Affinage

KIF1C

Kinesin-like protein KIF1C · UniProt O43896

Length
1103 aa
Mass
122.9 kDa
Annotated
2026-06-10
34 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: tie faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KIF1C is a plus-end-directed kinesin-3 motor that transports diverse membranous and ribonucleoprotein cargoes along microtubules and additionally scaffolds dynein-driven transport in both motor-dependent and non-motor capacities (PMID:31217419, PMID:31320392). The motor is held inactive by an intramolecular interaction between its microtubule-binding motor domain and stalk; this autoinhibition is relieved when the FERM domain of PTPN21 or the cargo adaptor Hook3 binds the KIF1C tail, increasing its landing rate on microtubules and converting it into a processive motor (PMID:31217419). Activation is further tuned by phosphorylation: casein kinase II phosphorylation of Ser1092 generates a 14-3-3 binding site (PMID:10559254), and c-Src-mediated tyrosine phosphorylation of the stalk enhances PTPD1 association to relieve autoinhibition (PMID:35654143), while Rab6A binding to the motor domain inhibits microtubule engagement (PMID:25821985). Once active, KIF1C delivers Rab6A-positive secretory vesicles to the cell surface and protects Golgi integrity (PMID:25821985), traffics α5β1-integrins to trailing focal adhesions to stabilize the cell rear during directional migration (PMID:23237952), and supports podosome and invadopodia dynamics in macrophages and cancer cells (PMID:16554367, PMID:35654143). KIF1C is also an mRNA transport motor: it carries APC-dependent and EJC-bound transcripts to cytoplasmic protrusions, with cargo specificity conferred by the RNA-binding adaptor CNBP recognizing GA-rich 3'UTR sequences (PMID:34493599, PMID:36316088, PMID:39982819). Its C-terminal intrinsically disordered region drives liquid-liquid phase separation that sequence-selectively clusters mRNA at the periphery (PMID:38898313). Beyond carrying cargo itself, KIF1C bridges dynein/dynactin via Hook3 to enable bidirectional transport (PMID:31320392), and in a non-motor mode activates dynein-driven retrograde lysosomal transport through a Hook3–RUFY3 link required for autophagic and endocytic degradation (PMID:39394274). The structural basis of the Hook3–KIF1C interaction has been resolved, defining an interface necessary for Hook3-activated anterograde transport (PMID:40312563).

Mechanistic history

Synthesis pass · year-by-year structured walk · 20 steps
  1. 1998 Medium

    Established KIF1C as a kinesin-like protein and proposed a first cellular role, framing it as a Golgi-associated motor potentially driving Golgi-to-ER retrograde transport.

    Evidence Yeast two-hybrid with PTPD1 ezrin domain, immunofluorescence localization, and dominant-negative overexpression with brefeldin A in cultured cells

    PMID:9685376

    Open questions at the time
    • Dominant-negative phenotype not confirmed by loss-of-function genetics
    • Direct motor activity not demonstrated
    • Cargo identity unresolved
  2. 1999 High

    Identified phosphoregulation of KIF1C, showing CK2 phosphorylation of Ser1092 creates a 14-3-3 docking site, the first regulatory input on the motor.

    Evidence In vitro CK2 kinase assay, co-IP of 14-3-3 isoforms, and CK2 inhibition in cells

    PMID:10559254

    Open questions at the time
    • Functional consequence of 14-3-3 binding for transport not defined
    • Connection to cargo selection unknown
  3. 2002 Medium

    Linked KIF1C function and localization to a physiological output, anthrax lethal toxin susceptibility in macrophages, acting at a post-entry step.

    Evidence Genetic mapping, allele-specific overexpression rescue, brefeldin A perturbation, and MKK3 cleavage assays

    PMID:11591317

    Open questions at the time
    • Molecular mechanism downstream of KIF1C not defined
    • Relevance to human cells unclear
  4. 2002 High

    Overturned the proposed Golgi-to-ER retrograde role by showing KIF1C knockout mice are viable with normal retrograde transport, redirecting the field toward other functions.

    Evidence Gene knockout with beta-gal knock-in and time-lapse BFA-induced transport analysis in primary fibroblasts

    PMID:11784862

    Open questions at the time
    • Did not identify the true physiological cargo or function
    • Possible redundancy with other motors not tested
  5. 2006 High

    Repositioned KIF1C as a plus-end-enriched motor at podosomes that physically bridges actin and microtubule cytoskeletons via non-muscle myosin IIA.

    Evidence siRNA/shRNA knockdown, dominant-negative constructs, co-IP, and live imaging in primary human macrophages

    PMID:16554367

    Open questions at the time
    • Cargo transported to podosomes not identified
    • Directness of myosin IIA interaction at structural level not resolved
  6. 2012 High

    Defined a concrete cargo and migration function: KIF1C transports α5β1-integrins to the trailing edge to stabilize the rear during directional cell migration.

    Evidence siRNA depletion, integrin trafficking and migration assays, and myosin II inhibition epistasis

    PMID:23237952

    Open questions at the time
    • Adaptor coupling KIF1C to integrin cargo not defined
    • Mechanism of rear-specific targeting unclear
  7. 2014 High

    Revealed Rab6A as a dual regulator/cargo factor whose binding to the motor domain inhibits microtubule interaction, while KIF1C is required for surface delivery and Golgi integrity.

    Evidence In vitro microtubule binding assays, co-IP, siRNA depletion, live vesicle imaging, and domain-deletion rescue in eLife study

    PMID:25821985

    Open questions at the time
    • How Rab6A inhibition is relieved in vivo not defined
    • Motor-independent Golgi protection mechanism unresolved
  8. 2014 Medium

    Showed KIF1C peripheral targeting depends on CLASP proteins and on microtubule acetylation, identifying track-selection inputs governing where KIF1C operates.

    Evidence CLASP siRNA, chimeric mitochondrial CLASP2 recruitment, MEC-17 perturbation, tubacin treatment, and live imaging in macrophages

    PMID:25151635 PMID:25344256

    Open questions at the time
    • Molecular nature of CLASP–KIF1C contact not mapped
    • Whether acetylation acts on motor or track recruitment unresolved
  9. 2019 High

    Established the core activation mechanism: full-length KIF1C is autoinhibited via a motor–stalk interaction that is released by PTPN21 FERM or Hook3 binding to the tail, converting it to a processive motor.

    Evidence Single-molecule motility with purified full-length KIF1C, domain-binding assays, neuronal DCV transport, and integrin trafficking rescue

    PMID:31217419

    Open questions at the time
    • Structural detail of the autoinhibited conformation not resolved
    • How phosphorylation integrates with adaptor-mediated release unclear
  10. 2019 High

    Demonstrated Hook3 scaffolds bidirectional transport, simultaneously binding dynein/dynactin and the KIF1C tail to couple opposing motors.

    Evidence In vitro reconstitution with purified dynein/dynactin, Hook3 and KIF1C, single-molecule motility, mass spectrometry, co-IP and live imaging

    PMID:31320392

    Open questions at the time
    • How directionality of the trimeric complex is biased in cells not defined
    • Cargo carried by the bidirectional complex not identified
  11. 2019 Medium

    Placed Kif1c in an osteoclast signaling pathway between p130Cas and c-Src controlling actin ring formation and bone resorption.

    Evidence shRNA knockdown, overexpression rescue in p130Cas and c-Src knockout backgrounds, and bone resorption assays

    PMID:31887784

    Open questions at the time
    • Molecular target of KIF1C in this pathway not defined
    • Whether motor activity is required not tested
  12. 2021 High

    Identified KIF1C as a direct mRNA transport motor carrying APC-dependent transcripts and its own mRNA to protrusions, with 3'UTR sufficiency for transport.

    Evidence Two-color single-molecule live imaging, siRNA depletion, mRNA localization and 3'UTR sufficiency assays

    PMID:34493599

    Open questions at the time
    • RNA-binding adaptor not yet identified in this study
    • Selectivity for specific transcripts unexplained
  13. 2022 Medium

    Extended the mRNA cargo model by showing RNA-dependent association of KIF1C with the exon junction complex during neurite transport.

    Evidence AP-MS in SH-SY5Y cells, co-IP with RNase sensitivity, and mutant KIF1C mislocalization imaging

    PMID:36316088

    Open questions at the time
    • Direct versus RNA-bridged EJC contact not distinguished
    • Functional consequence of EJC mislocalization for translation not assessed
  14. 2022 Medium

    Connected c-Src tyrosine phosphorylation of the stalk to PTPD1 recruitment and autoinhibition relief, linking the motor to invadopodia-driven cancer invasion.

    Evidence c-Src perturbation, phospho-mutant constructs, co-IP, microtubule-binding and invadopodia/invasion assays

    PMID:35654143

    Open questions at the time
    • Specific phosphorylated tyrosines and structural effect not mapped
    • Quantitative contribution relative to adaptor activation unknown
  15. 2023 Medium

    Showed that localization of Kif1c mRNA itself, rather than protein abundance, dictates the identity and number of KIF1C protein interactions and supports directed migration.

    Evidence mRNA mislocalization genetic perturbation, mass spectrometry of endogenous interactors, and migration assays

    PMID:36859340

    Open questions at the time
    • Mechanism coupling local translation to interaction specificity unresolved
    • Which mislocalized interactions are functionally decisive not defined
  16. 2024 High

    Demonstrated that the KIF1C C-terminal IDR drives liquid-liquid phase separation that sequence-selectively recruits and clusters mRNA at the periphery.

    Evidence In vitro LLPS with purified tail at near-endogenous concentrations, FRAP, IDR-deletion mutants, and RNA recruitment assays

    PMID:38898313

    Open questions at the time
    • How LLPS is spatially restricted to protrusions unclear
    • Relationship between condensate state and motility not fully defined
  17. 2024 Medium

    Uncovered a non-motor role in which KIF1C activates dynein-driven retrograde lysosomal transport via a Hook3–RUFY3 axis required for cargo degradation.

    Evidence KIF1C depletion, motor-dead mutant, co-IP of KIF1C–Hook3–RUFY3, lysosome positioning and degradation assays

    PMID:39394274

    Open questions at the time
    • How the same Hook3 scaffold switches between anterograde and retrograde modes not resolved
    • Stoichiometry of the KIF1C–Hook3–RUFY3 complex unknown
  18. 2025 Medium

    Defined the molecular CNBP–KIF1C motor-adaptor that couples GA-rich 3'UTR recognition to active mRNA transport, supplying the missing RNA-binding link.

    Evidence RNA pulldown, co-IP, siRNA depletion, and live-cell mRNA transport and 3'UTR binding assays

    PMID:39982819

    Open questions at the time
    • Whether CNBP acts within KIF1C condensates not tested
    • Generality across all protrusion mRNAs unresolved
  19. 2025 High

    Resolved the structural basis of Hook3-activated transport, defining the Hook3–KIF1C interface necessary and sufficient for anterograde motility.

    Evidence Crystal structure of Hook3(553–624)–KIF1C(714–809), structure-based mutagenesis, co-IP and anterograde transport assays

    PMID:40312563

    Open questions at the time
    • Structure of the autoinhibited full-length motor still lacking
    • How adaptor binding mechanically relieves autoinhibition not visualized
  20. 2025 Medium

    Proposed that KIF1C LLPS-driven multi-kinesin clusters generate mechanical force that fragments microtubules, implying an active role in cytoskeletal remodeling.

    Evidence Live-cell microtubule breakage imaging, computational simulation, IDR/motor mutants, and in vitro LLPS (preprint)

    PMID:bio_10.1101_2025.01.31.635950

    Open questions at the time
    • Not yet peer-reviewed
    • Physiological role of microtubule breakage unconfirmed
    • Whether this occurs at endogenous expression levels unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how the multiple activating inputs (phosphorylation, adaptor binding, Rab6A inhibition, mRNA localization) are integrated to select cargo, direction, and condensate state at specific subcellular sites.
  • No unified model coupling autoinhibition release to specific cargo classes
  • Structure of the full autoinhibited motor unknown
  • Switch between anterograde motor and non-motor dynein-activating modes undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003723 RNA binding 3 GO:0003774 cytoskeletal motor activity 3 GO:0008092 cytoskeletal protein binding 2 GO:0060090 molecular adaptor activity 2 GO:0098772 molecular function regulator activity 2 GO:0140657 ATP-dependent activity 1
Localization
GO:0005856 cytoskeleton 3 GO:0005794 Golgi apparatus 2 GO:0005829 cytosol 2 GO:0005764 lysosome 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 3 R-HSA-9609507 Protein localization 3 R-HSA-1474244 Extracellular matrix organization 1 R-HSA-9612973 Autophagy 1
Partners
14-3-3CLASP2CNBPHOOK3PTPD1PTPN21RAB6ARUFY3
Complex memberships
KIF1C–CNBP mRNA motor-adaptor complexKIF1C–Hook3–RUFY3 complexKIF1C–Hook3–dynein/dynactin complex

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 KIF1C was identified as a new kinesin-like protein (Unc104 subfamily) localized primarily at the Golgi apparatus; overexpression of catalytically inactive KIF1C inhibited brefeldin A-induced retrograde flow of Golgi membranes into the ER, implicating KIF1C in Golgi-to-ER vesicle transport. KIF1C was identified via yeast two-hybrid using the ezrin domain of PTPD1 as bait, and was found to be tyrosine-phosphorylated after peroxovanadate stimulation. Yeast two-hybrid, immunofluorescence, dominant-negative overexpression in 293/NIH3T3/C2C12 cells, brefeldin A treatment The Journal of biological chemistry Medium 9685376
1999 KIF1C dimerizes and associates with 14-3-3 proteins (beta, gamma, epsilon, zeta) via phosphorylation of Ser1092 (in a canonical 14-3-3 binding sequence). Ser1092 is a substrate for casein kinase II in vitro; inhibition of casein kinase II in cells reduced KIF1C–14-3-3γ association. Yeast two-hybrid, transient overexpression, co-immunoprecipitation, in vitro kinase assay, casein kinase II inhibition The Journal of biological chemistry High 10559254
2001 Kif1C alleles determine resistance or susceptibility of mouse macrophages to anthrax lethal toxin (LeTx). Brefeldin A treatment (which alters KIF1C cellular localization) converts resistant macrophages to susceptibility; ectopic expression of a resistance allele in susceptible macrophages increases survival. KIF1C acts downstream of toxin entry/processing (MKK3 cleavage still occurs in resistant cells), likely influencing a post-entry step. Genetic mapping, allele overexpression, brefeldin A treatment, LeTx susceptibility assay, MKK3 cleavage assay Current biology : CB Medium 11591317
2002 KIF1C knockout mice are viable with no obvious abnormalities; primary lung fibroblasts from kif1C−/− mice show no significant difference in Golgi distribution or brefeldin A-induced Golgi-to-ER retrograde transport, indicating KIF1C is dispensable for this retrograde transport in vivo. Gene knockout (knock-in of beta-gal into motor domain), immunocytochemistry, time-lapse analysis of BFA-induced transport Molecular and cellular biology High 11784862
2006 KIF1C is a microtubule plus-end-enriched kinesin that targets podosome turnover regions in primary human macrophages; KIF1C depletion (siRNA/shRNA) or expression of dominant-negative constructs decreases podosome dynamics and causes podosome deficiency. KIF1C binds non-muscle myosin IIA via its PTPD-binding domain, linking actin and tubulin cytoskeletons. siRNA/shRNA knockdown, dominant-negative overexpression, protein interaction studies (co-IP), live-cell imaging, immunofluorescence in primary human macrophages Molecular biology of the cell High 16554367
2012 KIF1C mediates transport of α5β1-integrins to trailing focal adhesions, which is required for maturation of these adhesions and resistance to tail retraction during directional cell migration. Loss of KIF1C leads to impaired rear stabilization and reduced directional persistence; the phenotype is suppressed by myosin II inhibition. Kif1C depletion (siRNA), live-cell migration assays, integrin trafficking assays, myosin II inhibition epistasis Developmental cell High 23237952
2014 Rab6A binds to both the motor domain and the C-terminus of KIF1C; Rab6A binding to the motor domain inhibits microtubule interaction in vitro and in cells, reducing the pool of motile KIF1C. KIF1C depletion slows protein delivery to the cell surface, disrupts vesicle motility, and triggers Golgi fragmentation. Protection of Golgi from fragmentation requires Rab6A-binding at both ends but not KIF1C motor activity. In vitro microtubule binding assay, co-IP, KIF1C depletion (siRNA), live-cell imaging of vesicle motility, Golgi fragmentation assay, rescue with deletion constructs eLife High 25821985
2014 KIF1C translocation to the cell periphery is dependent on CLASP proteins; upon PKC-induced podosome formation, KIF1C accumulates near CLASPs at peripheral microtubule plus ends. Chimeric mitochondrially-targeted CLASP2 recruits KIF1C, indicating a direct transient CLASP–KIF1C association that is required for KIF1C trafficking and podosome formation. CLASP siRNA knockdown, PKC activation, live-cell imaging, chimeric CLASP2 mitochondrial targeting assay, immunofluorescence Journal of cell science Medium 25344256
2014 Microtubule acetylation (regulated by MEC-17 acetyltransferase) influences the subcellular distribution, directionality, velocity, and run length of KIF1C-associated vesicles in primary human macrophages, as well as the targeting frequency of microtubule plus ends to podosomes. MEC-17 overexpression/siRNA, tubacin (deacetylase inhibitor) treatment, live-cell imaging of KIF1C vesicle dynamics, immunofluorescence European journal of cell biology Medium 25151635
2019 KIF1C is autoinhibited through an interaction between its microtubule-binding surface (motor domain) and its stalk. This autoinhibition is released by binding of PTPN21's FERM domain or the cargo adaptor Hook3 to the KIF1C tail. In vitro, full-length human KIF1C is a processive, plus-end-directed motor; its landing rate onto microtubules increases in the presence of PTPN21 FERM domain or Hook3. PTPN21 FERM domain stimulates dense core vesicle transport in primary hippocampal neurons and rescues integrin trafficking in KIF1C-depleted cells. In vitro single-molecule motility assay with purified full-length KIF1C, domain-binding assays, neuronal DCV transport assay, integrin trafficking rescue in KIF1C-depleted cells Nature communications High 31217419
2019 Hook3 acts as a scaffold that simultaneously binds dynein/dynactin (activating its motility) and the tail of KIF1C (without activating KIF1C). This trimeric complex allows dynein to transport KIF1C toward the minus end and KIF1C to transport dynein toward the plus end; in cells, KIF1C can recruit Hook3 to the cell periphery. In vitro reconstitution with purified components (dynein/dynactin, Hook3, KIF1C), single-molecule motility assays, mass spectrometry, co-IP, live-cell imaging The Journal of cell biology High 31320392
2021 KIF1C interacts with APC-dependent mRNAs and is required for their active transport to cytoplasmic protrusions along microtubules. Two-color live-cell imaging directly showed single mRNAs transported by single KIF1C motors; the mRNA 3'UTR is sufficient for KIF1C-dependent transport. KIF1C also maintains peripheral multimeric mRNA clusters and transports its own mRNA. Live-cell single-molecule imaging (two-color), siRNA KIF1C depletion, mRNA localization assay, 3'UTR sufficiency experiment RNA (New York, N.Y.) High 34493599
2019 Kif1c regulates actin ring formation and osteoclastic bone resorption downstream of p130Cas (and upstream of c-Src). Kif1c shRNA knockdown in wild-type osteoclasts suppressed actin ring formation; Kif1c overexpression rescued bone resorption in p130CasΔOCL−/− osteoclasts but not in c-Src−/− osteoclasts, placing Kif1c between p130Cas and c-Src in this signaling pathway. shRNA knockdown, overexpression rescue epistasis, cDNA microarray for pathway placement, bone resorption assay Cell biochemistry and function Medium 31887784
2022 c-Src phosphorylates tyrosine residues within the stalk domain of KIF1C, enhancing its association with PTPD1, which in turn activates KIF1C's microtubule-binding ability, likely by relieving autoinhibitory motor–stalk interactions. KIF1C localizes to invadopodium tips and is required for invadopodia elongation and cancer cell invasion. c-Src overexpression/inhibition, phospho-mutant constructs, co-IP, microtubule-binding assay, invadopodia elongation assay, invasion assay The Journal of biological chemistry Medium 35654143
2022 In neuronal cells, KIF1C interacts with all core components of the exon junction complex (EJC) in an RNA-mediated manner (abolished by RNase treatment); expression of mutant KIF1C causes loss of distal neurite EJC localization and pericentrosomal accumulation of EJC components, suggesting KIF1C transports mRNA in an EJC-bound state along neurites. Affinity proteomics (AP-MS) in SH-SY5Y cells, co-immunoprecipitation, RNase treatment, immunostaining of mutant KIF1C-expressing cells, UV-crosslinking RNA-protein extraction RNA (New York, N.Y.) Medium 36316088
2023 Localization of Kif1c mRNA to cell protrusions does not regulate KIF1C protein abundance or distribution but is required for directed cell migration and controls the specificity of KIF1C protein–protein interactions; mRNA mislocalization dramatically dysregulates the number and identity of KIF1C binding partners as determined by mass spectrometry. Kif1c mRNA mislocalization (genetic perturbation), mass spectrometry of endogenous KIF1C interactors, directed migration assays Genes & development Medium 36859340
2024 KIF1C's C-terminal tail contains an intrinsically disordered region (IDR) that drives liquid-liquid phase separation (LLPS). KIF1C forms dynamic liquid condensates in cellular protrusions that incorporate RNA molecules in a sequence-selective manner. Purified KIF1C tail constructs undergo LLPS in vitro at near-endogenous nM concentrations without crowding agents and directly recruit RNA. IDR-dependent LLPS is required for enrichment of mRNA cargoes at the cell periphery. In vitro LLPS with purified KIF1C tail, live-cell condensate imaging (FRAP, fluorescence recovery), IDR deletion mutants, RNA recruitment assay in vitro and in cells The EMBO journal High 38898313
2024 KIF1C unexpectedly supports retrograde transport of lysosomes toward the nucleus via dynein, without requiring its own motor activity (which is actually inhibitory for this process). Mechanistically, KIF1C interacts with dynein-activating adaptor Hook3, which associates with the lysosome-anchored protein RUFY3, thereby activating dynein-driven lysosomal transport. This non-motor role of KIF1C is required for efficient autophagic and endocytic cargo degradation. KIF1C depletion, motor-dead KIF1C mutant, co-IP (KIF1C–Hook3–RUFY3), lysosome positioning assay, autophagic/endocytic degradation assays Communications biology Medium 39394274
2025 Crystal structure of the Hook3(553–624)–KIF1C(714–809) complex was determined, revealing the molecular basis for Hook3–KIF1C interaction. Structure-based mutations in this interface abolish binding between full-length proteins in HEK293T cells and abrogate Hook3/KIF1C-mediated anterograde transport in RPE1 cells, demonstrating the complex is necessary and sufficient for Hook3-activated KIF1C transport. Crystal structure determination, structure-based mutagenesis, co-IP in HEK293T cells, anterograde transport assay in RPE1 cells EMBO reports High 40312563
2025 CNBP (RNA-binding protein) binds directly to GA-rich sequences in the 3'UTR of protrusion-targeted mRNAs and interacts with KIF1C; CNBP is required for KIF1C recruitment to mRNA cargo and for active mRNA transport on microtubules to the cell periphery, defining a KIF1C–CNBP motor-adaptor complex for mRNA transport. RNA pulldown, co-IP (CNBP–KIF1C), siRNA depletion, live-cell mRNA transport assay, 3'UTR binding assay Cell reports Medium 39982819
2025 Liquid-liquid phase separation of KIF1C generates multi-kinesin clusters that entangle neighboring microtubules and impose mechanical stress sufficient to cause microtubule breakage and disassembly in cells. Microtubule fragmentation requires a highly processive motor domain, a stiff clustering mechanism (IDR-driven LLPS), and sufficient drag force. Live-cell imaging of microtubule breakage, computational simulations, IDR/motor domain mutants, in vitro LLPS bioRxivpreprint Medium bio_10.1101_2025.01.31.635950

Source papers

Stage 0 corpus · 34 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 Characterization of KIF1C, a new kinesin-like protein involved in vesicle transport from the Golgi apparatus to the endoplasmic reticulum. The Journal of biological chemistry 116 9685376
2006 The kinesin KIF1C and microtubule plus ends regulate podosome dynamics in macrophages. Molecular biology of the cell 110 16554367
2012 Directional persistence of migrating cells requires Kif1C-mediated stabilization of trailing adhesions. Developmental cell 86 23237952
1999 The kinesin-like motor protein KIF1C occurs in intact cells as a dimer and associates with proteins of the 14-3-3 family. The Journal of biological chemistry 72 10559254
2001 Kif1C, a kinesin-like motor protein, mediates mouse macrophage resistance to anthrax lethal factor. Current biology : CB 70 11591317
2019 Hook3 is a scaffold for the opposite-polarity microtubule-based motors cytoplasmic dynein-1 and KIF1C. The Journal of cell biology 66 31320392
2013 KIF1C mutations in two families with hereditary spastic paraparesis and cerebellar dysfunction. Journal of medical genetics 63 24319291
2019 PTPN21 and Hook3 relieve KIF1C autoinhibition and activate intracellular transport. Nature communications 57 31217419
2015 Rab6 regulation of the kinesin family KIF1C motor domain contributes to Golgi tethering. eLife 53 25821985
2021 The kinesin KIF1C transports APC-dependent mRNAs to cell protrusions. RNA (New York, N.Y.) 37 34493599
2014 Microtubule acetylation regulates dynamics of KIF1C-powered vesicles and contact of microtubule plus ends with podosomes. European journal of cell biology 37 25151635
2014 Podosome-regulating kinesin KIF1C translocates to the cell periphery in a CLASP-dependent manner. Journal of cell science 30 25344256
2002 Molecular motor KIF1C is not essential for mouse survival and motor-dependent retrograde Golgi apparatus-to-endoplasmic reticulum transport. Molecular and cellular biology 27 11784862
2023 Localization of Kif1c mRNA to cell protrusions dictates binding partner specificity of the encoded protein. Genes & development 16 36859340
2024 The kinesin-3 KIF1C undergoes liquid-liquid phase separation for accumulation of specific transcripts at the cell periphery. The EMBO journal 15 38898313
2018 Progressive ataxia of Charolais cattle highlights a role of KIF1C in sustainable myelination. PLoS genetics 14 30067756
2018 Clinical phenotype of hereditary spastic paraplegia due to KIF1C gene mutations across life span. Brain & development 13 29544888
2022 c-Src-mediated phosphorylation and activation of kinesin KIF1C promotes elongation of invadopodia in cancer cells. The Journal of biological chemistry 11 35654143
2024 KIF1C facilitates retrograde transport of lysosomes through Hook3 and dynein. Communications biology 8 39394274
2022 The kinesin motor KIF1C is a putative transporter of the exon junction complex in neuronal cells. RNA (New York, N.Y.) 8 36316088
2019 Kif1c regulates osteoclastic bone resorption as a downstream molecule of p130Cas. Cell biochemistry and function 7 31887784
2025 A KIF1C-CNBP motor-adaptor complex for trafficking mRNAs to cell protrusions. Cell reports 6 39982819
2024 KIF1C and new Huntingtin-interacting protein 1 binding proteins regulate rheumatoid arthritis fibroblast-like synoviocytes' phenotypes. Frontiers in immunology 4 38726004
2020 Generation of the CRISPR/Cas9-mediated KIF1C knock-out human iPSC line HIHRSi003-A-1. Stem cell research 4 33161238
2023 Crosstalk between KIF1C and PRKAR1A in left atrial myxoma. Communications biology 2 37452081
2010 Exclusion of Kif1c as a candidate gene for anthrax toxin susceptibility. Microbial pathogenesis 2 20188815
2023 It's complicated: the interplay of Kif1c mRNA localization in cell protrusions, assembly of protein binding partners on the KIF1C protein, and cell migration. Genes & development 1 36889919
2026 Multi-Omics Characterization of a KIF1C Structural Variant in a Patient with a Complex Movement Disorder Partially Responsive to Deep Brain Stimulation. Cerebellum (London, England) 0 41874815
2025 Molecular basis for assembly and activation of the Hook3 - KIF1C complex-dependent transport machinery. EMBO reports 0 40312563
2025 KIF1C-related disorders: spastic ataxia or hypomyelinating leukodystrophy? A paradigm of classification ambiguity. Neurogenetics 0 40794111
2025 A Novel Homozygous KIF1C Variant in 2 Cases of Spastic Ataxia Type 2. Neurology. Genetics 0 41127312
2024 Genotyping KIF1C (c.608G>A) Mutant Reveals a Wide Distribution of Progressive Ataxia in German Charolais Cattle. Animals : an open access journal from MDPI 0 38338009
2024 A KIF1C-CNBP motor-adaptor complex for trafficking mRNAs to cell protrusions. bioRxiv : the preprint server for biology 0 38979199
2023 KIF1C, an RNA transporting kinesin-3, undergoes liquid-liquid phase separation through its C-terminal disordered domain. bioRxiv : the preprint server for biology 0 37961614

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