<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kita T</submitter><funding>Division for Interdisciplinary Advanced Research and Education, Tohoku University</funding><funding>Tohoku University</funding><funding>Japan Society for the Promotion of Science</funding><pagination>4348-4359</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10698283</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>122(22)</volume><pubmed_abstract>KIF1A is a member of the kinesin-3 motor protein family that transports synaptic vesicle precursors in axons. Mutations in the Kif1a gene cause neuronal diseases. Most patients are heterozygous and have both mutated and intact KIF1A alleles, suggesting that heterodimers composed of wild-type KIF1A and mutant KIF1A are likely involved in pathogenesis. In this study, we propose mathematical models to describe the motility of KIF1A heterodimers composed of wild-type KIF1A and mutant KIF1A. Our models precisely describe run length, run time, and velocity of KIF1A heterodimers using a few parameters obtained from two homodimers. The first model is a simple hand-over-hand model in which stepping and detachment rates from a microtubule of each head are identical to those in the respective homodim</pubmed_abstract><journal>Biophysical journal</journal><pubmed_title>Modeling the motion of disease-associated KIF1A heterodimers.</pubmed_title><pmcid>PMC10698283</pmcid><funding_grant_id>22H05523</funding_grant_id><funding_grant_id>23H02472</funding_grant_id><pubmed_authors>Sasaki K</pubmed_authors><pubmed_authors>Niwa S</pubmed_authors><pubmed_authors>Kita T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Modeling the motion of disease-associated KIF1A heterodimers.</name><description>KIF1A is a member of the kinesin-3 motor protein family that transports synaptic vesicle precursors in axons. Mutations in the Kif1a gene cause neuronal diseases. Most patients are heterozygous and have both mutated and intact KIF1A alleles, suggesting that heterodimers composed of wild-type KIF1A and mutant KIF1A are likely involved in pathogenesis. In this study, we propose mathematical models to describe the motility of KIF1A heterodimers composed of wild-type KIF1A and mutant KIF1A. Our models precisely describe run length, run time, and velocity of KIF1A heterodimers using a few parameters obtained from two homodimers. The first model is a simple hand-over-hand model in which stepping and detachment rates from a microtubule of each head are identical to those in the respective homodim</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Nov</publication><modification>2025-04-04T20:38:39.291Z</modification><creation>2025-04-04T20:38:39.291Z</creation></dates><accession>S-EPMC10698283</accession><cross_references><pubmed>37853694</pubmed><doi>10.1016/j.bpj.2023.10.014</doi></cross_references></HashMap>