Affinage

NFASC

Neurofascin · UniProt O94856

Length
1347 aa
Mass
150.0 kDa
Annotated
2026-06-14
40 papers in source corpus 19 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

Neurofascin (NFASC) is an immunoglobulin-superfamily cell adhesion molecule that organizes the molecular architecture of myelinated axons, producing distinct isoforms through spatio-temporally regulated alternative splicing that serve separable roles at the node of Ranvier, paranode, and axon initial segment (AIS) (PMID:24719087, PMID:28900163). The glial isoform NF155 binds directly to a contactin-1/Caspr1 complex to assemble paranodal axoglial junctions; crystallography of the contactin-1–NF155 adhesion complex defines an Ig1–Ig4 horseshoe architecture that sets the characteristic ~7.4 nm paranodal spacing, with competing heterophilic and homophilic interfaces and glycosylation/splice differences tuning complex formation (PMID:36329006). Caspr controls this interaction by regulating contactin glycoform processing and surface transport during biosynthesis (PMID:14676309), and NF155 production depends on QKI-mediated splicing in oligodendrocytes, whose loss collapses axoglial junctions and causes demyelination (PMID:27053216); NF155 separately governs both correct myelin targeting and myelin sheath growth (PMID:31761670). The neuronal isoform NF186 traffics to the membrane and diffuses laterally until immobilized at the AIS through AnkyrinG, where it also recruits Kv7.3 (PMID:32903174), is endocytically concentrated to the AIS via the adaptor Doublecortin (PMID:22649224), maintains nodal complexes differentially in PNS versus CNS (PMID:24719087), and serves as the AIS receptor for gliomedin to direct chandelier-cell synapse formation (PMID:41260922). The embryonic isoform NF140 independently clusters Nav channels at nascent nodes and is re-expressed in demyelinated multiple sclerosis lesions (PMID:25653379). Biallelic loss-of-function NFASC variants that abolish or destabilize NF155 disrupt paranodal junctions and cause a neurodevelopmental disorder with central and peripheral demyelination (PMID:31501903, PMID:30850329). NFASC isoforms are also targets of pathogenic autoantibodies in autoimmune nodopathies, where IgG4 antibodies against an NF155 Fn3–Fn4 epitope block paranodal assembly without complement activation, whereas IgG3 pan-neurofascin antibodies fix complement and are cytotoxic (PMID:30869655, PMID:40129269, PMID:36346134).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2003 High

    Established that paranodal assembly is gated upstream of NF155 binding by Caspr-dependent control of contactin maturation, explaining how the adhesion partner is licensed for surface engagement.

    Evidence Cell-based binding assays, co-expression, endoglycosidase H treatment, and Caspr knockout mice with biochemical fractionation

    PMID:14676309

    Open questions at the time
    • Did not resolve the structural basis of the NF155-contactin contact
    • Did not address how the complex achieves defined paranodal geometry
  2. 2005 Medium

    Distinguished opposing cell-biological activities of the two major isoforms, mapping NF155 adhesion/neurite outgrowth to an RGD motif and NF186 anti-adhesive activity to its mucin-like domain.

    Evidence Fc fusion protein binding, cell adhesion and neurite outgrowth assays with domain-deletion and RGD-mutant constructs

    PMID:16061393

    Open questions at the time
    • Single-study domain mapping not confirmed in vivo
    • RGD-mediated partner identity not defined
  3. 2012 High

    Identified a trafficking mechanism for AIS enrichment of neurofascin, showing DCX acts as an endocytic adaptor clearing somatodendritic neurofascin independently of its microtubule role.

    Evidence Live imaging and surface-distribution assays in cultured rat neurons with DCX microtubule and patient-allele (G253D) mutants

    PMID:22649224

    Open questions at the time
    • Molecular bridge between DCX and the endocytic machinery not defined
    • Relationship to AnkyrinG immobilization not addressed
  4. 2014 High

    Defined NF186 as a maintenance factor with PNS/CNS-distinct dependencies, showing nodal complex proteins are differentially destabilized while Nav channels partially persist.

    Evidence Inducible neuronal-specific conditional knockout mice with immunofluorescence and electrophysiology

    PMID:24719087

    Open questions at the time
    • Mechanism underlying differential PNS vs CNS protein stability unresolved
    • Did not separate nodal from paranodal contributions
  5. 2015 High

    Revealed a developmentally expressed NF140 isoform capable of independently clustering Nav channels and re-expressed in MS lesions, expanding isoform-specific node assembly mechanisms.

    Evidence Immunostaining of KO and WT mouse nerves, electrophysiology, and human MS postmortem tissue staining

    PMID:25653379

    Open questions at the time
    • Partner that recruits NF140 to nascent nodes not identified
    • Functional consequence of MS-lesion re-expression unknown
  6. 2016 High

    Linked NF155 isoform production to glial RNA processing, establishing QKI-dependent alternative splicing as required for axoglial junction integrity.

    Evidence Conditional (Olig2-Cre, inducible PLP-CreERT) knockout mice with immunostaining and splicing analysis

    PMID:27053216

    Open questions at the time
    • Direct QKI binding sites on Nfasc pre-mRNA not mapped
    • Whether QKI regulates other myelin transcripts contributing to phenotype not isolated
  7. 2017 Medium

    Demonstrated activity-dependent, Rbfox-controlled isoform switching, connecting neuronal depolarization to a shift from NF140 to NF186 splicing.

    Evidence RT-PCR splicing analysis, depolarization experiments in cerebellar granule cells, Rbfox manipulation

    PMID:28900163

    Open questions at the time
    • Single-lab finding
    • Signaling pathway coupling depolarization to splicing not defined
  8. 2017 Medium

    Extended NFASC function beyond myelinated axons by implicating it in NSCLC cell motility and actin cytoskeletal remodeling.

    Evidence siRNA knockdown in four NSCLC cell lines with migration assays and actin staining

    PMID:28418179

    Open questions at the time
    • Isoform responsible not specified
    • Molecular link to actin regulation not established
  9. 2019 High

    Resolved the trafficking-to-immobilization itinerary of NF186, showing vesicular delivery, bidirectional lateral diffusion, and AnkyrinG-dependent capture at the AIS that co-recruits Kv7.3.

    Evidence Live imaging, FRAP, and single-molecule surface diffusion tracking in neurons

    PMID:32903174

    Open questions at the time
    • Trigger that initiates AnkyrinG capture not defined
    • Relationship to DCX-mediated somatodendritic clearance not integrated
  10. 2019 High

    Established NFASC as a Mendelian disease gene, with biallelic loss-of-function variants abolishing NF155–CNTN1/Caspr1 binding and causing a neurodevelopmental disorder with central and peripheral demyelination.

    Evidence Exome/genome sequencing across families, patient tissue immunostaining, cell aggregation assays, plus iPSC-neuron protein-stability analysis of a transmembrane variant

    PMID:30850329 PMID:31501903

    Open questions at the time
    • Genotype-phenotype correlation across variant classes incomplete
    • No therapeutic rescue demonstrated
  11. 2019 High

    Dissected NF155's glial role into two separable functions, preventing mistargeting of myelin to neuronal somata and promoting sheath growth, with only the growth function requiring Caspr.

    Evidence Zebrafish genetic screen, complementary mouse knockout analyses, and time-lapse live imaging

    PMID:31761670

    Open questions at the time
    • Caspr-independent targeting partner not identified
    • Signaling downstream of NF155 driving growth not defined
  12. 2019 High

    Defined the pathogenic mechanism of anti-NF155 IgG4 autoantibodies as blockade of paranodal complex assembly with reduced NF155 levels, without competing with contactin-1/Caspr1 binding or driving internalization.

    Evidence Passive transfer in neonates, chronic intrathecal infusion in adults, nerve conduction studies, immunofluorescence, cell aggregation assays; plus a low-confidence single-patient anti-Caspr1 IgG4 study

    PMID:30869655 PMID:31753915

    Open questions at the time
    • Precise molecular step blocked by antibody not pinpointed at the time
    • Anti-Caspr1 finding limited to a single patient
  13. 2022 High

    Provided the structural basis for paranodal geometry, with crystal structures showing the contactin-1–NF155 Ig1–Ig4 horseshoe sets ~7.4 nm spacing and competing homophilic/heterophilic interfaces tuned by glycosylation and splicing.

    Evidence X-ray crystallography, biophysical binding assays, and cell-clustering assays

    PMID:36329006

    Open questions at the time
    • Caspr1 contribution to the structural complex not visualized
    • In vivo confirmation of competing interface usage absent
  14. 2023 High

    Mechanistically separated autoantibody pathogenicity by subclass, showing IgG3 pan-neurofascin antibodies fix complement and are cytotoxic whereas IgG4 NF155 antibodies act without complement.

    Evidence Myelinating DRG co-cultures, complement binding and cytotoxicity assays, ELISA, cell-based assays

    PMID:36346134

    Open questions at the time
    • In vivo correlation of complement effects with clinical severity not established
    • Access of antibodies to intact nodes in vivo not fully resolved
  15. 2025 High

    Localized the dominant anti-NF155 IgG4 epitope to the Fn3–Fn4 region, requiring both domains together and explaining isoform selectivity since none reacted with NF186.

    Evidence Flow-cytometric cell-based assay with NF155 truncation variants in HEK293 across 104 patients, with Western blotting

    PMID:40129269

    Open questions at the time
    • Structural map of how the Fn3-Fn4 epitope relates to the contactin-binding interface not provided
    • Why this epitope is immunogenic unknown
  16. 2025 Medium

    Characterized the nanoscale structural pathology of pan-neurofascin nodopathy, showing reduced NF155/Caspr-1 and NF186 density with preserved colocalization and sodium channel distribution, indicating potentially reversible adhesion loss.

    Evidence dSTORM super-resolution imaging of sural nerve biopsy teased fibers

    PMID:40051618

    Open questions at the time
    • Single-patient biopsy
    • Reversibility inferred structurally, not demonstrated functionally
  17. 2026 High

    Identified an inhibitory-circuit role for AIS NF186, showing it is required for chandelier-cell axon cartridge development with gliomedin serving as the intercellular receptor.

    Evidence Conditional NF186 deletion in pyramidal neurons, immunostaining, synaptic connectivity analysis

    PMID:41260922

    Open questions at the time
    • Downstream signaling driving cartridge assembly not defined
    • Whether gliomedin engagement at the AIS and at nodes uses identical machinery unclear

Open questions

Synthesis pass · forward-looking unresolved questions
  • How activity-dependent splicing, isoform-specific trafficking, and adhesion-complex geometry are coordinately controlled across development and disease remains unresolved.
  • No integrated model linking splicing regulators, trafficking adaptors, and structural assembly
  • Mechanism of reversibility in autoimmune nodopathy not established
  • Cancer-related NFASC function mechanistically uncharacterized

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098631 cell adhesion mediator activity 3 GO:0005198 structural molecule activity 2 GO:0008092 cytoskeletal protein binding 2
Localization
GO:0005886 plasma membrane 3 GO:0005856 cytoskeleton 1
Pathway
R-HSA-112316 Neuronal System 3 R-HSA-1266738 Developmental Biology 3 R-HSA-1643685 Disease 2 R-HSA-168256 Immune System 2
Partners
ANK3CASPR1CNTN1DCXGLDNKCNQ3NRCAM
Complex memberships
axon initial segment AnkyrinG complexnode of Ranvier nodal complexparanodal axoglial junction (NF155-contactin-1-Caspr1)

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2003 NF155 binds directly to contactin, but coexpression of Caspr inhibits this interaction by associating with contactin during biosynthesis and promoting a low-molecular-weight, endoglycosidase H-sensitive isoform of contactin at the cell membrane that cannot bind NF155. Deletion of Caspr in mice shifts contactin from the LMw to HMw glycoform, confirming Caspr regulates contactin processing and transport to the cell surface. Cell-based binding assays, co-expression studies, endoglycosidase H treatment, Caspr knockout mice with biochemical fractionation The Journal of cell biology High 14676309
2005 NF155 promotes neural cell adhesion and neurite outgrowth, and the RGD motif in its third FnIII repeat is critical for cell spreading and neurite outgrowth. Conversely, NF186 inhibits cell adhesion and neurite outgrowth, with inhibition associated with its mucin-like domain. Fc fusion protein binding assays, cell adhesion assays, neurite outgrowth assays with domain-deletion and RGD-mutant constructs Molecular and cellular neurosciences Medium 16061393
2012 Doublecortin (DCX) promotes endocytosis of neurofascin from soma and dendrites, thereby increasing neurofascin accumulation at the axon initial segment. This endocytic adaptor function is independent of DCX's microtubule-binding activity, and the patient allele DCX-G253D retains microtubule binding but is deficient in promoting neurofascin endocytosis. Live imaging and surface distribution assays in cultured rat neurons, DCX mutant constructs (microtubule-binding mutants, patient allele G253D), endocytosis assays The Journal of neuroscience High 22649224
2014 Inducible ablation of neuronal Neurofascin (Nfasc186) in adult mice causes >99% loss at PNS nodes and 94% loss at CNS nodes. Gliomedin and NrCAM at PNS nodes and brevican at CNS nodes are largely lost, Nav channels persist at nodes with ~40% reduction, and there is a 38% reduction in PNS conduction velocity. Loss of Nfasc186 also provokes CNS paranodal disorganization. This establishes distinct roles for Nfasc186 in node maintenance in PNS vs. CNS. Inducible conditional knockout mice (neuronal-specific Nfasc ablation), immunofluorescence, electrophysiology The Journal of neuroscience High 24719087
2015 Nfasc140 is a neuronal isoform strongly expressed during mouse embryonic development that can cluster voltage-gated sodium channels (Nav) at the developing node of Ranvier and restore electrophysiological function independently of Nfasc155 and Nfasc186. Nfasc140 is re-expressed in demyelinated white matter lesions of multiple sclerosis postmortem brain tissue. Immunostaining of knockout and wild-type mouse nerves, electrophysiology, human MS postmortem tissue immunostaining The Journal of neuroscience High 25653379
2016 The QKI RNA-binding proteins in oligodendrocytes regulate alternative splicing of the Nfasc gene to produce the Nfasc155 isoform. Deletion of QKI in oligodendrocytes results in loss of Nfasc155 and deterioration of axoglial junctions in the spinal cord, leading to demyelination and paralysis. Conditional knockout mice (Olig2-Cre and inducible PLP-CreERT), immunostaining, RNA splicing analysis The Journal of neuroscience High 27053216
2017 Alternative splicing of Nfasc is spatio-temporally regulated in cerebellar neurons. High K+-induced depolarization triggers a shift from Nfasc140 to Nfasc186 splicing in cerebellar granule cells. The neural RNA-binding protein Rbfox controls isoform selection at exons 26–29. RT-PCR splicing analysis in mouse brain, depolarization experiments in cerebellar granule cells, Rbfox functional assays Scientific reports Medium 28900163
2017 NFASC silencing in non-small cell lung cancer (NSCLC) cell lines decreased cell migration and caused morphological changes including rearrangements of the actin cytoskeleton and changes in F-actin networks in migrating cells, without affecting proliferation or viability. This identifies NFASC as a regulator of NSCLC cell motility. siRNA knockdown in four NSCLC cell lines, migration assays, actin cytoskeleton staining Molecular carcinogenesis Medium 28418179
2019 Patient-derived anti-Nfasc155 IgG4 antibodies target Nfasc155 on Schwann cell surface, reduce Nfasc155 protein levels, and prevent paranodal complex formation in neonatal animals without inhibiting Nfasc155 binding to contactin-1/CASPR1 or inducing target internalization. Chronic intrathecal infusion in adult animals induces loss of Nfasc155, paranodal specialization disruption, and conduction alterations in motor nerves. Passive transfer experiments in neonatal animals, chronic intrathecal infusion in adult animals, immunofluorescence, nerve conduction studies, cell aggregation assays The Journal of clinical investigation High 30869655
2019 Biallelic loss-of-function variants in NFASC (including a frameshift causing absent Nfasc155 expression and missense variants reducing expression) severely impair Nfasc155–CNTN1/CASPR1 complex interaction in cell aggregation assays, disrupt paranodal junction morphology in myelinated fibers of affected individuals, and cause neurodevelopmental disorder with central and peripheral demyelination. Exome/genome sequencing, immunostaining of patient myelinated fibers, cell aggregation assays, expression studies Brain High 31501903
2019 Anti-Caspr1 IgG4 antibodies can penetrate paranodal regions and disrupt the integrity of the Nfasc155/CNTN1/Caspr1 complex, as shown by intraneural injection and immunohistochemistry on skin biopsy of a single patient. Immunohistochemistry on skin biopsy, intraneural injection, cell aggregation assay Neurology(R) neuroimmunology & neuroinflammation Low 31753915
2019 A homozygous p.V1122E mutation in NFASC affecting a conserved transmembrane domain residue leads to significant loss of Neurofascin protein in iPSC-derived neurons from affected siblings, establishing this residue as critical for protein stability. iPSC-derived neurons from patients, immunostaining for Neurofascin protein levels Parkinsonism & related disorders Medium 30850329
2020 Neurofascin186 is transported to the soma and axon terminal via vesicles that fuse with the plasma membrane; after insertion, Nfasc186 is highly mobile in the axonal membrane and diffuses bidirectionally until immobilized at the axon initial segment through interaction with AnkyrinG. Kv7.3 is recruited to the AIS by the same mechanism. Live imaging (time-lapse fluorescence microscopy), FRAP, surface diffusion tracking in neurons eLife High 32903174
2022 Crystal structures of the contactin 1–NF155 adhesion complex reveal that conserved Ig1–2 interfaces form competing heterophilic contactin 1–NF155 and homophilic NF155 complexes. The Ig1–Ig4 horseshoe structure of the complex defines the ~7.4 nm paranodal spacing. Post-translational glycosylation and splice differences modulate complex formation. Contactin 1 also forms low-affinity clusters through Ig3–6 interfaces. X-ray crystallography, biophysical binding assays, cell-clustering assays Nature communications High 36329006
2023 Anti-pan-neurofascin antibodies (recognizing all NF isoforms) have direct access to nodes of Ranvier in myelinating dorsal root ganglia co-cultures and impair paranode formation, cause destruction of paranodal architecture, and alter paranodal myelin and sensory neurons in a titre-dependent manner. IgG3 subclass pan-neurofascin antibodies bind complement and exert cytotoxic effects in vitro, distinct from IgG4 NF155 antibodies which do not activate complement. Myelinating DRG co-cultures, immunofluorescence, complement binding and cytotoxicity assays, ELISA, cell-based assays Brain High 36346134
2025 Super-resolution imaging (dSTORM) of anti-pan-neurofascin nodopathy nerve biopsy reveals decreased NF155 and Caspr-1 density at paranodes and decreased NF186 density at nodes with preserved colocalization of adhesion proteins and intact sodium channel distribution. Axonal beta-IV spectrin is altered only in severely damaged nodes, indicating largely preserved axonal integrity with potentially reversible decreases in nodal/paranodal adhesion proteins. dSTORM super-resolution fluorescence microscopy on sural nerve biopsy teased fibers Frontiers in immunology Medium 40051618
2025 The epitope for anti-NF155 IgG4 autoantibodies in autoimmune nodopathy patients is located in the Fn3-Fn4 region (third to fourth fibronectin type III domain) of NF155 but not in the Fn3 or Fn4 domains alone. Autoantibodies in 104/104 anti-NF155+ patients bound Fn3-Fn4, and none reacted with NF186. Flow cytometric cell-based assay with truncation variants of NF155 stably/transiently expressed in HEK293 cells, Western blotting Annals of clinical and translational neurology High 40129269
2026 NF186 at the axon initial segment (AIS) of pyramidal neurons is necessary for chandelier cells (ChCs) to develop synaptic axon cartridges along the AIS. Gliomedin, a known NF186 receptor at nodes of Ranvier, is preferentially expressed in ChCs and mediates ChC axon cartridge development by acting as a major receptor for NF186 at the AIS. Conditional knockout mice (NF186 deletion in pyramidal neurons), immunostaining, synaptic connectivity analysis The Journal of neuroscience High 41260922
2019 Oligodendrocyte Neurofascin (Nfasc155) regulates two independent aspects of CNS myelination: (1) it prevents mistargeting of myelin to neuronal cell bodies (myelin targeting), and (2) it promotes myelin sheath growth. Disruption of Caspr (the neuronal binding partner of oligodendrocyte Neurofascin) impairs myelin sheath growth but does not affect myelin targeting, indicating these two functions are separable. Genetic screen in zebrafish, complementary knockout analyses in mice, time-lapse live imaging Developmental cell High 31761670

Source papers

Stage 0 corpus · 40 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2019 Antibodies to neurofascin, contactin-1, and contactin-associated protein 1 in CIDP: Clinical relevance of IgG isotype. Neurology(R) neuroimmunology & neuroinflammation 148 31753915
2003 Caspr regulates the processing of contactin and inhibits its binding to neurofascin. The Journal of cell biology 125 14676309
2017 Neurofascin antibodies in autoimmune, genetic, and idiopathic neuropathies. Neurology 89 29187518
2019 Anti-Neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo. The Journal of clinical investigation 83 30869655
2012 Neurofascin: a switch between neuronal plasticity and stability. The international journal of biochemistry & cell biology 65 22306302
1997 Organization of the neurofascin gene and analysis of developmentally regulated alternative splicing. The Journal of biological chemistry 53 9353344
2021 IgG1 pan-neurofascin antibodies identify a severe yet treatable neuropathy with a high mortality. Journal of neurology, neurosurgery, and psychiatry 51 34400540
2023 Anti-pan-neurofascin antibodies induce subclass-related complement activation and nodo-paranodal damage. Brain : a journal of neurology 50 36346134
2019 Biallelic mutations in neurofascin cause neurodevelopmental impairment and peripheral demyelination. Brain : a journal of neurology 47 31501903
2014 Differential stability of PNS and CNS nodal complexes when neuronal neurofascin is lost. The Journal of neuroscience : the official journal of the Society for Neuroscience 44 24719087
2018 Anti-neurofascin autoantibody and demyelination. Neurochemistry international 42 30582947
2015 Neurofascin 140 is an embryonic neuronal neurofascin isoform that promotes the assembly of the node of Ranvier. The Journal of neuroscience : the official journal of the Society for Neuroscience 41 25653379
2021 Anti-Neurofascin 155 Antibody-Positive Chronic Inflammatory Demyelinating Polyneuropathy/Combined Central and Peripheral Demyelination: Strategies for Diagnosis and Treatment Based on the Disease Mechanism. Frontiers in neurology 40 34177770
2016 Quaking Regulates Neurofascin 155 Expression for Myelin and Axoglial Junction Maintenance. The Journal of neuroscience : the official journal of the Society for Neuroscience 40 27053216
2012 Doublecortin (DCX) mediates endocytosis of neurofascin independently of microtubule binding. The Journal of neuroscience : the official journal of the Society for Neuroscience 40 22649224
2019 Oligodendrocyte Neurofascin Independently Regulates Both Myelin Targeting and Sheath Growth in the CNS. Developmental cell 35 31761670
2005 Cell adhesion and neurite outgrowth are promoted by neurofascin NF155 and inhibited by NF186. Molecular and cellular neurosciences 34 16061393
2023 Clinical profile of autoimmune nodopathy with anti-neurofascin 186 antibody. Annals of clinical and translational neurology 28 37060203
2019 Neurofascin (NFASC) gene mutation causes autosomal recessive ataxia with demyelinating neuropathy. Parkinsonism & related disorders 21 30850329
2015 Contactin-1 and Neurofascin-155/-186 Are Not Targets of Auto-Antibodies in Multifocal Motor Neuropathy. PloS one 21 26218529
2017 Copy number variation, increased gene expression, and molecular mechanisms of neurofascin in lung cancer. Molecular carcinogenesis 20 28418179
2022 Structural insights into the contactin 1 - neurofascin 155 adhesion complex. Nature communications 19 36329006
2022 Clinical and diagnostic features of anti-neurofascin-155 antibody-positive neuropathy in Han Chinese. Annals of clinical and translational neurology 17 35313093
2023 Pan-Neurofascin autoimmune nodopathy - a life-threatening, but reversible neuropathy. Current opinion in neurology 16 37639464
2018 Association of neurofascin IgG4 and atypical chronic inflammatory demyelinating polyneuropathy: A systematic review and meta-analysis. Brain and behavior 16 30240176
2020 Neurofascin and Kv7.3 are delivered to somatic and axon terminal surface membranes en route to the axon initial segment. eLife 13 32903174
2017 Spatio-temporal and dynamic regulation of neurofascin alternative splicing in mouse cerebellar neurons. Scientific reports 13 28900163
2019 Intrathecal cytokine profile in neuropathy with anti-neurofascin 155 antibody. Annals of clinical and translational neurology 12 31657126
2018 Neurofascin and Compact Myelin Antigen-Specific T Cell Response Pattern in Chronic Inflammatory Demyelinating Polyneuropathy Subtypes. Frontiers in neurology 11 29615965
2023 Anti-rituximab antibodies in patients with refractory autoimmune nodopathy with anti-neurofascin-155 antibody. Frontiers in immunology 10 37056784
2014 Organisation and control of neuronal connectivity and myelination by cell adhesion molecule neurofascin. Advances in neurobiology 10 25300139
2024 Clinical Features of Autoimmune Nodopathy With Anti-Neurofascin-155 Antibodies in South Koreans. Journal of clinical neurology (Seoul, Korea) 9 38171501
2021 Neurofascin antibodies in chronic inflammatory demyelinating polyradiculoneuropathy: from intrinsic genetic background to clinical manifestations. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 5 33782779
2021 The prevalence of anti-neurofascin-155 antibodies in patients with neuromyelitis optica spectrum disorders. Clinical and experimental immunology 5 33998675
2024 Anti-neurofascin-155 antibody mediated a distinct phenotype of chronic inflammatory demyelinating polyradiculoneuropathy. Journal of neurology 4 38771386
2025 Super-resolution of nodal and paranodal disruption in anti-pan-neurofascin-associated autoimmune nodopathy. Frontiers in immunology 2 40051618
2025 Epitope Mapping of Anti-Neurofascin 155 Antibody in a Large Cohort of Autoimmune Nodopathy Patients. Annals of clinical and translational neurology 1 40129269
2025 Clinical characteristics of anti-neurofascin 155 antibody-positive autoimmune nodopathy in children. Pediatric investigation 1 40969295
2026 The Highly Localized Interaction between Neurofascin-186 and Gliomedin Promotes Subcellular Innervation by the Chandelier Cell. The Journal of neuroscience : the official journal of the Society for Neuroscience 0 41260922
2025 Clinical and Radiological Heterogeneity in Anti-Neurofascin-155 Autoimmune Nodopathy: A Case Series Analysis. Journal of the peripheral nervous system : JPNS 0 41236406

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