| 1998 |
KIF5B (kinesin heavy chain) is essential for mitochondrial and lysosomal dispersion in extraembryonic cells; kif5B-/- knockout mice show perinuclear clustering of mitochondria and impaired lysosomal dispersion, and this phenotype is reversed by exogenous KIF5B expression. Subcellular fractionation confirmed KIF5B associates with mitochondria. |
Homologous recombination knockout mouse, subcellular fractionation, rescue by exogenous expression |
Cell |
High |
9657148
|
| 2001 |
RanBP2 contains a novel kinesin-binding domain (KBD) located between RBD2 and RBD3 that directly associates with KIF5B and KIF5C (but not KIF5A) both in vitro and in vivo; kinesin light chain and RanGTPase are also part of this macroassembly complex. |
Yeast two-hybrid, in vitro binding, co-immunoprecipitation, functional domain mapping |
The Journal of biological chemistry |
High |
11553612
|
| 2003 |
KIF5B mediates insulin-stimulated long-range movement of GLUT4-containing vesicles on microtubules in adipocytes through a PI3-kinase-independent mechanism; dominant-negative kinesin light chain mutants blocked outward GLUT4 vesicle movement and GLUT4 translocation to the plasma membrane. |
Live-cell imaging (GLUT4-YFP/tubulin-CFP), dominant-negative expression, wortmannin inhibition |
The EMBO journal |
High |
12743033
|
| 2004 |
The ribosome receptor p180 binds KIF5B; the binding site is residues 1294–1413 of p180 and the C-terminal cargo-binding domain of KIF5B (residues 867–907), and the interaction is likely coiled-coil in nature; the p180 binding site on KIF5B is homologous to the kinectin-binding site. |
Yeast two-hybrid screen, domain mapping |
Biochemical and biophysical research communications |
Low |
15184079
|
| 2007 |
The kinesin-binding domain (KBD) of RanBP2 selectively interacts with KIF5B and KIF5C via a ~100-residue segment spanning a coiled-coil and globular tail cargo-binding domain; a single residue conserved in KIF5B/KIF5C but absent in KIF5A confers isoform specificity. Selective inhibition of KBD–KIF5B/KIF5C interaction causes perinuclear mitochondrial clustering, reduced mitochondrial membrane potential, and cell shrinkage. |
Domain mutagenesis, cell-based KBD inhibition, mitochondrial localization assay, membrane potential measurement |
Traffic (Copenhagen, Denmark) |
High |
17887960
|
| 2007 |
KIF5B mediates post-Golgi transport of the apical marker p75-GFP in polarized MDCK epithelial cells but not in subconfluent cells; immunoprecipitation demonstrates a polarity-dependent interaction between KIF5B and p75-GFP that is absent before polarization. Dominant-negative KIF5B or function-blocking antibodies selectively block apical (but not basolateral) transport. |
Time-lapse microscopy, dominant-negative expression, microinjection of function-blocking antibodies, co-immunoprecipitation |
Developmental cell |
High |
17925227
|
| 2007 |
KIF5B interacts with Kv1 potassium channels via the T1 domain and mediates their axonal targeting; dominant-negative Kif5B blocks axonal localization of endogenous Kv1.1, Kv1.2, and Kv1.4 in cortical neurons, and Kv1.2 co-immunoprecipitates with Kif5B from brain lysate. |
Dominant-negative expression, co-immunoprecipitation from brain lysate, co-localization in cortical neurons |
The European journal of neuroscience |
Medium |
17241275
|
| 2007 |
Kif5B and the minus-end kinesin Kifc1 interact, co-localize on early endocytic vesicles (>90% of Kifc1-positive vesicles also contain Kif5B), mediate plus- and minus-end motility respectively, and both activities are required for vesicle fission; inhibition of either motor reduces fission frequency. |
In vitro microtubule-binding/motility assay, antibody inhibition, co-immunoprecipitation after FLAG-Kifc1 expression in 293T cells |
Molecular biology of the cell |
Medium |
17360972
|
| 2008 |
KIF5B (kinesin-1) is required for bidirectional positioning of COPII-coated ER exit sites (ERES) and for ER-to-Golgi transport; knockdown of KIF5B inhibits ER-to-Golgi transport and alters the morphology of transport carriers. |
siRNA knockdown, high-resolution 2D Gaussian localization of ERES, ER-to-Golgi trafficking assay |
Traffic (Copenhagen, Denmark) |
Medium |
18817524
|
| 2009 |
RANBP2, through its kinesin-binding domain flanked by RBD2 and RBD3, activates the ATPase activity of KIF5B ~30-fold in the presence of microtubules and ATP in a minimal purified system; activation is biphasic and cooperative, and deletion of one RBD reduces activation threefold and abolishes cooperativity. RBD2-KBD-RBD3 also induces KIF5B unfolding in the absence of microtubules. |
In vitro ATPase assay with purified components, domain deletion mutagenesis |
EMBO reports |
High |
19305391
|
| 2009 |
Syntabulin acts as a KIF5B motor adaptor mediating anterograde axonal transport of presynaptic cargoes and mitochondria in sympathetic neurons; interference with syntabulin–KIF5B interaction delays synaptic activity, impairs transmission, reduces mitochondrial distribution, and these defects are rescued by ATP application. |
RNAi knockdown, dominant-negative interference with syntabulin–KIF5B interaction, electrophysiology, mitochondrial distribution assay, ATP rescue |
The Journal of neuroscience |
High |
19828815
|
| 2009 |
Kif5b is essential for anterograde (forward) trafficking of the cardiac potassium channel Kv1.5 from the Golgi to the cell surface; overexpression of Kif5b increases Kv1.5 current density in a Golgi-dependent manner (blocked by Brefeldin A), and Kif5b dominant-negative blocks surface expression of newly induced Kv1.5. |
Patch-clamp electrophysiology, dominant-negative expression, Brefeldin A treatment, tetracycline-inducible Kv1.5 system |
The Journal of physiology |
High |
19675065
|
| 2009 |
Daxx functions as a scaffold assembling a complex of GLUT4, JNK1, and KIF5B; Daxx interacts with KIF5B through the 6xTPR domain of kinesin light chain. Depletion of Daxx causes partial translocation of GLUT4 from storage compartment to endosomes. |
Co-immunoprecipitation, two-hybrid protein-protein interaction, Daxx depletion |
Journal of cellular physiology |
Medium |
18932217
|
| 2010 |
KIF5B and KIF3A/KIF3B kinesins regulate bidirectional transport of MT1-MMP-positive vesicles along microtubules in human macrophages; siRNA knockdown of KIF5B reduces delivery of MT1-MMP to the cell surface and impairs surface-associated MT1-MMP functions including CD44 shedding and extracellular matrix degradation at podosomes. |
siRNA knockdown, live-cell vesicle tracking, MT1-MMP surface exposure assay, ECM degradation assay |
Blood |
High |
20505159
|
| 2013 |
KIF5B promotes anterograde transport of Nav1.8 to the plasma membrane and axons in DRG neurons; the N terminus of Nav1.8 directly interacts with the 511–620 aa stalk domain of KIF5B (co-immunoprecipitation); KIF5B mutants defective in ATP hydrolysis or cargo binding fail to increase Nav1.8 surface expression; disrupting the KIF5B–Nav1.8 interaction abolishes KIF5B-enhanced Nav1.8 current and axonal accumulation. |
Co-immunoprecipitation, domain mutagenesis, patch-clamp, overexpression/knockdown in DRG neurons, Brefeldin A treatment |
The Journal of neuroscience |
High |
24198377
|
| 2013 |
Kif5b mediates anterograde transport of α-sarcomeric actin, non-muscle myosin IIB, desmin, and nestin to the growing tips of elongating myotubes; conditional Kif5b knockout in myogenic cells causes aggregation of these proteins and defective myofibril assembly and linkage to myotendinous junctions. A 64-amino acid α-helix domain in the tail region of Kif5b directly interacts with desmin. |
Conditional knockout (Cre-loxP), immunofluorescence, rescue by Kif5b re-expression, functional domain mapping (direct interaction with desmin) |
Development (Cambridge, England) |
High |
23293293
|
| 2013 |
KIF5B is required for axonal localization of Kv1 channels and is required for female meiosis progression; RNAi silencing of Kif5b in mouse oocytes delays germinal vesicle breakdown and causes failure of first polar body extrusion; in mitotic cells, knockdown causes centrosome amplification and chromosomal segregation defects. |
RNAi silencing in mouse oocytes and mitotic cells, live imaging of meiotic progression |
PloS one |
Medium |
23560038
|
| 2013 |
For nuclear positioning during myogenesis, both the kinesin light chain (KLC) binding domain and the autoinhibitory peptide in the globular tail of Kif5b are indispensable; the coiled-coil stalk/tail domain (containing KLC-binding sites) targets to the perinuclear region, while the globular tail domain alone cannot, and rescue of nuclear positioning in Kif5b-deficient myoblasts requires both regions. |
Domain truncation rescue experiments in Kif5b-deficient myoblasts, immunofluorescence localization |
Biochemical and biophysical research communications |
Medium |
23402760
|
| 2014 |
KIF5B directly interacts with BNIP-2 via its BCH domain at both the motor and tail domains of KIF5B; KIF5B mediates microtubule-dependent anterograde transport of BNIP-2 to endosomes in C2C12 cells. KIF5B modulates p38MAPK activity through BNIP-2 transport, promoting myogenic differentiation; disruption of anterograde transport by dominant-negative KIF5B abolishes BNIP-2's promyogenic effects. |
Co-immunoprecipitation, far-Western blot, live microscopy with organelle markers, dominant-negative KIF5B, knockdown/gain-of-function |
Molecular biology of the cell |
High |
25378581
|
| 2014 |
Palmitate causes dissociation of KIF5B from mitochondria via Ca2+-dependent effects, disrupting mitophagy; Rheb and KIF5B interact with the mitochondrial outer membrane, and their disruption blocks mitochondrial degradation and promotes NLRP3 inflammasome activation and IL-1β-dependent insulin resistance; Rheb/KIF5B overexpression attenuates these effects. |
Overexpression/knockdown, Ca2+ signaling inhibitors, mitophagy assays, ROS measurement |
Redox biology |
Medium |
25462067
|
| 2014 |
PRIP and GABARAP function in a complex to regulate KIF5B-mediated insulin secretory vesicle transport; GABARAP knockdown reduces co-localization of insulin vesicles with KIF5B and decreases insulin secretion; free GABARAP (released by PRIP silencing or interference peptide) enhances co-localization of vesicles with microtubules and promotes mobility. |
siRNA knockdown, co-immunofluorescence, density step-gradient fractionation, live-cell vesicle tracking |
Biology open |
Medium |
24812354
|
| 2016 |
KIF5B induces relocalization of the nuclear pore component Nup358 into the cytoplasm during HIV-1 infection in a capsid-dependent manner; cytoplasmic Nup358 then directly associates with viral cores. KIF5B knockdown prevents nuclear entry and infection by HIV-1 but not by N74D or P90A capsid mutants that do not rely on Nup358. |
siRNA knockdown, fluorescence microscopy of Nup358 relocalization, infection assays with capsid mutants |
PLoS pathogens |
High |
27327622
|
| 2017 |
PLD2-generated phosphatidic acid (PA) directly and specifically binds to the C-terminus of KIF5B in vitro (liposome pull-down); this PA–KIF5B interaction is required for vesicular association of KIF5B, surface localization of MT1-MMP, invadopodia formation, and invasion in breast cancer cells. |
Liposome pull-down screen, in vitro binding assay, KIF5B C-terminal domain mapping, MT1-MMP surface localization assay, invasion assay |
Developmental cell |
High |
29033361
|
| 2018 |
Kif5b directly interacts with clathrin heavy chain (CHC) and preferentially localizes to relatively large clathrin-coated vesicles (CCVs); Kif5b promotes uncoating of large CCVs in vitro (uncoating decreased in cortex CCVs from kif5b cKO mice, increased by adding Kif5b fragments containing the CHC-binding site). Kif5b depletion inhibits cellular entry of vesicular stomatitis virus via large CCV, linking anterograde transport to clathrin-mediated endocytosis. |
Co-immunoprecipitation, in vitro CCV uncoating assay with kif5b cKO cortex, dominant-negative fragment, virus entry assay |
Cell discovery |
High |
30603101
|
| 2018 |
The dynamin-related GTPase Mx1 interacts (directly or indirectly) with Kif5B and α-tubulin as assessed by co-immunoprecipitation; Mx1 aids in vesicle fission and stabilizes the interaction between Kif5B, microtubules, and apical transport carriers in MDCK cells. |
Co-immunoprecipitation, live-cell microscopy, nocodazole disruption, Mx1 knockout/mutant |
Traffic (Copenhagen, Denmark) |
Low |
30246279
|
| 2019 |
Neuronal deletion of Kif5b reduces dopamine D2 receptor in synaptic plasma membranes (subcellular fractionation) causing D2-dependent movement initiation defects and hypo-locomotion; dopamine metabolism is impaired in neuronal Kif5b-KO. Deletion of Kif5b only in dopaminergic neurons is not sufficient to produce locomotor defects. |
Conditional knockout (neuronal and dopaminergic-specific), HPLC dopamine measurement, subcellular fractionation, pharmacological receptor agonist/antagonist testing |
Journal of neurochemistry |
High |
30664247
|
| 2019 |
KIF5B is concentrated in the central spindle during cytokinesis in chondrocytes; KIF5B null chondrocytes fail cytokinesis, leading to incomplete cell rotation, disrupted proliferation and differentiation, and disorganized growth plate. |
Conditional knockout in chondrocytes, immunofluorescence of central spindle during cytokinesis, growth plate histology |
Cell & bioscience |
Medium |
31636894
|
| 2020 |
KIF5B and KIF13B jointly transport Rab6-positive secretory vesicles from the Golgi to the cell periphery; KIF5B plays the dominant role while KIF13B helps vesicles reach freshly polymerized microtubule plus ends where KIF5B binds poorly (due to slow MAP7 family protein recruitment). Sub-pixel localization showed both motors localize to the vesicle front during plus-end transport; when vesicles reverse direction, KIF5B shifts to the back while KIF13B moves to the middle, suggesting KIF5B undergoes tug-of-war with a minus-end motor. |
siRNA depletion, live-cell imaging with sub-pixel localization, TIRF microscopy, co-localization of dual motors on same vesicle |
eLife |
High |
33174839
|
| 2020 |
KIF5B conditional knockout in CaMKIIα-positive neurons causes heightened turnover and lower stability of dendritic spines, reduced PSD95 acquisition, and abolishes the preceding FMRP translocation to the proximity of newly forming spines (both basally and after fear extinction learning). |
In vivo two-photon imaging, conditional knockout (CaMKIIα-Cre), spine morphogenesis quantification, FMRP localization tracking |
Cell reports |
High |
38451812
|
| 2020 |
KIF5B conditional knockout in hippocampal neurons causes deficits in dendritic spine morphogenesis, synaptic plasticity, and memory formation; these functional specificities relative to KIF5A are determined by their divergent carboxyl-termini, where arginine methylation of KIF5B regulates its function. |
Conditional knockout mouse, dendritic transport assays, electrophysiology (LTP), behavioral memory tests, domain-swap and arginine methylation experiments |
eLife |
High |
31961321
|
| 2020 |
L-dopa incorporated post-translationally into the C-terminus of α-tubulin reduces KIF5B binding affinity for microtubules; in L-dopa-treated neuronal cells, mitochondrial anterograde transport velocity is reduced, mitochondria spend more time paused, and fewer reach the distal axon segment. |
Biochemical binding assay (KIF5B affinity for dopa-tubulin microtubules), live-cell mitochondrial transport imaging in neuronal cell lines and primary hippocampal neurons |
Neurobiology of disease |
Medium |
33171229
|
| 2022 |
De novo heterozygous KIF5B variants at conserved amino acids in the ATPase activity-related motifs of the motor domain cause kyphomelic dysplasia in humans, establishing that KIF5B motor domain function is required for normal skeletal development. |
Whole-exome sequencing, de novo variant identification in four individuals, structural mapping to catalytic motifs |
Clinical genetics |
Medium |
35342932
|
| 2023 |
Dominant-negative KIF5B variants (p.Asn255del, p.Leu498Pro, p.Leu537Pro) disrupt lysosomal, autophagosome, and mitochondrial organization, and impact cilium biogenesis in vitro; all variants affect multiple developmental processes in zebrafish. One previously reported variant also showed these effects. |
In vitro cell microscopy (lysosomal/autophagosome/mitochondrial distribution), cilium biogenesis assay, zebrafish developmental analysis |
Human molecular genetics |
Medium |
36018820
|
| 2023 |
Dominant-negative KIF5B variants (modeled in C. elegans unc-116 Thr90Ile by CRISPR) cause defective mitochondria transport in neurons (time-lapse GFP-mitochondria imaging), abnormal body length and motility suppressed by extra wild-type allele; in human cells, the corresponding p.Thr87Ile variant causes dilated ER, intracellular vacuoles, Golgi maldistribution, and down-regulation of mTOR signaling (RNA-seq, proteomics, bone IHC); leucine supplementation partially rescues mTOR pathway in patient cells. |
CRISPR/Cas9 modeling in C. elegans, time-lapse GFP-mitochondria imaging, dominant negative suppression genetics, RNA-seq, proteomics, leucine rescue |
PLoS genetics |
High |
37934770
|
| 2025 |
KIF5B actively slides existing microtubules to the β-cell periphery in a glucose-stimulated manner, aligning the sub-membrane microtubule array in pancreatic β cells; this microtubule sliding is part of glucose-triggered microtubule remodeling that regulates insulin secretory granule positioning. |
Real-time live imaging, photokinetics (FRAP-like approaches), KIF5B manipulation in MIN6 cells and intact mouse islets |
eLife |
High |
41182903
|
| 2025 |
Cohesin-associated protein Pds5A recruits the deubiquitinase USP14 to the spindle apparatus, which stabilizes KIF5B by deubiquitination, regulating meiotic spindle elongation and chromosome segregation in mouse oocytes. |
Morpholino depletion, genetic ablation of Pds5A, spindle organization imaging, USP14 interaction assay, KIF5B ubiquitination/stability analysis |
Science advances |
Medium |
40215310
|