance transport.

Distinct Clinical Phenotypes in KIF1A-Associated Neurological Disorders Result from Different Amino Acid Substitutions at the Same Residue in KIF1A

The paper examines how different amino acid substitutions at the same KIF1A residue lead to distinct clinical and molecular outcomes in KIF1A-associated neurological disorders.

A Two-Heads-Bound State Drives KIF1A Superprocessivity

This study identifies a two-heads-bound state in KIF1A that enhances processivity and is critical for neuronal transport, contrasting with Kinesin-1's one-head-bound state.

The Power of Three: Dynactin associates with three dyneins under load for greater force production

The paper shows that mechanical tension recruits a third dynein motor to DDB complexes, enhancing force production and stability under load.

ALS-linked KIF5A ΔExon27 mutant causes neuronal toxicity through gain of function

This study shows that KIF5A ΔExon27 mutant causes neuronal toxicity through gain of function by forming aggregates and increasing motor activity.

Genotype and defects in microtubule-based motility correlate with clinical severity in KIF1A Associated Neurological Disorder

This study links KIF1A variants to clinical severity in KAND by analyzing transport defects and protein dysfunction.