Affinage

KIF21A

Kinesin-like protein KIF21A · UniProt Q7Z4S6

Length
1674 aa
Mass
187.2 kDa
Annotated
2026-06-10
49 papers in source corpus 15 papers cited in narrative 15 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

KIF21A is a plus-end-directed, neuron-enriched kinesin-4 motor that couples anterograde axonal cargo transport with spatial control of microtubule growth at the cell cortex (PMID:10225949, PMID:24120883). Through its C-terminal WD-40 repeat domain it binds cargo, including the K+-dependent Na+/Ca2+ exchanger NCKX2, whose polarized axonal delivery and consequent calcium homeostasis at boutons depend on KIF21A motor activity (PMID:22442075). At the cell edge KIF21A acts as a microtubule growth inhibitor that suppresses polymerization and catastrophes, and is recruited to cortical microtubule attachment complexes by direct binding to the ankyrin-repeat domain of KANK1/KANK2 — an interaction resolved at high resolution showing a conserved ~22-residue KIF21A peptide engaging two pockets of the KANK ankyrin domain together with its capping supramodule (PMID:24120883, PMID:29217769, PMID:29158259, PMID:29183992). Motor activity is held in check by an intramolecular autoinhibitory mechanism in which the third coiled-coil stalk forms an antiparallel coiled coil that binds and represses the motor domain (PMID:27485312). Heterozygous missense mutations clustered in the motor domain and third stalk cause congenital fibrosis of the extraocular muscles type 1 (CFEOM1) by relieving this autoinhibition; a knockin mouse model reproduces the disease with oculomotor axon stalling, enlarged growth cones, and ectopic branching (PMID:14595441, PMID:24656932, PMID:27485312). KIF21A additionally interacts with MAP1B to regulate axonal cytoskeleton and with BIG1 to control membrane trafficking (PMID:19020088, PMID:24656932), and the KIF21A–KANK1 axis supports dendritic spine morphogenesis, synaptic plasticity, and glomerular podocyte architecture (PMID:38767486, PMID:37932480).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1999 Medium

    Established KIF21A as a plus-end-directed kinesin motor with a candidate cargo-binding module, distinguishing it from its dendrite-restricted paralog KIF21B.

    Evidence Subcellular localization by immunofluorescence and neuronal fractionation, motor domain characterization

    PMID:10225949

    Open questions at the time
    • No cargo identified at this stage
    • WD-40 cargo-binding role only proposed, not functionally tested
  2. 2003 High

    Linked KIF21A to human disease by showing heterozygous missense mutations clustered in the third coiled-coil stalk cause CFEOM1, implicating the stalk in oculomotor axon development.

    Evidence Direct DNA sequencing and mutation mapping across a 45-proband cohort

    PMID:14595441

    Open questions at the time
    • Molecular consequence of the mutations unknown
    • Did not establish gain- vs loss-of-function
  3. 2008 Medium

    Connected KIF21A to membrane trafficking by identifying BIG1 as a WD-40-domain partner whose distribution depends on KIF21A.

    Evidence Reciprocal endogenous Co-IP, LC-MS/MS, fragment overexpression, and siRNA with distribution readout

    PMID:19020088

    Open questions at the time
    • No direct transport assay of BIG1 by KIF21A
    • Single lab, mechanism of trafficking control unresolved
  4. 2009 Medium

    Identified KANK1 as a stalk-domain partner and showed CFEOM1 mutations enhance both KIF21A self-association and KANK1 membrane translocation, hinting at altered protein interactions in disease.

    Evidence Co-IP, subcellular fractionation, knockdown, and wild-type/mutant construct overexpression

    PMID:19559006

    Open questions at the time
    • Functional consequence of enhanced KANK1 translocation unclear
    • Did not yet define the autoinhibition framework
  5. 2012 High

    Defined a concrete cargo for KIF21A, showing it drives anterograde axonal transport of NCKX2 to control bouton calcium homeostasis.

    Evidence Co-IP with WD-40 domain mapping, dominant-negative, siRNA, and live-cell calcium/surface imaging in hippocampal neurons

    PMID:22442075

    Open questions at the time
    • Whether other cargoes use the same WD-40 interface unknown
    • Link between cargo transport and CFEOM not established
  6. 2013 High

    Reframed KIF21A as a cortical microtubule growth inhibitor recruited by KANK1, and showed CFEOM1 mutations are activating by relieving autoinhibition.

    Evidence In vitro TIRF microtubule dynamics reconstitution, live-cell imaging, Co-IP, knockdown, and CFEOM1 mutant expression in neurons

    PMID:24120883

    Open questions at the time
    • Structural basis of autoinhibition not yet defined
    • Mechanism of microtubule catastrophe suppression unresolved
  7. 2014 High

    Confirmed in vivo that CFEOM1 mutations are gain-of-function attenuating autoinhibition, producing oculomotor axon stalling, and identified MAP1B as a functionally relevant partner.

    Evidence Knockin mouse with axon tracing, yeast two-hybrid and Co-IP for MAP1B, and Map1b-null genetic epistasis

    PMID:24656932

    Open questions at the time
    • Molecular interface of MAP1B binding not mapped
    • How motor hyperactivity translates to axon stalling not fully resolved
  8. 2016 High

    Provided the structural mechanism of autoinhibition, showing the stalk regulatory domain forms an antiparallel coiled coil that binds and represses the motor, with CFEOM1 mutations disrupting this fold.

    Evidence X-ray crystallography of the regulatory domain, in vitro binding, and disease-residue mutagenesis

    PMID:27485312

    Open questions at the time
    • Dynamics of inhibition release in cells not directly visualized
    • Regulatory triggers for activation unknown
  9. 2017 High

    Resolved the structural basis of cortical recruitment, showing a conserved KIF21A peptide is bound by a KANK ankyrin-repeat supramodule via combinatorial interfaces shared by KANK1 and KANK2.

    Evidence Multiple high-resolution crystal structures of KANK1/KANK2 ANKRD–KIF21A peptide complexes, mutagenesis, biochemical binding, and focal-adhesion localization

    PMID:29158259 PMID:29183992 PMID:29217769

    Open questions at the time
    • How recruitment couples to motor activation not defined
    • Regulation of the interaction in neurons not addressed
  10. 2021 Medium

    Showed the KANK2–KIF21A interface is disease-relevant, as a nephrotic-syndrome KANK2 mutation competitively displaces KIF21A via aberrant eIF4A1 binding and fails to rescue adhesion defects.

    Evidence Structural and biochemical competitive binding analysis with KANK2-knockout podocyte rescue

    PMID:34274317

    Open questions at the time
    • KIF21A-side consequences of displacement not directly tested
    • Single lab, focused on the KANK2 mutant
  11. 2023 Medium

    Extended KIF21A function to dendritic spine plasticity and podocyte architecture, in both cases requiring the KANK-dependent adhesion linkage.

    Evidence shRNA knockdown with binding-mutant rescue, LTP electrophysiology and behavior in rat, and zebrafish loss-of-function with podocyte ultrastructure and proteinuria readouts

    PMID:37932480 PMID:38767486

    Open questions at the time
    • Whether spine and podocyte roles use the same cortical microtubule mechanism unknown
    • Molecular cargo at spines/foot processes not identified
  12. 2025 Low

    Suggested a mechanistically distinct disease axis, with a second coiled-coil variant reducing TUBB3 binding and causing peripheral neuropathy rather than CFEOM.

    Evidence Single Co-IP for TUBB3 binding, protein modelling, and clinical/genetic characterization of one case

    PMID:39643435

    Open questions at the time
    • Single Co-IP without reciprocal or functional validation
    • TUBB3-binding role of the second coiled coil not independently confirmed
    • Genotype-phenotype link rests on a single case

Open questions

Synthesis pass · forward-looking unresolved questions
  • How cortical recruitment, autoinhibition release, and cargo selection are temporally coordinated to direct distinct axonal, dendritic, and non-neuronal outcomes remains unresolved.
  • No unified model linking motor activation to specific cargo at specific sites
  • Upstream signals controlling autoinhibition release unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003774 cytoskeletal motor activity 2 GO:0008092 cytoskeletal protein binding 2 GO:0098772 molecular function regulator activity 2 GO:0140657 ATP-dependent activity 1
Localization
GO:0005886 plasma membrane 2 GO:0005829 cytosol 1 GO:0005856 cytoskeleton 1
Pathway
R-HSA-112316 Neuronal System 2 R-HSA-1266738 Developmental Biology 2 R-HSA-5653656 Vesicle-mediated transport 2
Partners
BIG1KANK1KANK2MAP1BNCKX2TUBB3
Complex memberships
KANK1-KIF21A cortical microtubule attachment complex

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 enriched in neurons; KIF21A protein localizes throughout neurons (cell bodies, axons, and dendrites), whereas the closely related KIF21B is highly enriched in dendrites. KIF21A contains a domain of seven WD-40 repeats proposed to be involved in cargo binding. Subcellular localization by immunofluorescence/neuronal fractionation; motor domain characterization The Journal of cell biology Medium 10225949
2003 Heterozygous missense mutations in KIF21A cause CFEOM1; six different mutations were identified in 44/45 probands, with primary mutational hotspots in the third coiled-coil stalk domain, establishing that the stalk domain plays a critical role in oculomotor axis formation. Direct DNA sequencing and mutation mapping across patient cohort Nature genetics High 14595441
2008 KIF21A interacts with BIG1 (brefeldin A-inhibited guanine nucleotide-exchange protein 1); the C-terminal tail of KIF21A (containing seven WD-40 repeats) interacts with the C-terminal region of BIG1. Depletion of KIF21A by siRNA altered BIG1 distribution without changing intrinsic Golgi membrane proteins, implicating KIF21A in BIG1-dependent membrane trafficking. Co-immunoprecipitation (reciprocal IP of endogenous proteins), LC-MS/MS, overexpression of fragments, siRNA knockdown with subcellular distribution readout Proceedings of the National Academy of Sciences of the United States of America Medium 19020088
2009 KIF21A interacts with KANK1 through its third and fourth coiled-coil stalk domains; the CFEOM1-associated mutations R954W and M947T enhance KIF21A heterodimer formation with wild-type KIF21A and also enhance binding to KANK1, leading to significantly increased translocation of KANK1 to the membrane fraction. Co-immunoprecipitation, subcellular fractionation, knockdown of KIF21A, overexpression of wild-type and mutant KIF21A constructs Biochemical and biophysical research communications Medium 19559006
2012 KIF21A is the anterograde motor responsible for polarized axonal transport of NCKX2 in hippocampal neurons; the intracellular loop of NCKX2 specifically interacts with the WD-40 repeat domain of KIF21A. Dominant-negative KIF21A or KIF21A knockdown inhibits NCKX2-GFP axonal transport and causes calcium dysregulation at axonal boutons. Co-immunoprecipitation (WD-40 domain interaction mapping), dominant-negative overexpression, siRNA knockdown, live-cell calcium imaging, live-cell immunocytochemistry of surface NCKX2 The Journal of neuroscience High 22442075
2013 KIF21A functions as an inhibitor of microtubule growth at the cell cortex: 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 cortical microtubule attachment complexes. CFEOM1 mutations relieve autoinhibition of the KIF21A motor, leading to enhanced KIF21A accumulation in axonal growth cones, aberrant axon morphology, and reduced responsiveness to inhibitory cues. In vitro microtubule dynamics assay (TIRF microscopy), live-cell imaging, co-immunoprecipitation, siRNA knockdown, overexpression of CFEOM1 mutants in neurons Developmental cell High 24120883
2014 CFEOM1-associated mutations in the motor domain and third coiled-coil stalk of KIF21A attenuate KIF21A 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 ectopic branching. MAP1B was identified as a KIF21A-interacting protein, and Map1b-null mice also develop CFEOM. Knockin mouse model, axon morphology/tracing analysis, yeast two-hybrid and co-immunoprecipitation for MAP1B interaction, genetic epistasis (Map1b-/- phenotype) Neuron High 24656932
2016 The KIF21A stalk regulatory domain containing all CFEOM1-associated substitutions forms an intramolecular antiparallel coiled coil that mediates autoinhibition by binding the motor domain. CFEOM1 mutations hyperactivate KIF21A either by disrupting structural integrity of the antiparallel coiled coil or by reducing its affinity for the motor domain. This regulatory mechanism is conserved in KIF21B, KIF7, and KIF27. X-ray crystallography of regulatory domain, in vitro binding assays, mutagenesis of disease-associated residues, motor domain interaction assays Scientific reports High 27485312
2017 Crystal structure of the KANK1 ankyrin repeat domain (ANKRD) in complex with a KIF21A peptide at high resolution reveals that target recognition involves combinatorial use of two interfaces on the ANKRD. Mutations in either interface disrupt the KANK1-KIF21A interaction and block recruitment of KIF21A to focal adhesions. X-ray crystallography, mutagenesis of binding interface residues, co-immunoprecipitation, cellular immunofluorescence localization The Journal of biological chemistry High 29217769
2017 Crystal structure of the KANK1·KIF21A complex at 2.1 Å resolution shows that a five-helix-bundle-capping domain immediately preceding the ANK repeats of KANK1 forms a structural and functional supramodule with the ANK repeats to bind an evolutionarily conserved peptide in the middle of KIF21A. Cancer-associated missense mutations in KANK1 located at this interface destabilize the complex. X-ray crystallography (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; in each complex structure, KIF21A adopts helical conformations upon binding and is recognized by two distinct pockets of the ankyrin domain. X-ray crystallography of KIF21A peptide with KANK1 and KANK2 ankyrin domains, site-directed mutagenesis, biochemical binding assays The Journal of biological chemistry High 29183992
2021 An NS-associated KANK2 mutation (S684F) induces pathological binding of eIF4A1 at the physiological KIF21A-binding site of KANK2, competitively displacing KIF21A. In mouse podocytes, the S684F KANK2 mutant interfered with the KANK2/KIF21A interaction via eIF4A1 binding and failed to rescue focal adhesion or cell adhesion defects caused by KANK2 knockout. Structural analysis, biochemical co-immunoprecipitation, competitive binding assays, KANK2 knockout podocyte rescue experiments The Journal of biological chemistry Medium 34274317
2023 KIF21A localizes to a subset of dendritic spines; KIF21A-positive spines are larger and more structurally plastic. The KIF21A–KANK1 interaction is required for dendritic spine morphogenesis, dendritic branching, and synaptic plasticity; knockdown of either KIF21A or KANK1 inhibits spine morphogenesis, and rescue requires the ability to bind both KANK1 (via KIF21A) and talin1 (via KANK1). KIF21A knockdown in rat hippocampus impairs LTP amplitude and cognitive performance. shRNA knockdown, rescue with binding-deficient mutants, immunofluorescence localization, LTP electrophysiology, behavioral (cognitive) testing Neural regeneration research Medium 38767486
2023 Kif21a localizes specifically to podocytes in the zebrafish glomerulus; Kif21a deficiency causes podocyte foot process effacement, altered slit diaphragm formation, and severe proteinuria (leaky glomerular filtration barrier), establishing a role for KIF21A in podocyte architecture and glomerular filtration. Zebrafish loss-of-function model, immunofluorescence localization, electron microscopy of podocyte ultrastructure, functional proteinuria assay Scientific reports Medium 37932480
2025 A novel KIF21A variant (p.Leu664Pro) in the second coiled-coil domain, distinct from the autoinhibitory third coiled-coil domain, shows decreased binding to TUBB3 by co-immunoprecipitation in vitro, causing peripheral neuropathy rather than CFEOM, indicating that disruption of the KIF21A–TUBB3 interaction defines a mechanistically distinct disease phenotype. Co-immunoprecipitation (KIF21A variant vs. TUBB3), protein structure modelling, clinical/genetic characterization Journal of medical genetics Low 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 153 24120883
1999 Novel dendritic kinesin sorting identified by different process targeting of two related kinesins: KIF21A and KIF21B. The Journal of cell biology 142 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 37 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 25 29217769
2023 TUBB3 and KIF21A in neurodevelopment and disease. Frontiers in neuroscience 23 37600020
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
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
2023 The interaction between KIF21A and KANK1 regulates dendritic morphology and synapse plasticity in neurons. Neural regeneration research 9 38767486
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
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

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