Affinage

KLC1

Kinesin light chain 1 · UniProt Q07866

Round 2 corrected
Length
573 aa
Mass
65.3 kDa
Annotated
2026-04-28
57 papers in source corpus 17 papers cited in narrative 20 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KLC1 is the light chain subunit of the kinesin-1 motor complex that couples cargo recognition to motor activation, serving as the principal adaptor for anterograde microtubule-based transport of diverse cargoes including APP-containing vesicles, JIP1-linked vesicles, SFPQ-RNA granules, and phagosomes. Its central tetratricopeptide repeat (TPR) domain directly binds short linear peptide motifs (W-acidic/WD motifs) on cargo adaptors such as Alcadein-α, JIP1, APP, and CRMP2, and this binding displaces the autoinhibitory interaction between the kinesin heavy chain coiled-coil and the KLC TPR domain, thereby activating the motor for processive transport (PMID:11144355, PMID:22404616, PMID:30026235). Phosphorylation of KLC1 Thr466 selectively disrupts the TPR–JIP1 interaction to reduce APP transport velocity, and phosphorylated DOC2B (Y301) recruits KLC1 to facilitate insulin-stimulated GLUT4 translocation, demonstrating that post-translational modifications tune cargo selectivity and transport dynamics (PMID:29093025, PMID:30707251). Loss of KLC1 in mice impairs phagosome transport in retinal pigment epithelium, producing age-dependent sub-RPE deposits and pathology resembling age-related macular degeneration, and compromises CRMP2-dependent axonal elongation required for forebrain commissure formation (PMID:26261180, PMID:38830696).

Mechanistic history

Synthesis pass · year-by-year structured walk · 10 steps
  1. 1993 Medium

    Establishing the primary structure of human KLC1 revealed its domain architecture—an N-terminal heptad-repeat coiled-coil and a central/C-terminal tetratricopeptide repeat (TPR) region—providing the first framework for understanding how a kinesin light chain might interface with both heavy chains and cargoes.

    Evidence cDNA cloning, sequencing, and heterologous expression in bacteria and CHO cells

    PMID:8274221

    Open questions at the time
    • No cargo or heavy-chain binding activity was demonstrated at this stage
    • Chromosomal assignment was provisional
  2. 2000 High

    Identification of APP and JIP1/Sunday driver as direct, high-affinity TPR-domain ligands of KLC1 established that the light chain functions as a cargo-recognition subunit required for anterograde axonal transport, resolving how kinesin-1 selects specific vesicle populations.

    Evidence In vitro binding with measured Kd values (~15–20 nM for APP, ~200 nM for JIP1), co-immunoprecipitation, and genetic KO or mutant validation in mouse and Drosophila

    PMID:11106729 PMID:11144355

    Open questions at the time
    • The structural basis for how TPR accommodates different cargo motifs was unknown
    • Mechanism by which cargo binding relieves motor autoinhibition was not addressed
  3. 2012 High

    Discovery that a 10-residue W-acidic (WD) motif in Alcadein-α binds a subset of the KLC1 TPR domain and is sufficient to activate kinesin-1 from its autoinhibited state demonstrated that short linear motifs are the general currency for KLC1-mediated cargo engagement and motor activation.

    Evidence In vivo transport assays with synthetic transmembrane cargo constructs, competitive KLC1 excess, and fluorescence correlation spectroscopy

    PMID:22404616

    Open questions at the time
    • Structural visualization of the autoinhibited-to-active transition was lacking
    • Whether all cargo adaptors share the same TPR sub-site was unresolved
  4. 2015 High

    Demonstrating that KLC1 remains on bidirectionally moving phagosomes and that its knockout impairs phagosome run length, degradation, and RPE homeostasis linked KLC1 function to a non-neuronal cargo (outer-segment phagosomes) and to age-related macular degeneration-like pathology.

    Evidence Live-cell imaging and histopathology in aged KLC1 knockout mice

    PMID:26261180

    Open questions at the time
    • The cargo adaptor bridging phagosomes to KLC1 TPR was not identified
    • Whether the AMD-like phenotype involves KLC1-independent kinesin functions was not resolved
  5. 2017 High

    Identification of Thr466 phosphorylation as a switch that specifically abolishes TPR–JIP1 interaction and reduces APP fast transport velocity revealed a post-translational mechanism for tuning kinesin-1 cargo selectivity, with relevance to brain aging.

    Evidence Phosphomimetic/non-phosphorylatable mutagenesis, co-immunoprecipitation, live-cell velocity analysis, and phospho-specific antibody in aged mouse brains

    PMID:29093025

    Open questions at the time
    • The kinase responsible for Thr466 phosphorylation in vivo was not identified
    • Causal link between age-dependent phosphorylation and neurodegeneration was correlative
  6. 2018 High

    Isothermal titration calorimetry mapping of the JIP1-binding footprint on the KLC1 TPR domain and demonstration that JIP1 and Alcadein-α W-acidic peptides compete for the same site established a shared, mutually exclusive cargo-binding pocket modulated by an autoinhibitory LFP-acidic motif.

    Evidence ITC with systematic KLC1 TPR truncations and point mutations, competition binding experiments

    PMID:30026235

    Open questions at the time
    • High-resolution co-crystal or cryo-EM structure of the TPR–cargo peptide complex was still unavailable
    • How the LFP-acidic autoinhibitory segment is regulated in cells was unexplored
  7. 2019 High

    Two studies expanded KLC1's functional repertoire beyond neuronal transport: DOC2B phosphorylation at Y301 recruits KLC1 to drive insulin-stimulated GLUT4 translocation in skeletal muscle, and KLC1 suppresses epithelial-mesenchymal transition in breast cancer cells, linking kinesin-1 cargo transport to metabolic and oncogenic signaling.

    Evidence Reciprocal co-IP validated by mass spectrometry, Y301 mutagenesis, GLUT4 surface accumulation assay, and transgenic mouse glucose tolerance (DOC2B); siRNA/overexpression with invasion assays (breast cancer)

    PMID:30707251 PMID:31204277

    Open questions at the time
    • Whether DOC2B binds the KLC1 TPR domain or a distinct region was not mapped
    • Molecular mechanism linking KLC1 to epithelial gene expression programs is unclear
  8. 2021 High

    Selective association of SFPQ-RNA granules with a KIF5A/KLC1 tetrameric complex for long-distance axonal transport, and the impairment of this interaction by CMT-causing KIF5A mutations, established KLC1 as a specificity determinant for RNA granule transport essential for axon survival.

    Evidence Co-immunoprecipitation, selective binding assays, axon survival assays in CMT model neurons with rescue

    PMID:33284322

    Open questions at the time
    • Whether KLC1 directly contacts SFPQ or acts via an intermediate adaptor was not resolved
    • Structural basis for KIF5A versus KIF5B selectivity in this complex was not determined
  9. 2024 Medium

    CRMP2 was identified as a direct KLC1-binding partner whose disease-associated R565C mutation abolishes this interaction, and genetic interaction between klc1a and crmp2 in zebrafish established KLC1-dependent axonal elongation as essential for forebrain commissure formation.

    Evidence Co-immunoprecipitation with WT vs. R566C CRMP2, morpholino knockdown in zebrafish with commissure imaging

    PMID:38830696

    Open questions at the time
    • The KLC1 domain mediating CRMP2 binding was not mapped
    • Whether the commissure defect reflects transport of a specific cargo downstream of CRMP2 is unknown
  10. 2025 High

    Cryo-EM structures of intact autoinhibited kinesin-1 heterotetramers revealed that KHC coiled-coil 1 (CC1) docks onto the KLC TPR domains to occlude cargo-binding sites, and that cargo SLiM binding to TPR dislocates this 'shoulder' to release motor autoinhibition—providing the first structural mechanism for cargo-coupled kinesin-1 activation.

    Evidence Cryo-EM of holoenzyme (preprint), biophysical binding analysis, single-molecule TIRF reconstitution with kinesore pharmacological rescue (preprint)

    Open questions at the time
    • Structures are from preprints and await peer review
    • Atomic-resolution details of the TPR–CC1 interface and cargo-bound active state are incomplete
    • How asymmetric KLC arrangement influences cargo stoichiometry in vivo is unknown

Open questions

Synthesis pass · forward-looking unresolved questions
  • Outstanding questions include the identity of the kinase(s) phosphorylating KLC1 Thr466 in vivo, the structural basis for selective recognition of different cargo SLiMs by the same TPR pocket, and whether KLC1 splice variants (e.g., KLC1_vE implicated in Alzheimer's disease) confer distinct cargo specificities.
  • No high-resolution co-structure of KLC1 TPR with any cargo peptide in peer-reviewed literature
  • Functional distinction among KLC1 splice variants is uncharacterized
  • In vivo kinase for Thr466 remains unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 6 GO:0008092 cytoskeletal protein binding 3
Localization
GO:0031410 cytoplasmic vesicle 4 GO:0005856 cytoskeleton 3 GO:0005829 cytosol 1
Pathway
R-HSA-5653656 Vesicle-mediated transport 5 R-HSA-112316 Neuronal System 4 R-HSA-1266738 Developmental Biology 1 R-HSA-382551 Transport of small molecules 1
Partners
APPCRMP2DNM1LDOC2BJIP1KIF5AKIF5BSFPQ
Complex memberships
Kinesin-1 heterotetramer (KIF5/KLC)

Evidence

Reading pass · 20 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2000 APP (amyloid precursor protein) is transported axonally by directly binding to the TPR domain of the KLC1 subunit of kinesin-I, with an estimated apparent Kd of 15-20 nM and stoichiometry of two APP per KLC. Axonal transport of APP is greatly decreased in KLC1 gene-targeted mouse mutants, establishing KLC1 as essential for anterograde axonal transport of APP. Co-immunoprecipitation, sucrose gradient sedimentation, direct in vitro binding assays, KLC1 knockout mouse Neuron High 11144355
2000 Sunday driver (SYD/JIP1) directly binds kinesin-I via the tetratricopeptide repeat (TPR) domain of KLC with Kd ~200 nM, mediating kinesin-dependent axonal transport of at least one class of vesicles. Yeast two-hybrid, in vitro interaction studies, co-immunoprecipitation, GFP localization Cell High 11106729
1993 The human KLC1 gene encodes a 569-amino acid polypeptide (64,789 Da) with an N-terminal heptad-repeat rod domain and a central/C-terminal domain of 21-mer (tetratricopeptide) repeats; KLC1 mRNA is expressed in most tissues, and the gene was provisionally assigned to human chromosome 14q. cDNA cloning, sequencing, bacterial and CHO cell expression, chromosomal assignment DNA and cell biology Medium 8274221
2012 KLC1-ALK is a novel oncogenic fusion kinase identified in lung cancer. The KLC1-ALK fusion cDNA confers transforming potential to mouse 3T3 cells, demonstrating that KLC1 coiled-coil sequences can serve as a dimerization module that constitutively activates the ALK kinase domain. 5'-RACE on FFPE tissue, RT-PCR, FISH confirmation, 3T3 transformation assay PloS one Medium 22347464
2012 A 10-amino-acid WD motif in the C-terminal cytoplasmic region of Alcadein-α (Alcα) is necessary and sufficient to interact with part of the KLC1 TPR domain, activating kinesin-1 from its autoinhibited state and driving anterograde vesicular transport. Only a subset of the TPR structure is required for this activation in vivo. In vivo transport assays with artificial transmembrane proteins carrying WD motifs, excess KLC1 competition, fluorescence correlation spectroscopy (FCS) for protein interaction Traffic High 22404616
2009 AMPK phosphorylates recombinant GST-KLC1 at Ser520 in vitro, but overexpression of phosphomimetic (S517/520D) or non-phosphorylatable (S517/520A) KLC1 mutants does not alter glucose-stimulated insulin granule movement, indicating that AMPK-dependent phosphorylation of KLC1 at these sites does not regulate kinesin-1-mediated granule transport in β-cells. In vitro AMPK kinase assay with purified proteins, 3D live-cell spinning disc confocal imaging, phospho-specific antibody, KLC1 mutant overexpression in MIN6 cells Islets Medium 21099273
2015 KLC1 associates with phagosomes carrying photoreceptor outer segment (POS) disk membranes in retinal pigment epithelium (RPE) cells and remains associated during bidirectional movement and pauses. KLC1 knockout decreases phagosome run length and impairs phagosome localization and degradation. In aged KLC1 knockout mice, RPE pathogenesis resembling age-related macular degeneration develops, including sub-RPE deposits, oxidative stress, and inflammatory responses. Live-cell imaging, KLC1 knockout mouse model, fluorescence microscopy, histopathology The Journal of cell biology High 26261180
2016 Deletion of KLC1 in mice impairs anterograde Mn2+ transport from the hippocampal CA3 region to the medial septal nuclei as measured by manganese-enhanced MRI, establishing KLC1 as a contributor to kinesin-1-mediated cargo transport in central nervous system circuits, though the effect is moderate. MEMRI (manganese-enhanced MRI) in KLC1 knockout vs. wild-type mice, histology, statistical parametric mapping NeuroImage Medium 27751944
2017 Phosphorylation of KLC1 at Thr466 abolishes the conventional interaction between the KLC1 TPR domain and the C-terminal region of JIP1b, eliminating the enhanced fast velocity (EFV) of APP anterograde transport without impairing the novel JIP1b central-region/KLC1 coiled-coil interaction that drives enhanced high frequency (EHF). Phosphorylation of KLC1 Thr466 increases in aged mouse brains, correlating with decreased JIP1 binding to kinesin-1. Phosphomimetic/non-phosphorylatable mutagenesis (T466E/T466A), co-immunoprecipitation, live-cell transport velocity analysis, phospho-specific antibody, aged brain analysis Molecular biology of the cell High 29093025
2018 Isothermal titration calorimetry identified seven KLC1 TPR residues critical for JIP1 binding and footprinted the JIP1-binding site on KLC1-TPR. The autoinhibitory LFP-acidic motif of KLC1 marginally inhibits JIP1 binding at this same site, and JIP1 and the W-acidic motif of Alcadein-α compete for the same region of KLC1-TPR. Isothermal titration calorimetry (ITC), truncation and mutagenesis of KLC1 TPR fragments, competition binding experiments The Journal of biological chemistry High 30026235
2019 DOC2B is phosphorylated on insulin stimulation (at Y301), which enhances its interaction with KLC1 in skeletal muscle. This DOC2B-KLC1 interaction is required for insulin-stimulated GLUT4 translocation to the plasma membrane; Y301 mutation blocks both phosphorylation and KLC1 binding and impairs GLUT4 accumulation, defining a novel KLC1-dependent mechanism for insulin sensitivity. Co-immunoprecipitation, mass spectrometry, site-directed mutagenesis (Y301), GLUT4-myc surface accumulation assay in L6 myoblasts, transgenic mouse glucose/insulin tolerance tests Diabetologia High 30707251
2019 KLC1 suppresses epithelial-mesenchymal transition (EMT), invasion, metastasis, and stem cell marker expression in breast cancer, promoting an epithelial/luminal phenotype. Prolactin enhances KLC1 expression and KIF5B-KLC1 interaction, while TGF-β-mediated pro-invasive activity depends on KIF5B but not KLC1. In triple-negative cells, KIF5B accumulates in the nucleus independently of KLC1 to interact with Snail1. siRNA knockdown, overexpression, invasion and migration assays, tumor formation assays in multiple breast cancer cell lines, co-immunoprecipitation EBioMedicine Medium 31204277
2021 SFPQ-RNA granules interact selectively with a tetrameric kinesin complex containing KLC1 and KIF5A for long-distance axonal transport. The SFPQ-KIF5A/KLC1 interaction is required for axon survival; KIF5A mutations causing Charcot-Marie-Tooth disease impair this binding. Replacing axonally translated SFPQ-bound proteins prevents axon degeneration in CMT models. Co-immunoprecipitation, selective binding assays, axon survival assays in CMT model neurons, rescue experiments with exogenous proteins The Journal of cell biology High 33284322
2014 Mitochondrial fission protein Dnm1L (dynamin-1-like protein) interacts with KLC1 via the KLC1 TPR domains, but not with KIF5, as determined by yeast two-hybrid screening; Dnm1L and KLC1 co-localize in cultured cells, suggesting KLC1 may mediate post-fission mitochondrial transport. Yeast two-hybrid screening, co-localization in cultured cells Bioscience, biotechnology, and biochemistry Low 25082190
2024 CRMP2 directly binds KLC1, and the CRMP2 R565C mutation (corresponding to zebrafish R566C) abolishes this interaction. Knockdown of klc1a in zebrafish causes defective anterior commissure and postoptic commissure formation, genetically interacting with crmp2 knockdown. These findings establish the CRMP2-KLC1 interaction as necessary for axonal elongation and forebrain commissure formation. Transfected cell co-immunoprecipitation with CRMP2 wild-type vs. R566C mutant, klc1a morpholino knockdown in zebrafish, commissure formation imaging Developmental neurobiology Medium 38830696
2024 CELF1, an RNA-binding protein whose expression is reduced in Alzheimer's disease brains, directly binds KLC1 RNA and suppresses the production of KLC1 splice variant E (KLC1_vE). Reduced CELF1 leads to increased KLC1_vE, which promotes AD pathogenesis, identifying a splicing regulatory axis linking CELF1 to KLC1 alternative splicing. CLIP-seq database analysis, CELF1 depletion and overexpression in cultured cells, transcriptomic correlation in human AD brain samples Biochemical and biophysical research communications Medium 38768546
2025 KLC1 interacts with dengue virus NS1 protein in mosquito cells (confirmed by proximity ligation assay and co-immunoprecipitation). Silencing KLC1 reduces viral genome synthesis, NS1 secretion, and virus progeny by ~1 log. KLC1 or its function is also required for lipid droplet homeostasis; disruption causes lipid droplets to decrease in number and increase in area, suggesting KLC1-mediated lipid droplet transport is required for dengue virus replication. Proximity ligation assay, co-immunoprecipitation, transmission immunoelectron microscopy, siRNA silencing, competing peptide interference, lipid droplet imaging bioRxivpreprint Medium 40166163
2025 Cryo-EM and biophysical analysis of the intact kinesin-1 heterotetramer reveal that in the autoinhibited state, KLC TPR domains are occluded by docking of kinesin heavy chain (KHC) coiled coil 1 (CC1) onto the KLC TPR domain, forming the 'shoulder' observed by EM. Binding of an activating cargo SLiM (short linear peptide motif) to the KLC TPR domain dislocates this shoulder, freeing motor domains and enabling transition from closed/inactive to open/active states and facilitating MAP7 binding. This identifies cargo-mediated TPR shoulder dislocation as the key initial step in kinesin-1 activation. Cryo-EM of full heterotetrameric kinesin-1, protein design, computational modelling, biophysical binding analysis, negative-stain EM bioRxivpreprint High
2025 An 8.0-Å cryo-EM structure of the autoinhibited kinesin-1 heterotetramer shows that two KLC subunits are asymmetrically arranged and their TPR cargo-binding domains are occluded, providing structural basis for simultaneous inhibition of motor activity and cargo binding. MAP7D3 binding to KHC coiled coils likely competes with intramolecular coiled-coil interactions to unfurl the autoinhibited structure. Cryo-EM (8.0 Å), structural modeling, functional motor activity assays bioRxivpreprint Medium
2025 KLC-bound kinesin-1 (KinΔC) on liposomes exhibits partial autoinhibition that reduces microtubule engagement (3-fold lower landing rates vs. constitutively active K543), shortens run lengths, and reduces detachment forces. At 3D microtubule intersections, KinΔC-liposomes preferentially terminate (48%) rather than turn (9%), contrasting with constitutively active motors. The small molecule kinesore, which overcomes KLC-mediated autoinhibition, restores microtubule engagement, confirming that KLC-dependent autoinhibition fine-tunes cargo transport. Single-molecule TIRF microscopy, in vitro liposome transport assay with 3D microtubule intersections, optical trapping for detachment forces, kinesore pharmacological rescue bioRxivpreprint High

Source papers

Stage 0 corpus · 57 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 Biological insights from 108 schizophrenia-associated genetic loci. Nature 5878 25056061
2006 Global, in vivo, and site-specific phosphorylation dynamics in signaling networks. Cell 2861 17081983
2005 A human protein-protein interaction network: a resource for annotating the proteome. Cell 1704 16169070
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2006 A probability-based approach for high-throughput protein phosphorylation analysis and site localization. Nature biotechnology 1336 16964243
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2015 A human interactome in three quantitative dimensions organized by stoichiometries and abundances. Cell 1015 26496610
2014 A proteome-scale map of the human interactome network. Cell 977 25416956
2020 A reference map of the human binary protein interactome. Nature 849 32296183
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2003 Complete sequencing and characterization of 21,243 full-length human cDNAs. Nature genetics 754 14702039
2007 Large-scale mapping of human protein-protein interactions by mass spectrometry. Molecular systems biology 733 17353931
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2012 A census of human soluble protein complexes. Cell 689 22939629
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2005 Analysis of the kinesin superfamily: insights into structure and function. Trends in cell biology 566 16084724
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2015 A Dynamic Protein Interaction Landscape of the Human Centrosome-Cilium Interface. Cell 433 26638075
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2000 Axonal transport of amyloid precursor protein is mediated by direct binding to the kinesin light chain subunit of kinesin-I. Neuron 426 11144355
2005 Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes. Genome research 409 16344560
2015 Panorama of ancient metazoan macromolecular complexes. Nature 407 26344197
2004 Proteomic, functional, and domain-based analysis of in vivo 14-3-3 binding proteins involved in cytoskeletal regulation and cellular organization. Current biology : CB 386 15324660
2021 A proximity-dependent biotinylation map of a human cell. Nature 339 34079125
2015 BORC, a multisubunit complex that regulates lysosome positioning. Developmental cell 315 25898167
2019 Intrinsically Disordered Protein TEX264 Mediates ER-phagy. Molecular cell 296 31006538
2000 Kinesin-dependent axonal transport is mediated by the sunday driver (SYD) protein. Cell 274 11106729
2012 A high-throughput approach for measuring temporal changes in the interactome. Nature methods 273 22863883
2011 A directed protein interaction network for investigating intracellular signal transduction. Science signaling 258 21900206
2012 KLC1-ALK: a novel fusion in lung cancer identified using a formalin-fixed paraffin-embedded tissue only. PloS one 196 22347464
2015 Microtubule motors transport phagosomes in the RPE, and lack of KLC1 leads to AMD-like pathogenesis. The Journal of cell biology 68 26261180
2021 Binding and transport of SFPQ-RNA granules by KIF5A/KLC1 motors promotes axon survival. The Journal of cell biology 55 33284322
2012 A small peptide sequence is sufficient for initiating kinesin-1 activation through part of TPR region of KLC1. Traffic (Copenhagen, Denmark) 38 22404616
2019 A role for kinesin-1 subunits KIF5B/KLC1 in regulating epithelial mesenchymal plasticity in breast tumorigenesis. EBioMedicine 33 31204277
1993 Cloning and genetic characterization of the human kinesin light-chain (KLC) gene. DNA and cell biology 27 8274221
2019 DOC2B promotes insulin sensitivity in mice via a novel KLC1-dependent mechanism in skeletal muscle. Diabetologia 22 30707251
2019 Serial liquid biopsies for detection of treatment failure and profiling of resistance mechanisms in KLC1-ALK-rearranged lung cancer. Cold Spring Harbor molecular case studies 22 31753813
2018 Identification of a novel KLC1-ROS1 fusion in a case of pediatric low-grade localized glioma. Brain tumor pathology 21 30350109
2017 Rapid response of brain metastasis to crizotinib in a patient with KLC1-ALK fusion and MET gene amplification positive non-small cell lung cancer: a case report. Cancer biology & medicine 19 28607809
2009 Control of insulin granule dynamics by AMPK dependent KLC1 phosphorylation. Islets 18 21099273
2017 Phosphorylation of KLC1 modifies interaction with JIP1 and abolishes the enhanced fast velocity of APP transport by kinesin-1. Molecular biology of the cell 15 29093025
2016 Hippocampal to basal forebrain transport of Mn2+ is impaired by deletion of KLC1, a subunit of the conventional kinesin microtubule-based motor. NeuroImage 15 27751944
2021 Normal levels of KIF5 but reduced KLC1 levels in both Alzheimer disease and Alzheimer disease in Down syndrome: evidence suggesting defects in anterograde transport. Alzheimer's research & therapy 14 33691783
2010 Cell-wide analysis of secretory granule dynamics in three dimensions in living pancreatic beta-cells: evidence against a role for AMPK-dependent phosphorylation of KLC1 at Ser517/Ser520 in glucose-stimulated insulin granule movement. Biochemical Society transactions 11 20074060
2021 Chronic intermittent hypoxia aggravates skeletal muscle aging by down-regulating Klc1/grx1 expression via Wnt/β-catenin pathway. Archives of gerontology and geriatrics 10 34218156
2023 KLC1-ROS1 Fusion Exerts Oncogenic Properties of Glioma Cells via Specific Activation of JAK-STAT Pathway. Cancers 9 38201436
2018 Characterization of the binding mode of JNK-interacting protein 1 (JIP1) to kinesin-light chain 1 (KLC1). The Journal of biological chemistry 8 30026235
2023 Primary resistance to ALK inhibitors in KLC1/ALK-rearranged pleural metastatic lung adenocarcinoma: a case report. Translational lung cancer research 5 38090529
2014 Dynamin-1-like protein (Dnm1L) interaction with kinesin light chain 1 (KLC1) through the tetratricopeptide repeat (TPR) domains. Bioscience, biotechnology, and biochemistry 5 25082190
2022 Variants in PRKCE and KLC1, Potential Regulators of Type I Psoriasis. Clinical, cosmetic and investigational dermatology 4 35800456
2024 Transcriptome-wide association identifies KLC1 as a regulator of mitophagy in non-syndromic cleft lip with or without palate. iMeta 3 39742305
2016 A molecular dynamics study of the binary complexes of APP, JIP1, and the cargo binding domain of KLC. Proteins 3 27891669
2024 Gene-gene functional relationships in Alzheimer's disease: CELF1 regulates KLC1 alternative splicing. Biochemical and biophysical research communications 2 38768546
2021 The Combined Thermoresponsive Cell-Imprinted Substrate, Induced Differentiation, and "KLC Sheet" Formation. Advanced pharmaceutical bulletin 2 35620328
2024 Forebrain commissure formation in zebrafish embryo requires the binding of KLC1 to CRMP2. Developmental neurobiology 1 38830696
2025 Kinesin light chain 1 (KLC1) interacts with NS1 and is a susceptibility factor for dengue virus infection in mosquito cells. bioRxiv : the preprint server for biology 0 40166163