Affinage

NOS1AP

Carboxyl-terminal PDZ ligand of neuronal nitric oxide synthase protein · UniProt O75052

Length
506 aa
Mass
56.1 kDa
Annotated
2026-06-10
100 papers in source corpus 32 papers cited in narrative 33 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NOS1AP (CAPON) is a cytoplasmic adaptor protein that organizes neuronal nitric oxide synthase (nNOS/NOS1) signaling by competing with PSD95 for the nNOS PDZ domain and thereby tuning NMDA receptor-coupled NO output (PMID:9459447). The nNOS interaction is not a simple PDZ-motif contact: full-length NOS1AP forms an unusually stable heterodivalent interaction through both an internal ExF motif and the C-terminal PDZ ligand motif, whose concerted action efficiently excludes competing PDZ ligands from the nNOS binding pocket (PMID:25972165, PMID:28360833). Through its N-terminal PTB domain, NOS1AP scaffolds nNOS to additional partners that nucleate distinct downstream pathways: Dexras1, forming a ternary nNOS–CAPON–Dexras1 complex that enhances NO-mediated Dexras1 activation and ERK signaling (PMID:11086993, PMID:25129479); synapsins, which target nNOS to presynaptic sites (PMID:11867766); Scribble, which bridges NOS1AP to a β-Pix/Git1/PAK module and regulates Rac activity, dendritic protrusions, and the Lats1/YAP/TEAD axis (PMID:20357130, PMID:25918243); and MKK3, linking excitotoxic stimulation to p38MAPK activation and neuronal death (PMID:23658158). NOS1AP regulates dendrite outgrowth and spine morphology, with a central region (aa 181–307) binding carboxypeptidase E to control dendrite branching (PMID:19553464, PMID:26861996). Acute augmentation of the nNOS–CAPON interaction is pathogenic across neurological contexts—anxiety, ischemic stroke, amyloid-β toxicity, and neuropathic pain—and peptide disruptors of the complex are neuroprotective and behaviorally corrective (PMID:25129479, PMID:29319606, PMID:29577585, PMID:30727847). In the heart, NOS1AP co-localizes with NOS1 at the sarcoplasmic reticulum and intercalated discs, and through NOS1-dependent S-nitrosylation inhibits the L-type calcium channel to accelerate repolarization and shorten action potential duration; both overexpression and loss of NOS1AP are arrhythmogenic, the latter sensitizing cardiomyocytes to oxidative-stress-induced ventricular tachyarrhythmia (PMID:18337493, PMID:19800018, PMID:32061134, PMID:36352324, PMID:27170476). NOS1AP has been identified as a tau- and α-synuclein-interacting protein whose levels modulate tauopathy and synucleinopathy phenotypes (PMID:31160584, PMID:36012368).

Mechanistic history

Synthesis pass · year-by-year structured walk · 32 steps
  1. 1998 High

    Established NOS1AP's founding identity by showing it binds the nNOS PDZ domain and can displace PSD95, defining it as a competitive regulator of nNOS scaffolding.

    Evidence Co-immunoprecipitation and competition binding with overexpression in transfected cells

    PMID:9459447

    Open questions at the time
    • Did not resolve the binding determinants beyond the C-terminal motif
    • Functional consequence on NO output in neurons not addressed
  2. 2000 High

    Defined a downstream effector pathway by showing CAPON forms a ternary complex with nNOS and Dexras1, coupling NMDA-stimulated NO synthesis to small G-protein activation.

    Evidence Reciprocal Co-IP, ternary complex reconstitution, cortical neurons, nNOS-knockout mice

    PMID:11086993

    Open questions at the time
    • Did not map which CAPON domain binds Dexras1
    • Physiological readout of Dexras1 activation in vivo not established
  3. 2002 High

    Identified the PTB domain as a presynaptic targeting module by showing CAPON bridges nNOS to synapsins, with knockout altering nNOS localization.

    Evidence Co-IP with PTB domain mapping plus synapsin I/II double-knockout localization studies

    PMID:11867766

    Open questions at the time
    • Functional impact on presynaptic NO signaling not measured
  4. 2008 High

    Extended NOS1AP function to the heart by demonstrating it interacts with NOS1 and accelerates cardiac repolarization via L-type calcium channel inhibition.

    Evidence Co-IP and electrophysiology in isolated ventricular myocytes with CAPON overexpression

    PMID:18337493

    Open questions at the time
    • Molecular mechanism of channel inhibition (S-nitrosylation) not yet shown
    • Endogenous loss-of-function consequence not tested
  5. 2009 High

    Resolved cardiac subcellular organization, showing CAPON localizes with NOS1 at the sarcoplasmic reticulum and redistributes to caveolae after infarction, with NOS1 controlling CAPON abundance.

    Evidence Subcellular fractionation, Co-IP, dual immuno-gold EM, NOS1-knockout mice

    PMID:19800018

    Open questions at the time
    • Functional consequence of caveolar redistribution not established
  6. 2009 High

    Defined a non-canonical dendritic morphogenesis role by mapping dendrite branching to a central region binding carboxypeptidase E, distinct from the nNOS-binding domains.

    Evidence Deletion mutants, yeast two-hybrid, and cellular validation in cultured hippocampal neurons

    PMID:19553464

    Open questions at the time
    • Mechanism linking CPE binding to cytoskeletal remodeling unresolved
  7. 2010 High

    Connected NOS1AP to actin/polarity signaling by showing direct PTB-domain binding to Scribble, bridging to a β-Pix/Git1/PAK complex and regulating Rac and dendritic protrusions.

    Evidence Proteomic screen, direct binding assay, Co-IP, Rac activity assay in neurons

    PMID:20357130

    Open questions at the time
    • Whether nNOS participates in this complex not addressed
  8. 2010 Low

    Reported stimulus-dependent nuclear translocation of CAPON in astrocytes upon NO/NMDA stimulation, raising a possible nuclear function.

    Evidence Immunocytochemistry and Western blot with NO donors and MK801 in astrocytes

    PMID:20064573

    Open questions at the time
    • No functional consequence of nuclear localization established
    • Single lab, immunostaining-based observation
  9. 2011 Medium

    Extended Scribble-pathway involvement to cancer cell migration by placing NOS1AP in a SCRIB/VANGL1 complex required for polarity and motility.

    Evidence Mass spectrometry, confocal microscopy, shRNA knockdown with migration and growth assays in breast cancer cells

    PMID:22179838

    Open questions at the time
    • Single lab
    • Direct binding to VANGL1 vs indirect via Scribble not dissected
  10. 2011 Medium

    Linked CAPON to autonomic cardiovascular control by showing it is upregulated in the paraventricular nucleus during heart failure under Angiotensin II/AT1 signaling, contributing to sympathoexcitation.

    Evidence Western blot in CHF rat PVN, renal sympathetic nerve recording, losartan rescue, Ang II treatment in neuronal cells

    PMID:21831995

    Open questions at the time
    • Mechanism inferred from expression changes
    • Direct causal manipulation of CAPON in PVN not performed
  11. 2013 High

    Identified an excitotoxic death pathway by showing NOS1AP recruits MKK3 to nNOS to activate p38MAPK, with peptide disruption protective in hypoxia-ischemia.

    Evidence Co-IP, siRNA knockdown, cell-permeable competing peptide, rat neonatal hypoxia-ischemia model

    PMID:23658158

    Open questions at the time
    • Whether MKK3 binds the same domain as other partners not mapped
  12. 2014 High

    Demonstrated behavioral significance of the nNOS–CAPON interaction in anxiety, with bidirectional manipulation acting through Dexras1-ERK signaling.

    Evidence Viral overexpression and Tat-peptide disruption in mouse hippocampus, chronic mild stress, pathway analysis

    PMID:25129479

    Open questions at the time
    • Circuit-level locus of action beyond hippocampus not defined
  13. 2014 High

    Provided a human-genetic mechanistic link by showing an enhancer polymorphism increases NOS1AP expression and that NOS1AP at intercalated discs alters cardiomyocyte electrophysiology.

    Evidence Enhancer reporter assays, human genetics, localization by immunostaining, cardiomyocyte electrophysiology

    PMID:24857694

    Open questions at the time
    • Precise conduction mechanism at intercalated discs unresolved
  14. 2015 High

    Overturned the simple PDZ-motif model by demonstrating that an internal ExF motif, not the C-terminal PDZ ligand alone, is required for nNOS binding, with full-length NOS1AP forming a stable heterodivalent interaction.

    Evidence Multiple in vitro and cellular binding assays with mutagenesis of PDZ and ExF motifs, neuronal excitotoxicity assays

    PMID:25972165

    Open questions at the time
    • Structural basis of dual-motif engagement not solved
  15. 2015 Medium

    Connected NOS1AP to Hippo signaling by showing it promotes Lats1 and YAP phosphorylation, restraining TEAD activity and proliferation, with PTB-domain phospholipid recognition.

    Evidence Co-IP, siRNA, TEAD reporter and proliferation assays

    PMID:25918243

    Open questions at the time
    • Single lab
    • Direct vs Scribble-mediated effect on Lats1 not separated
  16. 2015 High

    Identified a sympathetic-neuron protective role, where CAPON upregulation enhances NOS1 activity and cGMP to reduce calcium currents and norepinephrine release, deficient in pre-hypertensive rats.

    Evidence Noradrenergic-specific viral overexpression in stellate ganglia, patch-clamp, calcium imaging, NOS1 activity and norepinephrine release assays

    PMID:25916729

    Open questions at the time
    • Whether CAPON loss drives hypertension causally not proven
  17. 2015 Medium

    Described a regulatory PTM by mapping O-GlcNAc sites on NOS1AP that stabilize nNOS binding and are protective against glutamate-induced apoptosis.

    Evidence Mass spectrometry site identification, mutagenesis, Co-IP, neuronal apoptosis assay

    PMID:26197318

    Open questions at the time
    • Enzyme responsible for site-specific modification not identified
    • Single lab
  18. 2016 Medium

    Defined cardiac calcium-handling function by showing NOS1AP silencing reduces calcium transients and S-nitrosylation, with selective co-localization to L-type calcium and Kir3.1 channels.

    Evidence siRNA knockdown, calcium imaging, S-nitrosylation assay, confocal co-localization in cardiac myocytes

    PMID:24665357

    Open questions at the time
    • Single lab
    • Causal nitrosylation targets beyond L-type channel not fully mapped
  19. 2016 Medium

    Showed dose-sensitivity of NOS1AP in dendritic spine plasticity, where overexpression produces aberrant filopodia-like protrusions dependent on nNOS PDZ interaction.

    Evidence Co-IP, overexpression of isoforms and deletion mutants, Sholl and spine analysis in primary neurons

    PMID:26861996

    Open questions at the time
    • Single lab
    • Endogenous role at physiological levels not isolated
  20. 2016 Medium

    Established loss-of-function cardiac vulnerability, showing Nos1ap-null mice are normal at baseline but highly arrhythmia-prone under oxidative stress, rescued by antioxidant.

    Evidence Nos1ap knockout mice, ECG/telemetry, echocardiography, optical mapping, calcium imaging, N-acetyl-cysteine rescue

    PMID:27170476

    Open questions at the time
    • Single lab
    • Molecular link between NOS1AP loss and oxidative sensitivity not fully resolved
  21. 2017 Medium

    Refined the binding mechanism by showing the ExF and PDZ motifs act concertedly to exclude competing ligands, with an additional structured element required for efficient competition.

    Evidence In vitro binding competition assays, mutagenesis, denaturation experiments with affinity measurement

    PMID:28360833

    Open questions at the time
    • Identity of the structured element not determined
    • No high-resolution structure
  22. 2018 Medium

    Demonstrated therapeutic disruption of nNOS-NOS1AP in neuropathic pain, with the TAT-GESV peptide reducing allodynia and p38-dependent p53 phosphorylation while sparing nNOS-PSD95.

    Evidence In vitro binding assay, rodent paclitaxel and nerve-ligation pain models, signaling readout

    PMID:29319606

    Open questions at the time
    • Peptide specificity relies on prior characterization
    • Single lab
  23. 2018 Medium

    Implicated NOS1AP in amyloid pathology by showing amyloid-β increases nNOS-CAPON interaction, with disruption rescuing memory via Dexras1 S-nitrosylation and ERK-CREB-BDNF signaling.

    Evidence Co-IP, proximity ligation assay, APP/PS1 mice, behavioral and dendritic readouts, pathway Western blots

    PMID:29577585

    Open questions at the time
    • Single lab
    • Causal sequence linking interaction to BDNF suppression not fully dissected
  24. 2019 High

    Identified CAPON as a tau-binding protein whose dosage bidirectionally controls tauopathy, with overexpression driving neuronal death and deficiency ameliorating pathology.

    Evidence IP/LC-MS tau interactome, AAV overexpression and knockout in tauopathy mice, histopathology and tau biochemistry

    PMID:31160584

    Open questions at the time
    • Whether tau binding depends on nNOS interaction not determined
    • Binding domain on CAPON not mapped
  25. 2019 High

    Demonstrated that nNOS-CAPON disruption promotes post-stroke recovery and dendritic/synaptic remodeling without altering infarct size, separating repair from initial injury.

    Evidence Co-IP, AAV and peptide/small-molecule disruption in two stroke models, behavior, Golgi staining, electrophysiology

    PMID:30727847

    Open questions at the time
    • Mechanism of dendritic remodeling downstream of disruption not detailed
  26. 2019 Medium

    Linked CAPON to depression by showing it is elevated in patient prefrontal cortex, interacts with spinophilin, and its knockdown reverses depression-like behavior.

    Evidence Postmortem immunohistochemistry, Co-IP in human brain, AAV knockdown with behavioral assays in mice

    PMID:30307500

    Open questions at the time
    • Single lab
    • Causal direction of spinophilin/synapsin changes not established
  27. 2021 High

    Provided patient-derived mechanistic evidence that NOS1AP risk alleles reduce NOS1 expression and co-localization, causing NOS1 loss-of-function electrophysiology and arrhythmia phenotype.

    Evidence hiPSC-CMs from LQT1 patients, guinea pig cardiomyocyte NOS1 inhibition, patch-clamp, calcium imaging, AP clamp

    PMID:32061134

    Open questions at the time
    • Allele-specific regulatory mechanism on NOS1 expression not fully resolved
  28. 2021 Medium

    Showed that excess nNOS-CAPON pairing recruits PSD-95, reduces spine density, and impairs social and working memory, defining a dose-dependent cognitive role.

    Evidence AAV overexpression in mouse hippocampus, Co-IP, Golgi spine analysis, behavioral testing

    PMID:34455393

    Open questions at the time
    • Single lab
    • Mechanism by which CAPON increases nNOS-PSD-95 binding unclear
  29. 2022 Medium

    Confirmed the cardiac S-nitrosylation mechanism in vivo, showing Nos1ap overexpression increases L-type channel nitrosylation, shortens APD, and is arrhythmogenic.

    Evidence Cardiac-specific transgenic mice, patch-clamp, optical mapping, ECG/telemetry, nitrosylation immunochemistry

    PMID:36352324

    Open questions at the time
    • Single lab
    • cGMP/ROS-independent nitrosylation route not mechanistically detailed
  30. 2022 Medium

    Placed NOS1AP downstream of TDP-43, showing it is a direct TDP-43 mRNA target controlling NMDA-receptor signaling and that NOS1AP modulation rescues TDP-43 pathology.

    Evidence Transcriptome analysis, Drosophila genetic rescue, primary cortical neuron NMDA signaling assays

    PMID:36267332

    Open questions at the time
    • Single lab
    • Relevance to human ALS/FTD pathology not established
  31. 2022 Low

    Reported that NOS1AP interacts with and co-aggregates with α-synuclein, implicating it in synucleinopathies.

    Evidence Bioinformatic prediction and overexpression in yeast and mammalian cells with co-aggregation assay

    PMID:36012368

    Open questions at the time
    • Direct binding not rigorously demonstrated
    • No in vivo validation
    • Aggregation shown only by overexpression
  32. 2022 Medium

    Localized cognitive function of the nNOS/NOS1AP interaction to the medial prefrontal cortex, with disruption selectively impairing social recognition and working memory.

    Evidence Stereotaxic AAV manipulation in mouse mPFC with construct controls and behavioral battery

    PMID:36513018

    Open questions at the time
    • Single lab
    • Downstream signaling in mPFC not dissected

Open questions

Synthesis pass · forward-looking unresolved questions
  • The high-resolution structural basis of the heterodivalent ExF/PDZ nNOS engagement and the identity of the additional structured element remain unresolved, as does whether the disease-relevant partners (tau, α-synuclein, MKK3) bind through shared or distinct surfaces.
  • No crystal/cryo-EM structure of NOS1AP–nNOS
  • Binding domains for tau and α-synuclein unmapped
  • Whether neuronal and cardiac functions share regulatory mechanisms unknown

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 6 GO:0098772 molecular function regulator activity 5 GO:0008289 lipid binding 1
Localization
GO:0005886 plasma membrane 3 GO:0005634 nucleus 1 GO:0005783 endoplasmic reticulum 1 GO:0005829 cytosol 1
Pathway
R-HSA-112316 Neuronal System 4 R-HSA-397014 Muscle contraction 4 R-HSA-162582 Signal Transduction 3 R-HSA-5357801 Programmed Cell Death 3
Partners
CPEDEXRAS1MAP2K3MAPTNOS1SCRIBSYN1YAP1
Complex memberships
SCRIB–VANGL1–NOS1AP complexScribble–β-Pix/Git1/PAK complexnNOS–CAPON–Dexras1 ternary complexnNOS–CAPON–synapsin I complex

Evidence

Reading pass · 33 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1998 CAPON (NOS1AP) was identified as a novel nNOS-associated protein that interacts with the nNOS PDZ domain through its C-terminus. CAPON competes with PSD95 for interaction with nNOS, and overexpression of CAPON results in loss of PSD95/nNOS complexes in transfected cells. Co-immunoprecipitation, transfection/overexpression in cells, competition binding assay Neuron High 9459447
2000 CAPON (NOS1AP) selectively interacts with Dexras1, a brain-enriched Ras-family small G protein, forming a ternary complex with nNOS and CAPON that enhances NO-mediated activation of Dexras1. NMDA receptor-stimulated NO synthesis activates Dexras1 in cortical neurons, and this activation is selectively reduced in nNOS-knockout mice. Co-immunoprecipitation, ternary complex reconstitution, cortical neuron experiments, nNOS-knockout mouse model Neuron High 11086993
2002 CAPON (NOS1AP) interacts with synapsins I, II, and III through an N-terminal phosphotyrosine-binding (PTB) domain interaction, forming a ternary complex comprising nNOS, CAPON, and synapsin I. Loss of synapsin I and II in double-knockout mice alters the subcellular localization of nNOS, demonstrating the functional importance of this complex for nNOS targeting to presynaptic sites. Co-immunoprecipitation, PTB domain binding assay, synapsin I/II double-knockout mouse localization studies Proceedings of the National Academy of Sciences of the United States of America High 11867766
2008 CAPON (NOS1AP) protein is expressed in the heart, interacts with NOS1, and accelerates cardiac repolarization by inhibition of the L-type calcium channel in ventricular myocytes. Protein expression analysis (Western blot), co-immunoprecipitation, electrophysiology in isolated ventricular myocytes with CAPON overexpression Proceedings of the National Academy of Sciences of the United States of America High 18337493
2009 NOS1AP (long isoform, NOS1AP-L) regulates dendrite outgrowth and branching in cultured hippocampal neurons. The middle region (amino acids 181–307), not the PDZ-binding or PTB domains, mediates this effect, and carboxypeptidase E (CPE) was identified as a binding partner for this middle region that mediates NOS1AP's effects on dendrite morphology. Overexpression/knockdown in cultured hippocampal neurons, NOS1AP deletion mutants, yeast two-hybrid screen, biochemical and cellular validation of CPE interaction The Journal of neuroscience : the official journal of the Society for Neuroscience High 19553464
2010 NOS1AP associates directly with Scribble through the NOS1AP PTB domain and the fourth PDZ domain of Scribble. Scribble bridges NOS1AP to a β-Pix/Git1/PAK complex. Overexpression of NOS1AP increases dendritic protrusions in a PTB domain-dependent manner, and both full-length NOS1AP and the PTB domain influence Rac activity. Proteomic screen, direct binding assay, co-immunoprecipitation, overexpression in neurons, Rac activity assay The Journal of neuroscience : the official journal of the Society for Neuroscience High 20357130
2011 NOS1AP forms a protein complex with SCRIB and VANGL1 along cellular protrusions in metastatic breast cancer cells. shRNA-mediated knockdown of NOS1AP slows breast cancer cell migration and prevents establishment of leading-trailing polarity; reduction of NOS1AP also enhances anchorage-independent growth. Mass spectrometry, confocal microscopy, shRNA knockdown, cell migration assay, anchorage-independent growth assay Oncogene Medium 22179838
2013 NOS1AP interacts with p38MAPK-activating kinase MKK3. Excitotoxic stimulation induces recruitment of NOS1AP to nNOS in rat cortical neurons. Excitotoxic activation of p38MAPK and subsequent neuronal death are reduced by competing with the nNOS:NOS1AP interaction or by NOS1AP siRNA knockdown. A cell-permeable peptide competing for nNOS:NOS1AP interaction doubles surviving tissue in a rat neonatal hypoxia-ischemia model. Co-immunoprecipitation, siRNA knockdown, cell-permeable competing peptide, in vivo rat hypoxia-ischemia model The Journal of neuroscience : the official journal of the Society for Neuroscience High 23658158
2014 Augmenting nNOS-CAPON interaction in mouse hippocampus by CAPON overexpression produces anxiogenic behaviors, while dissociating CAPON from nNOS by overexpressing truncated CAPON fragments or delivering Tat-CAPON-12C peptide produces anxiolytic effects. The mechanism involves Dexras1-ERK signaling downstream of nNOS-CAPON association. Viral overexpression in mouse hippocampus, behavioral assays (anxiety), chronic mild stress model, Dexras1-ERK signaling pathway analysis Nature medicine High 25129479
2014 A noncoding polymorphism (rs7539120) within an enhancer of NOS1AP affects cardiac function by increasing NOS1AP transcript expression. NOS1AP localizes to cardiomyocyte intercalated discs, and overexpression of NOS1AP in cardiomyocytes alters cellular electrophysiology. Enhancer reporter assays, human genetic and molecular genetic assays, NOS1AP localization by cellular fractionation/immunostaining, cardiomyocyte electrophysiology with overexpression American journal of human genetics High 24857694
2015 NOS1AP functionally associates with the transcriptional coactivator YAP. Silencing NOS1AP reduces phosphorylation of YAP and of the upstream kinase Lats1; conversely, NOS1AP expression promotes YAP and Lats1 phosphorylation, correlating with reduced TEAD activity and restricted cell proliferation. NOS1AP isoforms with a membrane-interacting PTB domain associate with Scribble and recognize acidic phospholipids. Co-immunoprecipitation (NOS1AP-YAP complex), siRNA silencing with YAP/Lats1 phosphorylation readout, TEAD reporter assay, cell proliferation assays Molecular and cellular biology Medium 25918243
2015 The interaction of NOS1AP with nNOS is not mediated solely by the classical C-terminal PDZ motif as previously assumed. The PDZ motif of NOS1AP is neither sufficient nor necessary for binding nNOS as measured by multiple methods; instead, a novel internal ExF motif is required for interaction. Full-length NOS1AP forms an unusually stable heterodivalent interaction with nNOS through both the ExF motif and the PDZ ligand motif. Multiple binding assays (in vitro and cellular), domain mapping, mutagenesis of PDZ and ExF motifs, cortical neuron excitotoxicity assays The Journal of neuroscience : the official journal of the Society for Neuroscience High 25972165
2016 NOS1AP overexpression in hippocampal and cortical neurons causes highly altered spine morphology and excessive growth of filopodia-like protrusions. Interaction with the NOS-I PDZ domain (confirmed by co-immunoprecipitation) contributes to these effects on dendritic spine plasticity. Co-immunoprecipitation, overexpression of NOS1AP isoforms and deletion mutants in primary cultured neurons, Sholl analysis, spine morphology quantification European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology Medium 26861996
2017 The concerted action of the ExF motif and PDZ ligand motif of NOS1AP efficiently excludes an alternate ligand from the nNOS PDZ ligand-binding pocket. An additional structured element (denaturable) contributes to the interaction; its denaturation selectively prevents the concerted action of the two motifs, resulting in ~30-fold reduction in competition with alternate PDZ ligands despite only ~3-fold drop in overall binding affinity. In vitro binding competition assays, mutagenesis of ExF and PDZ motifs, denaturation experiments with binding affinity measurements Frontiers in molecular neuroscience Medium 28360833
2018 TAT-GESV, a peptide inhibitor of the nNOS-NOS1AP complex, disrupts in vitro binding between nNOS and NOS1AP but not between nNOS and its upstream partner PSD95. Disruption of nNOS-NOS1AP interaction suppresses mechanical and cold allodynia in paclitaxel-induced and nerve ligation neuropathic pain models, and blocks paclitaxel-induced phosphorylation of p53 at Ser15 (a p38 MAPK substrate). In vitro binding assay, cortical neuron excitotoxicity assay, intrathecal peptide administration in rodent pain models, p38 MAPK substrate phosphorylation measurement Pain Medium 29319606
2018 Increased nNOS-CAPON interaction was detected after amyloid-β treatment in cultured neurons and in the hippocampus of APP/PS1 transgenic mice. Blocking nNOS-CAPON interaction rescued memory in 4-month-old APP/PS1 mice and ameliorated dendritic impairments. S-nitrosylation of Dexras1 and inhibition of the ERK-CREB-BDNF pathway were identified as downstream consequences of nNOS-CAPON interaction. Co-immunoprecipitation, proximity ligation assay, APP/PS1 mouse model, behavioral memory testing, dendritic spine analysis, Dexras1 S-nitrosylation measurement, ERK-CREB-BDNF pathway Western blot Aging cell Medium 29577585
2019 CAPON (NOS1AP) was identified as a novel tau-binding protein by immunoprecipitation/LC-MS screening. CAPON overexpression in AppNL-G-F/human-tau knock-in mice produced significant hippocampal atrophy, caspase3-dependent neuronal death, and higher levels of phosphorylated, oligomerized, and insoluble tau. CAPON deficiency ameliorated AD-related pathological phenotypes in a tauopathy model. Immunoprecipitation/LC-MS (tau interactome screen), AAV overexpression in transgenic mice, histopathology, tau biochemical fractionation, CAPON knockout in tauopathy model Nature communications High 31160584
2019 Stroke increases nNOS-CAPON association in the peri-infarct cortex during the delayed period. Inhibiting the ischemia-induced nNOS-CAPON association promotes functional recovery (reduced foot faults, forelimb asymmetry), facilitates dendritic remodeling (increased spine density, branching), and enhances synaptic transmission (increased mEPSC frequency), but does not affect neuronal loss or infarct size. Co-immunoprecipitation, AAV-mediated NOS1AP fragment overexpression, Tat-CAPON-12C and ZLc-002 peptide/small molecule in photothrombotic stroke and tMCAO mouse models, behavioral assessment, Golgi staining, electrophysiology Stroke High 30727847
2019 CAPON-immunoreactivity is increased in the DLPFC and anterior cingulate cortex in MDD patients, accompanied by upregulation of spinophilin and downregulation of synapsin. CAPON colocalizes with spinophilin in the DLPFC of MDD patients and interacts with spinophilin in human brain. Viral-mediated CAPON downregulation in mouse medial PFC reverses depression-like behaviors in CUMS mice. Immunohistochemistry in postmortem brain, co-immunoprecipitation (CAPON-spinophilin interaction in human brain), AAV-mediated knockdown in mouse PFC with behavioral assays Cerebral cortex (New York, N.Y. : 1991) Medium 30307500
2009 CAPON (NOS1AP) localizes with NOS1 in cardiac sarcoplasmic reticulum (SR) fractions; co-immunoprecipitation confirmed CAPON interaction with mu and alpha isoforms of NOS1 in whole heart lysates. Following myocardial infarction, CAPON and NOS1 redistribute to caveolae and colocalize with caveolin-3. In NOS1-deficient cardiomyocytes, CAPON abundance in the SR is reduced. CAPON also associates with xanthine oxidoreductase and plasma membrane calcium ATPase (PMCA) in infarcted hearts. Subcellular fractionation, co-immunoprecipitation, dual immuno-gold electron microscopy, NOS1-knockout mice Nitric oxide : biology and chemistry High 19800018
2011 In chronic heart failure (CHF), CAPON expression is augmented in the paraventricular nucleus (PVN), concomitant with decreased nNOS, disconnecting the NR1-nNOS link and contributing to enhanced sympathoexcitation. Angiotensin II type 1 receptor (AT1) antagonist losartan treatment normalizes CAPON and nNOS expression and reduces renal sympathetic nerve activity. Ang II directly increases CAPON expression in NG108 neuronal cells, reversed by AT1 blockade. Western blot in PVN of CHF rats, renal sympathetic nerve activity recording, losartan pharmacological intervention, Ang II treatment in neuronal cell culture Cardiovascular research Medium 21831995
2015 CAPON expression is significantly reduced in stellate ganglia of spontaneously hypertensive rats before development of hypertension. Targeted upregulation of CAPON using a noradrenergic-specific viral vector significantly upregulated NOS1 activity and cGMP, reduced neuronal calcium current (ICa) and intracellular calcium transients, and reduced norepinephrine release from atria. These effects were reversed by NOS1 inhibition. Viral vector (Ad.PRSx8-mCherry/CAPON) overexpression in stellate ganglia neurons, patch-clamp electrophysiology, calcium imaging, NOS1 activity assay, cGMP measurement, 3H-norepinephrine release assay Hypertension (Dallas, Tex. : 1979) High 25916729
2015 O-GlcNAc modification occurs on NOS1AP at Ser47, Ser183, Ser204, Ser269, and Ser271 (identified by mass spectrometry). O-GlcNAc modification levels of NOS1AP increase during glutamate-induced neuronal apoptosis. Mutation of O-GlcNAc sites decreases the interaction of NOS1AP with nNOS. Decreasing NOS1AP O-GlcNAc modification results in more severe neuronal apoptosis. Mass spectrometry (O-GlcNAc site identification), site-directed mutagenesis, co-immunoprecipitation, neuronal apoptosis assay International journal of molecular sciences Medium 26197318
2021 NOS1AP minor alleles (rs16847548 and rs4657139) are associated with reduced NOS1 expression, reduced NOS1AP-NOS1 co-localization in hiPSC-CMs from symptomatic LQT1 patients, and functional NOS1 loss of function (prolonged APD, enhanced ICaL, and perturbed calcium handling). In guinea pig cardiomyocytes, NOS1 inhibition prolonged APD, enhanced ICaL and INaL, slowed Ca2+ decay, and induced delayed afterdepolarizations, establishing a mechanistic link between NOS1AP variants and arrhythmia phenotype. hiPSC-CMs from LQT1 patients with different NOS1AP genotypes, guinea pig cardiomyocyte pharmacological NOS1 inhibition, patch-clamp electrophysiology, calcium imaging, action potential clamp Cardiovascular research High 32061134
2021 Hippocampal overexpression of NOS1AP markedly increased the interaction of nNOS with PSD-95, reduced dendritic spine density, and changed dendritic spine morphology at CA1 synapses. This produced behavioral impairment in social memory and spatial working memory. AAV overexpression in mouse hippocampus, co-immunoprecipitation (nNOS-PSD-95 interaction), Golgi staining and spine morphology analysis, behavioral testing EBioMedicine Medium 34455393
2022 NOS1AP mRNA is a direct TDP-43 target (identified by transcriptome analysis). TDP-43-mediated downregulation of NOS1AP expression strongly affects NMDA-receptor signaling in primary mouse cortical neurons. In Drosophila, modulation of NOS1AP alone can rescue TDP-43 pathology. Transcriptome analysis, Drosophila genetic rescue experiments, primary mouse cortical neuron NMDA-receptor signaling assays Brain communications Medium 36267332
2022 NOS1AP interacts with α-synuclein and forms detergent-resistant non-amyloid aggregates when overproduced. This interaction was demonstrated in yeast and mammalian cells, suggesting NOS1AP may be implicated in synucleinopathies. Bioinformatics aggregation prediction, overexpression in yeast and mammalian cells (detergent-resistant aggregate detection), co-aggregation assay with α-synuclein International journal of molecular sciences Low 36012368
2022 Cardiac-specific overexpression of Nos1ap in transgenic mice leads to increased L-type calcium channel nitrosylation (S-nitrosylation via NOS1), shortening of APD90, decreased QT interval duration, increased susceptibility to ventricular tachycardias, and reduced survival. Overexpression did not alter cGMP or ROS levels. Conditional transgenic mouse model with cardiac-specific Nos1ap overexpression, whole-cell patch-clamp, optical mapping, ECG/telemetry, immunochemistry for nitrosylation FEBS open bio Medium 36352324
2014 NOS1AP enhancer polymorphism rs7539120 increases NOS1AP transcript expression, and NOS1AP localizes to cardiomyocyte intercalated discs. Overexpression in cardiomyocytes leads to altered cellular electrophysiology, supporting a role for NOS1AP in cardiac electrical conductance and QT interval regulation through propagation defects. Enhancer reporter assay, immunostaining for intercalated disc localization, cardiomyocyte electrophysiology with NOS1AP overexpression American journal of human genetics Medium 24857694
2010 CAPON (NOS1AP) undergoes nuclear translocation in astrocytes stimulated with NO donors (SNP, GSNO) or NMDA receptor agonist; it localizes predominantly in the cytoplasm under basal conditions. nNOS co-localizes with CAPON in the nucleus of stimulated astrocytes. NMDA receptor antagonist MK801 reverses the nuclear localization of CAPON induced by SNP. Immunocytochemistry, real-time PCR, Western blot, pharmacological manipulation (NO donors, MK801) Neurochemistry international Low 20064573
2016 NOS1AP silencing in cardiac myocytes reduces electrically evoked calcium transient amplitude and degree of S-nitrosylation. NOS1AP shows high co-localization with the L-type calcium channel and inwardly rectifying potassium channel Kir3.1, low co-localization with RyR2, and no co-localization with connexin 43. NOS1AP is upregulated in dystrophic cardiomyopathy mice. siRNA knockdown, calcium imaging, S-nitrosylation assay, confocal co-localization microscopy, immunofluorescence/Western blot in dystrophic cardiomyopathy model International journal of physiology, pathophysiology and pharmacology Medium 24665357
2016 Nos1ap knockout mice develop normally but are highly susceptible to oxidative stress (doxorubicin)-induced ventricular tachyarrhythmias, QTc prolongation, impaired cardiac function (reduced fractional shortening), and increased mortality. Ex vivo optical mapping showed APD90 is prolonged at baseline and further lengthened by doxorubicin in Nos1ap-/- mice. Calcium transient amplitude is reduced in Nos1ap-/- cardiomyocytes after doxorubicin, and antioxidant N-acetyl-L-cysteine rescued these phenotypes. Nos1ap knockout mouse model, ECG/telemetry, echocardiography, ex vivo optical mapping, calcium imaging in isolated cardiomyocytes, pharmacological rescue with antioxidant International heart journal Medium 27170476
2022 Disruption of NOS1AP/nNOS interaction in the medial prefrontal cortex (by AAV overexpression of NOS1AP, NOS1AP396-503, or nNOS1-133) impairs social recognition and spatial working memory capacity in mice, without affecting anxiety, social interaction, or spatial reference memory. Stereotaxic AAV injection in mouse mPFC, comprehensive behavioral battery, genetic dissection of nNOS/NOS1AP/PSD-95 interactions European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology Medium 36513018

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1998 CAPON: a protein associated with neuronal nitric oxide synthase that regulates its interactions with PSD95. Neuron 307 9459447
2000 Dexras1: a G protein specifically coupled to neuronal nitric oxide synthase via CAPON. Neuron 272 11086993
2009 NOS1AP is a genetic modifier of the long-QT syndrome. Circulation 201 19822806
2010 Polymorphisms in the NOS1AP gene modulate QT interval duration and risk of arrhythmias in the long QT syndrome. Journal of the American College of Cardiology 133 20538168
2004 Linkage disequilibrium mapping of schizophrenia susceptibility to the CAPON region of chromosome 1q22. American journal of human genetics 127 15065015
2008 CAPON modulates cardiac repolarization via neuronal nitric oxide synthase signaling in the heart. Proceedings of the National Academy of Sciences of the United States of America 120 18337493
2007 Common NOS1AP variants are associated with a prolonged QTc interval in the Rotterdam Study. Circulation 119 17576865
2011 A protein complex of SCRIB, NOS1AP and VANGL1 regulates cell polarity and migration, and is associated with breast cancer progression. Oncogene 101 22179838
2002 Neuronal nitric-oxide synthase localization mediated by a ternary complex with synapsin and CAPON. Proceedings of the National Academy of Sciences of the United States of America 99 11867766
2015 Neuronal nitric oxide synthase (NOS1) and its adaptor, NOS1AP, as a genetic risk factors for psychiatric disorders. Genes, brain, and behavior 95 25612209
2005 Increased expression in dorsolateral prefrontal cortex of CAPON in schizophrenia and bipolar disorder. PLoS medicine 95 16146415
2014 CAPON-nNOS coupling can serve as a target for developing new anxiolytics. Nature medicine 88 25129479
2013 The nNOS-p38MAPK pathway is mediated by NOS1AP during neuronal death. The Journal of neuroscience : the official journal of the Society for Neuroscience 85 23658158
2012 Common variation in the NOS1AP gene is associated with drug-induced QT prolongation and ventricular arrhythmia. Journal of the American College of Cardiology 84 22682551
2019 Tau binding protein CAPON induces tau aggregation and neurodegeneration. Nature communications 81 31160584
2014 An enhancer polymorphism at the cardiomyocyte intercalated disc protein NOS1AP locus is a major regulator of the QT interval. American journal of human genetics 70 24857694
2010 NOS1AP associates with Scribble and regulates dendritic spine development. The Journal of neuroscience : the official journal of the Society for Neuroscience 62 20357130
2007 Associations between genetic variants in the NOS1AP (CAPON) gene and cardiac repolarization in the old order Amish. Human heredity 60 17565224
2009 Identification of a schizophrenia-associated functional noncoding variant in NOS1AP. The American journal of psychiatry 58 19255043
2009 NOS1AP regulates dendrite patterning of hippocampal neurons through a carboxypeptidase E-mediated pathway. The Journal of neuroscience : the official journal of the Society for Neuroscience 54 19553464
2009 Genetic variation in NOS1AP is associated with sudden cardiac death: evidence from the Rotterdam Study. Human molecular genetics 53 19643915
2014 Mechanisms of NOS1AP action on NMDA receptor-nNOS signaling. Frontiers in cellular neuroscience 51 25221472
2008 Identification of a common variant at the NOS1AP locus strongly associated to QT-interval duration. Human molecular genetics 49 18927126
2008 Association of NOS1AP genetic variants with QT interval duration in families from the Diabetes Heart Study. Diabetes 48 18235038
2011 Common variants in CASQ2, GPD1L, and NOS1AP are significantly associated with risk of sudden death in patients with coronary artery disease. Circulation. Cardiovascular genetics 46 21685173
2011 Decreased nNOS in the PVN leads to increased sympathoexcitation in chronic heart failure: role for CAPON and Ang II. Cardiovascular research 46 21831995
2009 Association of genetic variants of NOS1AP with type 2 diabetes in a Chinese population. Diabetologia 43 19937226
2017 Nitric oxide pathway genes (NOS1AP and NOS1) are involved in PTSD severity, depression, anxiety, stress and resilience. Gene 42 28465168
2005 CAPON expression in skeletal muscle is regulated by position, repair, NOS activity, and dystrophy. Experimental cell research 40 15561099
2008 NOS1AP in schizophrenia. Current psychiatry reports 36 18474209
2018 nNOS-CAPON interaction mediates amyloid-β-induced neurotoxicity, especially in the early stages. Aging cell 35 29577585
2022 Requirement of hippocampal DG nNOS-CAPON dissociation for the anxiolytic and antidepressant effects of fluoxetine. Theranostics 34 35664081
2012 NOS1AP is associated with increased severity of PTSD and depression in untreated combat veterans. Journal of affective disorders 34 23146198
2010 Mutation screening of NOS1AP gene in a large sample of psychiatric patients and controls. BMC medical genetics 32 20602773
2019 Dissociating nNOS (Neuronal NO Synthase)-CAPON (Carboxy-Terminal Postsynaptic Density-95/Discs Large/Zona Occludens-1 Ligand of nNOS) Interaction Promotes Functional Recovery After Stroke via Enhanced Structural Neuroplasticity. Stroke 31 30727847
2008 Common variation in the NOS1AP gene is associated with reduced glucose-lowering effect and with increased mortality in users of sulfonylurea. Pharmacogenetics and genomics 31 18551039
2015 Unexpected Heterodivalent Recruitment of NOS1AP to nNOS Reveals Multiple Sites for Pharmacological Intervention in Neuronal Disease Models. The Journal of neuroscience : the official journal of the Society for Neuroscience 30 25972165
2016 Research progress in NOS1AP in neurological and psychiatric diseases. Brain research bulletin 29 27237129
2008 Evidence for a role of the NOS1AP (CAPON) gene in schizophrenia and its clinical dimensions: an association study in a South American population isolate. Human heredity 28 19077434
2020 nNOS-CAPON blockers produce anxiolytic effects by promoting synaptogenesis in chronic stress-induced animal models of anxiety. British journal of pharmacology 26 32343840
2016 Interaction of NOS1AP with the NOS-I PDZ domain: Implications for schizophrenia-related alterations in dendritic morphology. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology 26 26861996
2005 Failure to confirm allelic association between markers at the CAPON gene locus and schizophrenia in a British sample. Biological psychiatry 26 16202394
2021 NOS1AP polymorphisms reduce NOS1 activity and interact with prolonged repolarization in arrhythmogenesis. Cardiovascular research 25 32061134
2018 Disruption of nNOS-NOS1AP protein-protein interactions suppresses neuropathic pain in mice. Pain 25 29319606
2015 NOS1AP Functionally Associates with YAP To Regulate Hippo Signaling. Molecular and cellular biology 25 25918243
2009 Common variation in NOS1AP and KCNH2 genes and QT interval duration in young adults. The Cardiovascular Risk in Young Finns Study. Annals of medicine 25 18785031
2009 Cardiac nitric oxide synthase-1 localization within the cardiomyocyte is accompanied by the adaptor protein, CAPON. Nitric oxide : biology and chemistry 25 19800018
2008 A common NOS1AP genetic polymorphism is associated with increased cardiovascular mortality in users of dihydropyridine calcium channel blockers. British journal of clinical pharmacology 25 19076153
2016 Physicochemical composition and sensory quality evaluation of capon and rooster meat. Poultry science 24 26957630
2010 A variation in NOS1AP gene is associated with repaglinide efficacy on insulin resistance in type 2 diabetes of Chinese. Acta pharmacologica Sinica 24 20305679
2010 Childhood trauma and genetic factors in familial schizophrenia associated with the NOS1AP gene. Schizophrenia research 24 20541371
2009 Calcium channel blockers, NOS1AP, and heart-rate-corrected QT prolongation. Pharmacogenetics and genomics 24 19247217
2007 Involvement of CAPON and nitric oxide synthases in rat muscle regeneration after peripheral nerve injury. Journal of molecular neuroscience : MN 24 18157660
2007 Changes in mRNA for CAPON and Dexras1 in adult rat following sciatic nerve transection. Journal of chemical neuroanatomy 22 17768032
2015 CAPON modulates neuronal calcium handling and cardiac sympathetic neurotransmission during dysautonomia in hypertension. Hypertension (Dallas, Tex. : 1979) 21 25916729
2015 Association of NOS1AP variants and depression phenotypes in schizophrenia. Journal of affective disorders 21 26384012
2018 ZLc002, a putative small-molecule inhibitor of nNOS interaction with NOS1AP, suppresses inflammatory nociception and chemotherapy-induced neuropathic pain and synergizes with paclitaxel to reduce tumor cell viability. Molecular pain 18 30157705
2019 CAPON Is a Critical Protein in Synaptic Molecular Networks in the Prefrontal Cortex of Mood Disorder Patients and Contributes to Depression-Like Behavior in a Mouse Model. Cerebral cortex (New York, N.Y. : 1991) 17 30307500
2010 A common variant of NOS1AP is associated with QT interval duration in a Chinese population with Type 2 diabetes. Diabetic medicine : a journal of the British Diabetic Association 17 20722683
2010 Inhibition of nitric oxide-induced nuclear localization of CAPON by NMDA receptor antagonist in cultured rat primary astrocytes. Neurochemistry international 16 20064573
2021 Hippocampal overexpression of NOS1AP promotes endophenotypes related to mental disorders. EBioMedicine 15 34455393
2017 The interaction of NOS1AP, DISC1, DAOA, and GSK3B confers susceptibility of early-onset schizophrenia in Chinese Han population. Progress in neuro-psychopharmacology & biological psychiatry 15 29100974
2016 Oxidative Stress Induced Ventricular Arrhythmia and Impairment of Cardiac Function in Nos1ap Deleted Mice. International heart journal 15 27170476
2012 Positive association between rs10918859 of the NOS1AP gene and coronary heart disease in male Han Chinese. Genetic testing and molecular biomarkers 15 23171141
2005 Does the CAPON gene confer susceptibility to schizophrenia? PLoS medicine 15 16231981
2022 NOS1AP Interacts with α-Synuclein and Aggregates in Yeast and Mammalian Cells. International journal of molecular sciences 14 36012368
2017 NOS1AP genetic variation is associated with impaired healing of diabetic foot ulcers and diminished response to healing of circulating stem/progenitor cells. Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society 13 28755516
2016 Sex-dichotomous effects of NOS1AP promoter DNA methylation on intracranial aneurysm and brain arteriovenous malformation. Neuroscience letters 13 27080431
2015 NOS1AP O-GlcNAc Modification Involved in Neuron Apoptosis Induced by Excitotoxicity. International journal of molecular sciences 13 26197318
2009 NOS1AP variant associated with incidence of type 2 diabetes in calcium channel blocker users in the Atherosclerosis Risk in Communities (ARIC) study. Diabetologia 13 19943157
2008 Family-based association studies of CAPON and schizophrenia in the Chinese Han population. Progress in neuro-psychopharmacology & biological psychiatry 13 18430503
2008 Lack of association between PKLR rs3020781 and NOS1AP rs7538490 and type 2 diabetes, overweight, obesity and related metabolic phenotypes in a Danish large-scale study: case-control studies and analyses of quantitative traits. BMC medical genetics 13 19111066
2009 SNP association and sequence analysis of the NOS1AP gene in SIDS. Legal medicine (Tokyo, Japan) 12 19289301
2022 NOS1AP is a novel molecular target and critical factor in TDP-43 pathology. Brain communications 11 36267332
2007 Expression of CAPON after spinal cord injury in rats. Journal of molecular neuroscience : MN 11 18074109
2016 Low Expression of CAPON in Glioma Contributes to Cell Proliferation via the Akt Signaling Pathway. International journal of molecular sciences 10 27869735
2010 Elevated expression of CAPON and neuronal nitric oxide synthase in the sciatic nerve of rats following constriction injury. Veterinary journal (London, England : 1997) 10 20202870
2014 NOS1AP modulates intracellular Ca(2+) in cardiac myocytes and is up-regulated in dystrophic cardiomyopathy. International journal of physiology, pathophysiology and pharmacology 9 24665357
2011 Cardiac levels of NOS1AP RNA from right ventricular tissue recovered during lead extraction. Heart rhythm 9 22019493
2023 The Physiological Function of nNOS-Associated CAPON Proteins and the Roles of CAPON in Diseases. International journal of molecular sciences 8 37958792
2020 Neuroprotective Effect of N-Cyclohexylethyl-[A/G]-[D/E]-X-V Peptides on Ischemic Stroke by Blocking nNOS-CAPON Interaction. ACS chemical neuroscience 8 33356131
2019 Systematic Meta-Analysis of the Association Between a Common NOS1AP Genetic Polymorphism, the QTc Interval, and Sudden Death. International heart journal 8 31447468
2019 Effects of Long Form of CAPON Overexpression on Glioma Cell Proliferation are Dependent on AKT/mTOR/P53 Signaling. International journal of medical sciences 7 31171914
2017 Efficient Binding of the NOS1AP C-Terminus to the nNOS PDZ Pocket Requires the Concerted Action of the PDZ Ligand Motif, the Internal ExF Site and Structural Integrity of an Independent Element. Frontiers in molecular neuroscience 7 28360833
2022 Inducible over-expression of cardiac Nos1ap causes short QT syndrome in transgenic mice. FEBS open bio 6 36352324
2022 Disrupting the nNOS/NOS1AP interaction in the medial prefrontal cortex impairs social recognition and spatial working memory in mice. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology 6 36513018
2017 Sex is a moderator of the association between NOS1AP sequence variants and QTc in two long QT syndrome founder populations: a pedigree-based measured genotype association analysis. BMC medical genetics 6 28720088
2015 NOS1AP Polymorphisms Modify QTc Interval Duration But Not Cardiac Arrest Risk in Hypertrophic Cardiomyopathy. Journal of cardiovascular electrophysiology 6 26332198
2010 The nuclear localization of CAPON in hippocampus and cerebral cortex neurons after lipopolysaccharide stimulation. Neuroimmunomodulation 6 20962540
2024 NOS1AP Gene Variants and Their Role in Metabolic Syndrome: A Study of Patients with Schizophrenia. Biomedicines 5 38540239
2022 Influence of NOS1AP Risk Variants on the Corrected QT (QTc) Interval in the Pharmacotherapy of Schizophrenia. Pharmacopsychiatry 5 35732169
2020 Effects of interaction of NOS1AP gene polymorphisms and childhood abuse on paranoid personality disorder features among male violent offenders in China. Journal of psychiatric research 5 32828023
2014 Association of common variants in NOS1AP gene with sudden unexplained nocturnal death syndrome in the southern Chinese Han population. International journal of legal medicine 5 24504561
2023 Cardiac muscle-restricted partial loss of Nos1ap expression has limited but significant impact on electrocardiographic features. G3 (Bethesda, Md.) 4 37708408
2021 A NOS1AP gene variant is associated with a paradoxical increase of the QT-interval shortening effect of digoxin. The pharmacogenomics journal 4 34616002
2019 Author Correction: Tau binding protein CAPON induces tau aggregation and neurodegeneration. Nature communications 4 31263162
2021 PPARD rs2016520 (T/C) and NOS1AP rs12742393 (A/C) polymorphisms affect therapeutic efficacy of nateglinide in Chinese patients with type 2 diabetes mellitus. BMC medical genomics 3 34772419
2020 Characterization hiPSC-derived neural progenitor cells and neurons to investigate the role of NOS1AP isoforms in human neuron dendritogenesis. Molecular and cellular neurosciences 3 32987141
2017 The role of Capon in multiple myeloma. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 3 28671047
2014 Generation of a cre recombinase-conditional Nos1ap over-expression transgenic mouse. Biotechnology letters 3 24563304

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