Affinage

KIF21A

Kinesin-like protein KIF21A · UniProt Q7Z4S6

Length
1674 aa
Mass
187.2 kDa
Annotated
2026-04-28
49 papers in source corpus 15 papers cited in narrative 15 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KIF21A is a plus-end-directed kinesin-4 family motor protein that functions both as an anterograde axonal transporter and as a cortical microtubule growth inhibitor, with critical roles in oculomotor axon guidance, dendritic spine morphogenesis, and glomerular podocyte integrity. Its C-terminal WD-40 repeat domain engages cargo such as the sodium/calcium exchanger NCKX2 for axonal transport and interacts with the Arf-GEF BIG1, while its coiled-coil stalk mediates recruitment to the cell cortex through binding to KANK1/KANK2 ankyrin-repeat supramodules, where KIF21A suppresses microtubule growth and catastrophes (PMID:24120883, PMID:29158259, PMID:22442075). Motor activity is held in check by an intramolecular antiparallel coiled-coil autoinhibitory interaction between the stalk regulatory domain and the motor domain; heterozygous missense mutations in either domain relieve this autoinhibition, causing the congenital eye movement disorder CFEOM1 through oculomotor axon stalling, growth-cone enlargement, and aberrant pathfinding (PMID:14595441, PMID:27485312, PMID:24656932). KIF21A also directly binds TUBB3, and disruption of this interaction by a coiled-coil variant produces a neurological syndrome distinct from classic CFEOM (PMID:39643435).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1999 Medium

    Establishing that KIF21A exists as a distinct plus-end kinesin with WD-40 repeats and pan-neuronal distribution resolved the identity of this motor and distinguished it from the dendrite-restricted paralog KIF21B.

    Evidence Identification via novel kinesin screen, domain architecture analysis, and immunolocalization in neurons

    PMID:10225949

    Open questions at the time
    • No cargo or functional role identified
    • Motor directionality inferred from kinesin family membership, not directly measured for KIF21A
  2. 2003 High

    Discovery that heterozygous KIF21A stalk-domain mutations cause CFEOM1 established the gene as essential for oculomotor circuit development and pinpointed the third coiled-coil as a functionally critical region.

    Evidence Direct sequencing of KIF21A in 45 CFEOM1 probands with mutation clustering in third coiled-coil stalk domain

    PMID:14595441

    Open questions at the time
    • Mechanism by which stalk mutations alter motor function unknown
    • No animal model to confirm causality
  3. 2008 High

    Identification of the BIG1–KIF21A interaction via the WD-40 tail showed that KIF21A connects to Arf-GTPase signaling and membrane trafficking, broadening its functional scope beyond simple cargo transport.

    Evidence LC-MS/MS, reciprocal co-immunoprecipitation, fragment mapping, siRNA knockdown altering BIG1 distribution

    PMID:19020088

    Open questions at the time
    • Physiological cargo transported via BIG1 link unclear
    • Whether BIG1 interaction is relevant to CFEOM pathogenesis untested
  4. 2009 Medium

    Demonstration that KIF21A binds KANK1 through its coiled-coil domains—and that CFEOM1 mutations enhance this interaction—revealed a cortical recruitment axis and suggested disease mutations are gain-of-function.

    Evidence Co-immunoprecipitation and subcellular fractionation comparing wild-type and CFEOM1 mutant KIF21A

    PMID:19559006

    Open questions at the time
    • No structural basis for KANK1 binding determined
    • Single-study observation of enhanced binding by mutants
  5. 2012 High

    Establishing NCKX2 as a WD-40-dependent KIF21A cargo that requires KIF21A for anterograde axonal transport linked this motor to calcium homeostasis at presynaptic terminals.

    Evidence Co-immunoprecipitation, dominant-negative and siRNA experiments with live-cell NCKX2-GFP tracking and calcium imaging

    PMID:22442075

    Open questions at the time
    • Whether NCKX2 transport defects contribute to CFEOM unknown
    • Additional axonal cargoes not systematically identified
  6. 2013 High

    Reconstitution of KIF21A's microtubule growth-inhibitory activity in vitro, combined with demonstration that CFEOM1 mutations relieve autoinhibition and cause growth-cone accumulation, unified the transport and cytoskeletal regulation functions and provided the first mechanistic disease model.

    Evidence In vitro microtubule dynamics assays, TIRF microscopy, KANK1-dependent cortical recruitment, primary neuron assays with CFEOM1 mutants

    PMID:24120883

    Open questions at the time
    • Structural basis of autoinhibition not yet resolved
    • Relative contribution of growth inhibition vs. cargo transport to CFEOM unclear
  7. 2014 High

    A knockin mouse carrying the commonest human CFEOM1 mutation recapitulated oculomotor axon stalling and growth-cone defects, confirming the gain-of-function mechanism in vivo and identifying MAP1B as an interacting partner whose loss phenocopies CFEOM.

    Evidence Knockin mouse model with axon tracing and growth-cone morphology; co-immunoprecipitation for MAP1B; Map1b-null mouse phenotyping

    PMID:24656932

    Open questions at the time
    • How MAP1B functionally intersects KIF21A autoinhibition unknown
    • Whether MAP1B interaction is direct or bridged not resolved
  8. 2016 High

    The crystal structure of the KIF21A stalk regulatory domain revealed an antiparallel coiled-coil fold whose disruption by CFEOM1 mutations weakens motor-domain binding, providing the atomic-level explanation for disease-associated hyperactivation.

    Evidence Crystal structure, analytical ultracentrifugation, in vitro binding assays with disease-mimicking mutations

    PMID:27485312

    Open questions at the time
    • Full-length structure of autoinhibited KIF21A not available
    • Dynamics of autoinhibition relief in vivo uncharacterized
  9. 2017 High

    High-resolution crystal structures of KANK1 and KANK2 ankyrin domains complexed with a short KIF21A peptide defined the cortical recruitment interface at atomic detail, showing a supramodule recognition mechanism conserved across KANK family members.

    Evidence Crystal structures (2.1 Å for KANK1·KIF21A; separate KANK2·KIF21A structure), mutagenesis disrupting binding and focal-adhesion recruitment

    PMID:29158259 PMID:29183992 PMID:29217769

    Open questions at the time
    • How KANK-mediated cortical anchoring coordinates with autoinhibition release unknown
    • Whether all KANK family members equally recruit KIF21A in vivo untested
  10. 2021 High

    Discovery that a nephrotic syndrome-associated KANK2 mutation allows eIF4A1 to competitively displace KIF21A from the shared binding site demonstrated that the KANK–KIF21A axis operates in podocyte adhesion and can be pathologically disrupted by heterologous competitors.

    Evidence Structural analysis, competitive binding assays, co-immunoprecipitation, KANK2-knockout podocyte rescue

    PMID:34274317

    Open questions at the time
    • Whether KIF21A loss per se drives podocyte pathology or acts through KANK2 dysfunction unresolved
  11. 2023 High

    Identification of KIF21A in dendritic spines and demonstration that the KIF21A–KANK1 axis drives spine morphogenesis, LTP, and cognitive function extended the motor's role from axonal guidance to postsynaptic plasticity.

    Evidence shRNA knockdown in primary neurons and rat hippocampus in vivo, rescue with binding-deficient mutants, electrophysiology, behavioral assays

    PMID:38767486

    Open questions at the time
    • Cargo transported by KIF21A into spines not identified
    • Whether microtubule growth inhibition or transport underlies spine effects unknown
  12. 2023 Medium

    Zebrafish loss-of-function showed KIF21A is required in podocytes for foot process formation and slit diaphragm integrity, establishing an in vivo role in glomerular filtration.

    Evidence Zebrafish knockout, electron microscopy of foot processes, proteinuria assay

    PMID:37932480

    Open questions at the time
    • Not replicated in mammalian kidney models
    • Molecular mechanism of podocyte foot process regulation by KIF21A unclear
  13. 2025 Medium

    A novel KIF21A coiled-coil variant that reduces TUBB3 binding defined a direct KIF21A–TUBB3 interaction and a distinct clinical phenotype (peripheral neuropathy, corpus callosum hypoplasia) outside classic CFEOM.

    Evidence Co-immunoprecipitation comparing mutant vs. reference KIF21A with TUBB3, protein modelling, clinical phenotyping

    PMID:39643435

    Open questions at the time
    • Single family; independent replication needed
    • Mechanism by which reduced TUBB3 binding alters neuronal development not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the full-length structure of autoinhibited KIF21A, the identity of dendritic-spine cargoes, the relative contributions of microtubule regulation versus transport to each tissue-specific phenotype, and whether KIF21A has catalytic or regulatory roles beyond its motor activity.
  • No full-length autoinhibited structure
  • Spine-specific cargo unknown
  • Relative contribution of growth inhibition vs. transport to axonal and podocyte phenotypes unresolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003774 cytoskeletal motor activity 3 GO:0008092 cytoskeletal protein binding 3
Localization
GO:0005829 cytosol 2 GO:0005856 cytoskeleton 2 GO:0005886 plasma membrane 2
Pathway
R-HSA-112316 Neuronal System 2 R-HSA-1266738 Developmental Biology 2 R-HSA-1852241 Organelle biogenesis and maintenance 2 R-HSA-9609507 Protein localization 2
Partners
BIG1KANK1KANK2MAP1BNCKX2TUBB3

Evidence

Reading pass · 15 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 KIF21A is a plus-end-directed kinesin motor protein containing seven WD-40 repeats; it localizes throughout neurons (axons and dendrites), whereas the paralog KIF21B is enriched specifically in dendrites, demonstrating a novel kinesin sorting mechanism in neurons. Identification of novel kinesin-like proteins, immunolocalization in neurons, domain architecture analysis The Journal of cell biology Medium 10225949
2003 Heterozygous missense mutations in KIF21A, predominantly in the third coiled-coil stalk domain, cause CFEOM1, identifying the stalk as critical for KIF21A function in oculomotor axis formation. Direct DNA sequencing of KIF21A in 45 CFEOM1 probands; mutation mapping to stalk domain Nature genetics High 14595441
2008 KIF21A physically interacts with BIG1 (brefeldin A-inhibited guanine nucleotide-exchange protein 1); the C-terminal WD-40 repeat tail of KIF21A interacts with the C-terminal region of BIG1. ARF1 activity modulates this interaction, and KIF21A depletion alters BIG1 distribution without changing intrinsic Golgi membrane protein distribution. LC-MS/MS of co-precipitated proteins, reciprocal co-immunoprecipitation, overexpression of full-length and fragment constructs, siRNA knockdown, immunofluorescence Proceedings of the National Academy of Sciences of the United States of America High 19020088
2009 KIF21A interacts with KANK1 via the third and fourth coiled-coil domains of KIF21A and the ankyrin-repeat domain of KANK1. CFEOM1 mutations (R954W, M947T) enhance heterodimer formation with wild-type KIF21A and increase KANK1 translocation to the membrane fraction, suggesting KIF21A regulates KANK1 subcellular distribution. Co-immunoprecipitation, subcellular fractionation, knockdown experiments Biochemical and biophysical research communications Medium 19559006
2012 KIF21A mediates anterograde axonal transport of NCKX2 via direct interaction between the intracellular loop of NCKX2 and the WD-40 repeat domain of KIF21A. Dominant-negative KIF21A or KIF21A knockdown inhibits axonal transport of NCKX2 and causes calcium dysregulation at axonal boutons. Co-immunoprecipitation, dominant-negative overexpression, siRNA knockdown, live-cell imaging of NCKX2-GFP transport, calcium imaging The Journal of neuroscience High 22442075
2013 KIF21A acts as a cortical microtubule growth inhibitor: in vitro it suppresses microtubule growth and inhibits catastrophes; in cells it restricts microtubule growth at the cell edge. KIF21A is recruited to the cortex by KANK1, which co-clusters with liprin-α1/β1 and LL5β-containing complexes. CFEOM1 mutations relieve autoinhibition of KIF21A motor activity, leading to enhanced KIF21A accumulation in axonal growth cones, aberrant axon morphology, and reduced responsiveness to inhibitory cues. In vitro microtubule dynamics assay, live-cell imaging, TIRF microscopy, co-immunoprecipitation, dominant-negative and overexpression constructs, primary neuron culture assays Developmental cell High 24120883
2014 CFEOM1 mutations in both the motor domain and third coiled-coil stalk of KIF21A attenuate autoinhibition (gain-of-function mechanism). Knockin mice with the most common human mutation develop CFEOM with oculomotor axon stalling, enlarged growth cones, excessive filopodia, and random trajectories. MAP1B was identified as a KIF21A-interacting protein, and Map1b-null mice also develop CFEOM. Knockin mouse model, axon tracing, growth cone morphology analysis, co-immunoprecipitation (KIF21A–MAP1B interaction), in vitro autoinhibition assays Neuron High 24656932
2016 The KIF21A stalk regulatory domain containing all CFEOM1-associated substitutions forms an intramolecular antiparallel coiled coil that inhibits the motor domain. CFEOM1 mutations disrupt the structural integrity of this antiparallel coiled coil or its autoinhibitory binding interface, reducing affinity for the motor domain and causing KIF21A hyperactivation. This regulatory mechanism is conserved in KIF21B, KIF7, and KIF27. Crystal structure of regulatory domain, in vitro binding assays, mutagenesis, analytical ultracentrifugation Scientific reports High 27485312
2017 Crystal structure of the KANK1 ankyrin repeat domain (ANKRD) in complex with a short KIF21A peptide at high resolution reveals that the ANKRD uses two distinct interfaces (combinatorial use) to recognize KIF21A. Mutations at either interface disrupt the KANK1–KIF21A interaction and block KIF21A recruitment to focal adhesions. Crystal structure (high-resolution), site-directed mutagenesis, biochemical binding assays, cellular immunofluorescence localization The Journal of biological chemistry High 29217769
2017 Crystal structure of the KANK1·KIF21A complex at 2.1 Å resolution reveals that a five-helix-bundle-capping domain immediately preceding the ANK repeats of KANK1 forms a structural and functional supramodule with its ANK repeats to bind an evolutionarily conserved KIF21A peptide. Cancer-associated missense mutations at the KANK1–KIF21A interface destabilize complex formation. Crystal structure (2.1 Å), biochemical binding assays, mutagenesis The Journal of biological chemistry High 29158259
2017 A stretch of ~22 amino acids in KIF21A is sufficient for binding to both KANK1 and KANK2 ankyrin domains. Structures of KIF21A peptide complexed with KANK1 and KANK2 ankyrin domains show KIF21A adopts helical conformations recognized by two distinct pockets of the ankyrin domain. Crystal structure of KIF21A peptide–KANK1 ANK domain and KIF21A peptide–KANK2 ANK domain complexes, site-directed mutagenesis, biochemical binding assays The Journal of biological chemistry High 29183992
2021 An NS-associated KANK2 mutation (S684F) induces abnormal binding of eIF4A1 to KANK2 at the physiological KIF21A-binding site; eIF4A1 can competitively displace KIF21A from this site. This pathological competition disrupts KANK2/KIF21A interaction and impairs focal adhesion and cell adhesion in podocytes. Structural analysis, competitive binding assays, co-immunoprecipitation, KANK2 knockout podocyte rescue experiments The Journal of biological chemistry High 34274317
2023 KIF21A localizes to a subset of dendritic spines in neurons; KIF21A-positive spines are larger and more structurally plastic. The KIF21A–KANK1 interaction is required for dendritic spine morphogenesis and synaptic plasticity; knockdown of either protein inhibits spine morphogenesis and dendritic branching, and hippocampal KIF21A knockdown impairs long-term potentiation and cognitive function in rats. Immunofluorescence, shRNA knockdown in primary neurons and in vivo rat hippocampus, rescue with wild-type vs. binding-deficient mutants, electrophysiology (LTP), behavioral assays Neural regeneration research High 38767486
2023 Kif21a localizes specifically to podocytes in the zebrafish glomerulus; its deficiency causes podocyte foot process effacement, altered slit diaphragm formation, and severe proteinuria, establishing a role for KIF21A in maintaining glomerular filtration barrier integrity. Zebrafish loss-of-function model, immunolocalization, electron microscopy (foot process morphology), functional proteinuria assay Scientific reports Medium 37932480
2025 A novel KIF21A variant (p.Leu664Pro) in the second coiled-coil domain causes decreased binding of KIF21A to TUBB3 (β-tubulin III) as demonstrated by co-immunoprecipitation, defining a KIF21A–TUBB3 interaction whose disruption produces peripheral neuropathy, corpus callosum hypoplasia, and strabismus without classic CFEOM. Co-immunoprecipitation (KIF21A p.Leu664Pro vs. reference with TUBB3 in vitro), protein structure modelling Journal of medical genetics Medium 39643435

Source papers

Stage 0 corpus · 49 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2003 Heterozygous mutations of the kinesin KIF21A in congenital fibrosis of the extraocular muscles type 1 (CFEOM1). Nature genetics 201 14595441
2013 CFEOM1-associated kinesin KIF21A is a cortical microtubule growth inhibitor. Developmental cell 152 24120883
1999 Novel dendritic kinesin sorting identified by different process targeting of two related kinesins: KIF21A and KIF21B. The Journal of cell biology 140 10225949
2014 Human CFEOM1 mutations attenuate KIF21A autoinhibition and cause oculomotor axon stalling. Neuron 94 24656932
2004 Identification of KIF21A mutations as a rare cause of congenital fibrosis of the extraocular muscles type 3 (CFEOM3). Investigative ophthalmology & visual science 74 15223798
2007 Three novel mutations in KIF21A highlight the importance of the third coiled-coil stalk domain in the etiology of CFEOM1. BMC genetics 41 17511870
2005 A novel KIF21A mutation in a patient with congenital fibrosis of the extraocular muscles and Marcus Gunn jaw-winking phenomenon. Archives of ophthalmology (Chicago, Ill. : 1960) 41 16157808
2021 Bi-allelic loss-of-function variants in KIF21A cause severe fetal akinesia with arthrogryposis multiplex. Journal of medical genetics 36 34740919
2012 KIF21A-mediated axonal transport and selective endocytosis underlie the polarized targeting of NCKX2. The Journal of neuroscience : the official journal of the Society for Neuroscience 30 22442075
2009 A major mutation of KIF21A associated with congenital fibrosis of the extraocular muscles type 1 (CFEOM1) enhances translocation of Kank1 to the membrane. Biochemical and biophysical research communications 30 19559006
2008 Novel and recurrent KIF21A mutations in congenital fibrosis of the extraocular muscles type 1 and 3. Archives of ophthalmology (Chicago, Ill. : 1960) 29 18332320
2008 Interaction of brefeldin A-inhibited guanine nucleotide-exchange protein (BIG) 1 and kinesin motor protein KIF21A. Proceedings of the National Academy of Sciences of the United States of America 28 19020088
2017 Structural insights into ankyrin repeat-mediated recognition of the kinesin motor protein KIF21A by KANK1, a scaffold protein in focal adhesion. The Journal of biological chemistry 24 29217769
2016 Structural basis for misregulation of kinesin KIF21A autoinhibition by CFEOM1 disease mutations. Scientific reports 23 27485312
2005 KIF21A gene c.2860C>T mutation in congenital fibrosis of extraocular muscles type 1 and 3. Molecular vision 20 15827546
2012 Spatiotemporal expression pattern of KIF21A during normal embryonic development and in congenital fibrosis of the extraocular muscles type 1 (CFEOM1). Gene expression patterns : GEP 19 22465342
2004 Mutation analysis of KIF21A in congenital fibrosis of the extraocular muscles (CFEOM) patients. Ophthalmic genetics 18 15621876
2023 TUBB3 and KIF21A in neurodevelopment and disease. Frontiers in neuroscience 17 37600020
2004 Mutation analysis of the KIF21A gene in an Indian family with CFEOM1: implication of CpG methylation for most frequent mutations. Ophthalmic genetics 17 15621877
2011 KIF21A novel deletion and recurrent mutation in patients with congenital fibrosis of the extraocular muscles-1. International journal of molecular medicine 16 21805025
2017 Structural analyses of key features in the KANK1·KIF21A complex yield mechanistic insights into the cross-talk between microtubules and the cell cortex. The Journal of biological chemistry 15 29158259
2017 Structural basis for the recognition of kinesin family member 21A (KIF21A) by the ankyrin domains of KANK1 and KANK2 proteins. The Journal of biological chemistry 15 29183992
2010 KIF21A mutations in two Chinese families with congenital fibrosis of the extraocular muscles (CFEOM). Molecular vision 14 21042561
2014 A novel de novo KIF21A mutation in a patient with congenital fibrosis of the extraocular muscles and Möbius syndrome. Molecular vision 13 24715754
2009 Germline Mosaicism for KIF21A Mutation (p.R954L) Mimicking Recessive Inheritance for Congenital Fibrosis of the Extraocular Muscles. Ophthalmology 13 19896199
2003 A Japanese family with FEOM1-linked congenital fibrosis of the extraocular muscles type 1 associated with spinal canal stenosis and refinement of the FEOM1 critical region. Neuromuscular disorders : NMD 13 12899874
2011 Lack of KIF21A mutations in congenital fibrosis of the extraocular muscles type I patients from consanguineous Saudi Arabian families. Molecular vision 10 21264235
2005 Recurrent mutation of the KIF21A gene in Japanese patients with congenital fibrosis of the extraocular muscles. Japanese journal of ophthalmology 10 16365788
2015 A rare case of congenital fibrosis of extraocular muscle type 1A due to KIF21A mutation with Marcus Gunn jaw-winking phenomenon. European journal of paediatric neurology : EJPN : official journal of the European Paediatric Neurology Society 9 26190014
2020 KIF21A pathogenic variants cause congenital fibrosis of extraocular muscles type 3. Ophthalmic genetics 8 33251926
2023 The interaction between KIF21A and KANK1 regulates dendritic morphology and synapse plasticity in neurons. Neural regeneration research 7 38767486
2012 KIF21A mRNA expression in patients with Down syndrome. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 7 22968744
2009 KIF21A variant R954W in familial or sporadic cases of CFEOM1. European journal of ophthalmology 7 19551685
2021 Nephrotic-syndrome-associated mutation of KANK2 induces pathologic binding competition with physiological interactor KIF21A. The Journal of biological chemistry 5 34274317
2013 Inherited KIF21A and PAX6 gene mutations in a boy with congenital fibrosis of extraocular muscles and aniridia. BMC medical genetics 5 23799907
2006 Mutation p.Arg954Trp of KIF21A causes congenital fibrosis of the extraocular muscles in a Chinese family. Yi chuan xue bao = Acta genetica Sinica 5 16939002
2017 Clinical characteristics of a KIF21A mutation in a Chinese family with congenital fibrosis of the extraocular muscles type 1. Medicine 4 28930843
2014 Maternal germline mosaicism of kinesin family member 21A (KIF21A) mutation causes complex phenotypes in a Chinese family with congenital fibrosis of the extraocular muscles. Molecular vision 4 24426772
2023 Phenotypic heterogeneity associated with KIF21A: Two new cases and review of the literature. American journal of medical genetics. Part A 3 37921537
2022 [Identification of a novel KIF21A gene mutation in a Chinese family with congenital fibrosis of the extraocular muscles]. [Zhonghua yan ke za zhi] Chinese journal of ophthalmology 3 35280030
2020 A 63-bp insertion in exon 2 of the porcine KIF21A gene is associated with arthrogryposis multiplex congenita. Animal genetics 3 32686171
2016 KIF21A mutation in two Chinese families with congenital fibrosis of the extraocular muscles type 1 and 3. Molecular medicine reports 3 27513105
2012 [R954 mutations in KIF21A gene in Chinese patients with congenital fibrosis of extraocular muscles]. [Zhonghua yan ke za zhi] Chinese journal of ophthalmology 3 23336411
2023 Kif21a deficiency leads to impaired glomerular filtration barrier function. Scientific reports 2 37932480
2018 KIF21A Gene c.2860C>T Mutation in CFEOM1A: The First Report from Iran. Avicenna journal of medical biotechnology 2 30555664
2013 Congenital fibrosis of extraocular muscle type 1A due to KIF21A mutation: first case report from Hong Kong. Hong Kong medical journal = Xianggang yi xue za zhi 2 23535681
2011 [Mutation analysis of KIF21A gene in a Chinese family with congenital fibrosis of the extraocular muscles type I]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 2 21983718
2025 KIF21A-associated peripheral neuropathy defined by impaired binding with TUBB3. Journal of medical genetics 1 39643435
2025 Case Report: autosomal dominant distal motor neuropathy as a new phenotype of KIF21A-related disorders. Frontiers in genetics 0 41282472