S. Niwa

The chromokinesin Kid (KIF22) forms a homodimer, moves processively along microtubules and transports double-stranded DNA

This study shows that Kid (KIF22) forms a homodimer, moves processively along microtubules, and transports double-stranded DNA, reclassifying it as a processive and dimeric motor.

SLC-25A46 Regulates Mitochondrial Fusion through FZO-1/Mitofusin and is Essential for Maintaining Neuronal Morphology

This study identifies SLC-25A46 as a regulator of mitochondrial fusion through FZO-1/Mitofusin and shows its role in maintaining neuronal morphology.

The FHA domain is essential for the autoinhibition of KIF1A/UNC-104

The paper investigates the role of the FHA domain in regulating dimerization of DmUNC-104 and links abnormal dimerization to human diseases.

Characterizing Human KIF1Bβ Motor Activity by Single-Molecule Motility Assays and Caenorhabtidis elegans Genetics.

This study characterizes KIF1Bβ motor activity using single-molecule assays and C. elegans genetics, showing reduced activity due to a disease mutation.

Modeling the motion of disease-associated KIF1A heterodimers

This paper develops mathematical models to explain the motility of KIF1A heterodimers, showing that a coordinated head model better predicts experimental results than an independent head model.

Comparative analysis of two Caenorhabditis elegans kinesins KLP-6 and UNC-104 reveals common and distinct activation mechanisms in kinesin-3

This study compares KLP-6 and UNC-104, two Caenorhabditis elegans kinesin-3 proteins, revealing that autoinhibition release triggers dimerization and processive movement in UNC-104 but not in KLP-6.

Diversification of the recombinant anti-kinesin monoclonal antibody H2

The paper demonstrates that recombinant H2 monoclonal antibody performs equivalently to hybridoma-derived H2 in detecting KHCs and ALS-associated aggregates.

An ALS-associated mutant KIF5A forms oligomers and aggregates and induces neuronal toxicity

This study shows that an ALS-associated KIF5A mutant forms oligomers and aggregates, leading to neuronal toxicity rather than loss of function.

Structural model of microtubule dynamics inhibition by Kinesin-4 from the crystal structure of KLP-12 - tubulin complex

The paper reports the crystal structure of KLP-12-tubulin complex, revealing how KLP-12 inhibits microtubule dynamics by altering tubulin curvature.

Extreme value analysis of intracellular cargo transport by motor proteins

The paper applies extreme-value analysis to study motor protein transport in C. elegans neurons, finding differences in distribution shape parameters between anterograde and retrograde transport.

De novo disease-associated mutations in KIF1A dominant negatively inhibit axonal transport of synaptic vesicle precursors

This study establishes C. elegans models for KIF1A-associated neuronal disorder and shows that disease mutations inhibit wild-type KIF1A function in heterodimers.

Effects of the dynein inhibitor dynarrestin on the number of motor proteins transporting synaptic cargos

The paper measures how dynarrestin affects motor protein transport by estimating force-producing units in hippocampal neurons.

Reconstitution of Kinesin-1 Activation

This study reconstitutes kinesin-1 activation in vitro, revealing that KLC-based inhibition and cargo-adaptor binding regulate motor activity, with a third non-motor MAP required for robust motility.

CAMSAP2 organizes a γ-tubulin-independent microtubule nucleation centre

The paper shows CAMSAP2 nucleates microtubules from soluble β-tubulin without γ-tubulin, reducing the nucleation barrier and forming aster-like structures.

A Highly Conserved 310-Helix Within the Kinesin Motor Domain is Critical for Kinesin Function and Human Health.

This study identifies a conserved 310-helix in KIF1A critical for motor function and human health, showing that the P305L mutation disrupts microtubule association and motor performance.

Disease-associated mutations hyperactivate KIF1A motility and anterograde axonal transport of synaptic vesicle precursors

This study shows that disease-associated KIF1A mutations hyperactivate motor activity, leading to increased anterograde axonal transport of synaptic vesicle precursors and contributing to motor neuron disease.