| 2000 |
GAKIN (KIF13B) binds directly to the guanylate kinase-like (GUK) domain of hDlg (DLG1) and PSD-95, but not p55, among MAGUK family proteins. The interaction was identified by affinity protein purification and peptide sequencing. KIF13B contains a motor domain at the NH2 terminus, a central stalk domain, and a CAP-Gly domain at the COOH terminus. In resting T lymphocytes both proteins are cytoplasmic; upon CD2 receptor cross-linking, hDlg translocates to the lymphocyte cap. |
Affinity protein purification, peptide sequencing, cDNA cloning, GST pulldown, immunolocalization |
The Journal of biological chemistry |
Medium |
10859302
|
| 2005 |
KIF13B directly interacts with centaurin-alpha1 (an ARF6 GAP and PIP3-binding protein); the interaction is mediated by the GAP domain of centaurin-alpha1 and the stalk domain of KIF13B. KIF13B binding suppresses the ARF6 GAP activity of centaurin-alpha1 in intact cells, and both proteins colocalize at cell-periphery leading edges; a deletion mutant of centaurin-alpha1 lacking the KIF13B-binding site fails to colocalize. |
Yeast two-hybrid, GST pulldown, co-immunoprecipitation, ARF6 GAP activity assay, immunofluorescence |
Journal of cell science |
Medium |
15923660
|
| 2006 |
KIF13B (GAKIN) directly interacts with PIP3BP (a PIP3-interacting protein) and, together with PIP3BP, assembles onto PIP3-containing liposomes and drives their motility along microtubules in vitro. In PC12 cells and hippocampal neurons, KIF13B transport activity promotes PIP3 accumulation at neurite tips; overexpression of KIF13B constructs that alter PIP3 distribution causes loss of axonally differentiated neurites, indicating KIF13B-PIP3BP complex is required for neuronal polarity formation. |
In vitro liposome motility assay, co-immunoprecipitation, overexpression/dominant-negative in PC12 cells and hippocampal neurons, immunofluorescence |
The Journal of cell biology |
High |
16864656
|
| 2007 |
KIF13B (GAKIN) exists in an autoinhibited conformation in solution—it shows potent microtubule gliding activity but minimal microtubule-stimulated ATPase activity. Intramolecular interaction between the MAGUK binding stalk (MBS) domain and the motor domain confers this globular autoinhibited state. Direct binding of the SH3-I3-GUK module of hDlg to the MBS domain of KIF13B activates microtubule-stimulated ATPase activity ~10-fold, demonstrating cargo-mediated relief of autoinhibition. |
Microtubule gliding assay, ATPase assay, in vitro binding (pull-down), domain-deletion analysis |
Biochemistry |
High |
17696365
|
| 2010 |
Par1b/MARK2 phosphorylates KIF13B and is identified as a KIF13B-binding protein. KIF13B accumulates at the distal microtubule tips in axons but not dendrites. Overexpression of KIF13B induces extra axon formation; co-expression of Par1b kinase suppresses this in a kinase-activity-dependent manner. KIF13B siRNA knockdown retards neurite extension and causes an axonless phenotype. The extra-axon phenotype of Par1b siRNA is rescued by KIF13B siRNA, placing KIF13B downstream of Par1b. KIF13B also acts downstream of PI3K signaling via Par1b phosphorylation. |
Co-immunoprecipitation, kinase assay, siRNA knockdown, overexpression, epistasis in hippocampal neurons |
Molecular and cellular biology |
High |
20194617
|
| 2010 |
KIF13B (GAKIN) negatively regulates TCR signaling to NF-κB by associating with the scaffold protein CARD11 in a signal-dependent manner and competing with Bcl10 for CARD11 binding. KIF13B dynamically localizes to the immunological synapse and regulates redistribution of CARD11 from the central synapse region to a distal region. |
Expression-cloning screen, co-immunoprecipitation, NF-κB reporter assay, immunofluorescence live-cell imaging at immunological synapse |
Molecular cell |
Medium |
21145487
|
| 2010 |
Xenopus KIF13B (xKIF13B) is required for primordial germ cell (PGC) migration; knockdown inhibits bleb formation and PIP3 accumulation at PGC blebs, causing PGC mismigration in vivo and in vitro. Interference with PIP3 synthesis similarly causes PGC mismigration, linking KIF13B function to polarized PIP3 accumulation for directional cell migration. |
Morpholino knockdown in Xenopus embryos, PIP3 imaging, PGC migration assay in vivo and explant |
Developmental biology |
Medium |
21029731
|
| 2012 |
KIF13B transports TRPV1-containing vesicles to the cell surface via its FHA domain. Cdk5 phosphorylates KIF13B at Thr-506 within the FHA domain to promote motor-cargo association; T506A mutation reduces KIF13B-TRPV1 interaction. Cdk5/p35 overexpression promotes and Cdk5 inhibition prevents KIF13B-TRPV1 association. CFA-induced Cdk5 activation increases TRPV1 anterograde transport, contributing to heat hyperalgesia; a cell-permeable TAT-T506 peptide decreases TRPV1 surface localization and alleviates CFA-induced heat hyperalgesia. |
Co-immunoprecipitation, kinase assay (Cdk5 phosphorylation of KIF13B), site-directed mutagenesis (T506A), surface biotinylation, TAT peptide delivery in vivo, behavioral pain assays |
The Journal of neuroscience |
High |
23077056
|
| 2014 |
KIF13B enhances caveolin-dependent endocytosis of LRP1 by acting as a scaffold that recruits LRP1 to caveolae via an LRP1–hDLG1–KIF13B–utrophin–caveolae linkage. KIF13B KO mice show elevated serum cholesterol and factor VIII; KO MEFs show decreased LDL uptake. Exogenous KIF13B localizes on the plasma membrane with caveolae and translocates to cytoplasmic vesicles with LRP1 and caveolin-1. |
KIF13B knockout mice, co-immunoprecipitation, serum/endocytosis assays in MEFs, live-cell imaging/trafficking |
The Journal of cell biology |
High |
24469637
|
| 2014 |
KIF13B directly interacts with VEGFR2 and mediates its transport from the Golgi to the endothelial cell surface. KIF13B depletion diverts VEGFR2 to lysosomal degradation, prevents VEGF-induced endothelial migration and capillary tube formation, and blocks neovascularization in mice. |
Co-immunoprecipitation, KIF13B knockdown, truncation/dominant-negative overexpression, in vitro tube formation assay, in vivo Matrigel plug/neovascularization assay |
Journal of cell science |
High |
25128562
|
| 2016 |
KIF13B regulates PNS and CNS myelination through the DLG1 scaffold. In Schwann cells, KIF13B promotes myelination by driving p38γ MAPK-mediated phosphorylation and ubiquitination of DLG1, which downregulates PI3K/AKT signaling (DLG1 is a brake on myelination). In oligodendrocytes, KIF13B negatively regulates myelination by destabilizing DLG1, which in that context enhances AKT activation. |
Kif13b conditional knockout mice, co-immunoprecipitation, phosphorylation/ubiquitination assays, myelin analysis in PNS/CNS |
PLoS biology |
High |
27070899
|
| 2016 |
The crystal structure of DLG4 GK domain in complex with the KIF13B MBS (MAGUK binding stalk) domain reveals an atypical MAGUK GK target recognition mode in which the GK domain binds an unphosphorylated, autonomously folded domain (MBS) rather than a phosphopeptide. This structural insight explains the molecular basis of DLG/KIF13B complex formation and autoinhibition relief. |
X-ray crystallography, in vitro binding measurements, mutagenesis |
Structure |
High |
27642159
|
| 2017 |
KIF13B is a novel member of the RPGRIP1N-C2 domain family and is recruited to the ciliary base by NPHP4, which binds two distinct sites in the KIF13B tail including an RPGRIP1N-C2 domain. KIF13B and NPHP4 are both required for establishing a CAV1-enriched membrane microdomain at the transition zone, which is necessary for Shh-induced ciliary SMO accumulation. |
Co-immunoprecipitation, domain mapping, siRNA knockdown, immunofluorescence, SMO accumulation assay, ciliogenesis analysis |
Nature communications |
High |
28134340
|
| 2018 |
Drosophila KIF13B ortholog Khc-73 (a plus-end kinesin) regulates sorting of endosomes in larval motor neurons. Loss of Khc-73 impairs retrograde BMP signaling: activated BMP transcription factor Mad nuclear accumulation is reduced, and retrograde-bound endosomes fail to leave the synapse and join the retrograde axonal pathway. Genetic enhancement/suppression with BMP pathway components places Khc-73 in the BMP retrograde signaling pathway. |
Drosophila genetics (mutant analysis, epistasis), live imaging of endosomes in motor neurons, pMad immunostaining, electrophysiology |
PLoS genetics |
Medium |
29373576
|
| 2019 |
Rab10 interacts with KIF13B (and KIF13A) and is required for tubular endosome formation; Rab10 knockout abolishes tubular endosomal structures in HeLaM cells. KIF13B was identified as a Rab10-interacting protein by in silico screening and validated experimentally, and both the Rab10-binding homology domain and the motor domain of KIF13A are required for Rab10-positive tubular endosome formation. |
Rab GTPase localization screen, Rab10 knockout (CRISPR), co-immunoprecipitation, domain-deletion analysis, fluorescence microscopy |
Journal of cell science |
Medium |
30700496
|
| 2019 |
The cytoplasmic domain of LRP1 interacts specifically with the alternatively spliced I3 domain of DLG1, which in turn complexes with KIF13B via GUK-MBS domain interaction. The CAP-Gly domain of KIF13B is required for proper subcellular localization of KIF13B and LRP1; mice expressing KIF13B lacking the CAP-Gly domain (KIF13BΔCG) show higher serum cholesterol and reduced LDL uptake. KIF13A null mice show no such cholesterol or factor VIII elevation. |
Mouse knockout/truncation models, co-immunoprecipitation, domain-binding assays, serum/endocytosis assays, immunolocalization |
Biochimica et biophysica acta. Molecular cell research |
High |
31487503
|
| 2020 |
KIF13B and KIF5B cooperate to transport Rab6-positive secretory vesicles from the Golgi to the cell periphery. KIF13B assists Rab6 vesicles in reaching freshly polymerized microtubule plus ends (where KIF5B binds poorly due to slow MAP7 population). Sub-pixel localization showed both kinesins localize to the vesicle front during plus-end directed transport; upon reversal, KIF13B relocates to the middle while KIF5B shifts to the back, suggesting KIF5B (not KIF13B) undergoes tug-of-war with minus-end motors. |
siRNA knockdown, live-cell imaging (TIRF), sub-pixel localization microscopy, kymograph analysis |
eLife |
High |
33174839
|
| 2020 |
Netrin-1 induces KIF13B interaction with Myosin X (Myo X); KIF13B mediates anterograde transport of Myo X into axons, which is required for Netrin-1-DCC-regulated axon initiation and contralateral branching in developing mouse neocortex. KIF13B KD results in axon initiation deficits similar to those seen with Myo X KO/KD and Netrin-1 KO. |
Proteomic analysis of Myo X binding proteins, co-immunoprecipitation, KIF13B knockdown in embryonic cortical neurons, axon morphology analysis in vivo |
The Journal of neuroscience |
Medium |
33097641
|
| 2021 |
EC-specific KIF13B knockout mice demonstrate that endothelial KIF13B is required for VEGF-A-induced vascular leakage, angiogenesis, tumor growth, and cancer metastasis in vivo, confirming KIF13B-mediated VEGFR2 trafficking to the endothelial surface as an essential step in pathological VEGF-A signaling. |
Endothelial cell-specific Kif13b conditional knockout mice, VEGF-A vascular leakage assays, tumor growth/metastasis models |
Life science alliance |
High |
34670814
|
| 2022 |
KIF13B undergoes bursts of bidirectional motor-driven movement within primary cilia of human RPE1 cells, with anterograde and retrograde velocities similar to IFT. Intraciliary movement requires KIF13B's own motor domain and appears cell-type specific, representing the first demonstration of intraciliary motor-driven movement by a vertebrate kinesin-3. |
Live-cell imaging (TIRF/fluorescence), KIF13B-eGFP constructs including motor-domain mutants, velocity analysis compared to IFT172-eGFP |
Journal of cell science |
Medium |
35403186
|
| 2022 |
Angiomotin isoform 2 (Ap80) is a novel KIF13B interactor that promotes binding of the MAGUK PALS1 to KIF13B. Ap80 concentrates at the ciliary base and recruits PALS1 there. Ap80 depletion leads to elongated primary cilia and reduced SMO ciliary accumulation; Ap80 overexpression causes ciliary shortening, indicating Ap80 activates KIF13B cargo binding at the ciliary base to regulate ciliary length and Hedgehog signaling. |
Co-immunoprecipitation, siRNA knockdown, overexpression, live-cell imaging, ciliary SMO accumulation assay |
Journal of cell science |
Medium |
35673984
|
| 2023 |
KIF13B mediates recycling of internalized VEGFR2 through Rab11-positive recycling vesicles back to the cell surface. After VEGF stimulation, phosphorylated VEGFR2 at cell-cell junctions is internalized into Rab5-positive early endosomes where it associates with KIF13B. Inhibition of KIF13B attenuates phosphorylation of VEGFR2-Y951, SRC-Y416, and VE-cadherin-Y685 and diverts VEGFR2 to lysosomal degradation. |
Co-immunoprecipitation, Rab5/Rab11 vesicle trafficking assays, phospho-specific immunoblotting, KIF13B inhibition (dominant-negative/peptide), live-cell trafficking imaging |
Cellular and molecular life sciences |
Medium |
36928770
|
| 2024 |
KIF13B is recruited to polarized vesicles at the trans-Golgi network through interaction with the heterotetrameric adaptor protein complex AP-1. In hippocampal neurons, KIF13B mediates both dendrite- and axon-selective transport; interference with KIF13B binding to AP-1 disrupts both transport modes. |
Live-cell imaging in hippocampal neurons, AP-1 binding domain interference (dominant-negative), KIF13B-fluorescent fusions, kymograph analysis |
Molecular biology of the cell |
Medium |
38446634
|
| 2025 |
KIF13B interacts with AMPKα1 and regulates its phosphorylation, governing mitochondrial homeostasis and suppressing SREBP1-mediated de novo lipogenesis in the liver. Kif13b deficiency increases hepatic lipid synthesis and impairs mitochondrial oxidative phosphorylation; liver-specific Kif13b knockout causes spontaneous hepatic steatosis. |
Co-immunoprecipitation, Kif13b whole-body and liver-specific knockout mice, phosphorylation assays, lipid synthesis assays, mitochondrial function assays |
Military Medical Research |
Medium |
40038775
|
| 2025 |
In macrophages, KIF13B maintains MERTK expression by enhancing its deubiquitination through interaction with the deubiquitinase USP9X; loss of KIF13B decreases ITCH expression and leads to accelerated CBL-mediated ubiquitination and degradation of MERTK, impairing macrophage efferocytosis and promoting atherosclerosis. |
Co-immunoprecipitation (KIF13B-USP9X), Kif13b macrophage-specific knockout mice, MERTK ubiquitination assays, bone marrow transplantation, efferocytosis assays |
European heart journal |
Medium |
40709729
|
| 2025 |
KIF13B regulates ciliary protein composition and extracellular vesicle (EV) shedding from cilia. KIF13B knockout causes aberrant accumulation of polycystin-2 (PC2) within cilia, increased release of large EVs enriched with CCDC198 and CCDC92, and altered small EV composition. KIF13B acts at centriole distal appendages to limit ciliary protein entry and promote endocytic retrieval downstream of the BBSome, suppressing EV release from cilia. |
Kif13b knockout cells, super-resolution microscopy, EV characterization (proteomics), live imaging, PC2 and BBSome localization analysis |
Current biology |
Medium |
40930094
|
| 2025 |
In vascular smooth muscle cells (VSMCs), KIF13B facilitates ubiquitination and proteasomal degradation of KLF4 through a KCTD10-dependent pathway. VSMC-specific Kif13b deletion exacerbates atherosclerotic lesion development and impairs plaque stability; adverse effects were rescued by the KLF4 inhibitor Kenpaullone. |
VSMC-specific Kif13b KO mice (PCSK9 AAV model), Co-immunoprecipitation (KIF13B-KCTD10), KLF4 ubiquitination/degradation assays, pharmacological rescue |
The Journal of clinical investigation |
Medium |
41609725
|
| 2025 |
KIF13B stabilizes PLIN5 by preventing its lysosomal degradation; loss of KIF13B impairs mitochondrial localization of PLIN5, disrupting cardiac lipid homeostasis and mitochondrial function in sepsis-induced cardiac dysfunction. AAV9-PLIN5 gene therapy rescues cardiac dysfunction in Kif13b KO mice. |
Kif13b global KO mice, cardiomyocyte PLIN5 localization assays, lysosomal degradation assays, AAV9-PLIN5 rescue, cardiac function measurements |
Research (Washington, D.C.) |
Medium |
41531892
|
| 2025 |
KIF13B is enriched at photoreceptor synaptic ribbons in addition to the primary photoreceptor cilium. This synaptic localization requires intact synaptic ribbon structure, as shown by loss of KIF13B enrichment at ribbons in RIBEYE knockout mice. |
Confocal microscopy, super-resolution SIM, immunogold electron microscopy, RIBEYE KO mice |
International journal of molecular sciences |
Medium |
40649824
|
| 2026 |
In macrophages, KIF13B loss impairs proteasome-dependent degradation of the glycosyltransferase STT3A, enhancing cathepsin D (CTSD) glycosylation and secretion, which promotes lipid accumulation and inflammatory responses in liver cells via CTSD interaction with hepatocyte THBS1. Transcription factor ZNF384 is identified as an upstream regulator that binds the KIF13B promoter to activate its transcription. |
Myeloid-specific Kif13b KO mice, STT3A proteasome degradation assay, CTSD glycosylation/secretion assay, Co-IP (CTSD-THBS1), ZNF384 ChIP/promoter binding assay |
Hepatology |
Medium |
41746601
|