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Last update 08 May 2025

NOS1AP

Last update 08 May 2025

Basic Info

Synonyms

C-terminal PDZ ligand of neuronal nitric oxide synthase protein, CAPON, Carboxyl-terminal PDZ ligand of neuronal nitric oxide synthase protein

+ [3]

Introduction

Adapter protein involved in neuronal nitric-oxide (NO) synthesis regulation via its association with nNOS/NOS1. The complex formed with NOS1 and synapsins is necessary for specific NO and synapsin functions at a presynaptic level. Mediates an indirect interaction between NOS1 and RASD1 leading to enhance the ability of NOS1 to activate RASD1. Competes with DLG4 for interaction with NOS1, possibly affecting NOS1 activity by regulating the interaction between NOS1 and DLG4 (By similarity). In kidney podocytes, plays a role in podosomes and filopodia formation through CDC42 activation (PubMed:33523862).

Drugs associated with NOS1AP

NOS1AP inhibitors(Northwestern University)

Target

NOS1AP

Mechanism

NOS1AP inhibitors

Active Org.-

Originator Org.

Northwestern University

Active Indication-

Inactive Indication-

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ZLc002

Target

NOS1AP

Mechanism

NOS1AP inhibitors

Active Org.-

Originator Org.

Indiana University

Active Indication-

Inactive Indication

Inflammation [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with NOS1AP

100 Translational Medicine associated with NOS1AP

0 Patents (Medical) associated with NOS1AP

248

Literatures (Medical) associated with NOS1AP

11 Feb 2025·S.S. Korsakov Journal of Neurology and Psychiatry

The association of NOS1AP gene polymorphisms with the duration of the QT interval in patients with schizophrenia receiving antipsychotic therapy

Article

Author: Mednova, I.A. ; Tiguntsev, V.V. ; Galkin, S.A. ; Paderina, D.Z. ; Kornetova, E.G. ; Ivanova, S.A.

Objective. To study the associations of NOS1AP gene polymorphisms with the duration of the QT interval (QTc) in patients with schizophrenia receiving antipsychotics. Material and methods. One hundred and sixty-eight patients (78 men and 90 women) with an established diagnosis of schizophrenia were examined. The patients received basic antipsychotic therapy. At the time of admission to the hospital, a standard 12-lead electrocardiogram recording was performed. The calculation of the QTc interval was carried out using the Bazett formula. Three NOS1AP polymorphisms (rs12029454, rs10494366 and rs12143842) were selected for genotyping. Results. Spearman’s correlation revealed a significant relationship between CPZeq and the duration of the QTc interval in the group of men (rs=0.262; p=0.021; pBonf=0.042). CPZeq was positively correlated with the duration of the QTc interval in men with AA and AG rs12029454 (rs=0.717; p=0.00025; pbonf=0.0015), GG and GT rs10494366 (rs=0.381; p=0.008; pbonf=0.048), TT and CT rs12143842 (rs=0.389; p=0.003; pbonf=0.018) genotypes. We did not find any significant correlations in the group of women. Conclusion. Genetic variants rs12029454, rs10494366 and rs12143842 of the NOS1AP gene are associated with the duration of the QTc interval in men with schizophrenia in response to antipsychotics. The AA/AG rs12029454, GG/GT rs10494366 and TT/CT rs12143842 genotypes in men contribute to the prolongation of the QTc interval and the development of undesirable cardiovascular disorders against the background of antipsychotic therapy.

01 Jan 2025·CNS Neuroscience & Therapeutics

S‐Nitrosylation of Dexras1 Controls Post‐Stroke Recovery via Regulation of Neuronal Excitability and Dendritic Remodeling

Article

Author: Ni, Huanyu ; Qin, Cheng ; Song, Yixuan ; Zhou, Haihui ; Han, Zhou ; Han, Dan ; Yan, Simin

ABSTRACTAimsStroke is a major public health concern leading to high rates of death and disability worldwide, unfortunately with no effective treatment available for stroke recovery during the repair phase.MethodsPhotothrombotic stroke was induced in mice. Adeno‐associated viruses (AAV) were microinjected into the peri‐infarct cortex immediately after photothrombotic stroke. Grid‐walking task and cylinder task were used to assess motor function. Western blotting, Golgi staining, and electrophysiology recordings were performed to uncover the mechanisms.ResultsThe ternary complex of neuronal nitric oxide synthase (nNOS), carboxy‐terminal PDZ ligand of nNOS (CAPON) and dexamethasone‐induced ras protein 1 (Dexras1) is structurally beneficial for S‐nitrosylation of Dexras1 (SNO‐Dexras1). In our previous study, uncoupling nNOS‐CAPON interaction by Tat‐CAPON‐12C promoted functional recovery after stroke. Here, we show that ischemia elevated the levels of nNOS‐Dexras1 complex and SNO‐Dexras1 in the peri‐infarct cortex in the days 4–10 after stroke induction, and as excepted, Tat‐CAPON‐12C, a peptide disrupting nNOS‐CAPON interaction, significantly reversed these changes. The above information implies that repressed SNO‐Dexras1 may mediate functional‐promoting effects of Tat‐CAPON‐12C and SNO‐Dexras1 could be the vital molecular substrate for post‐stroke functional recovery in the repair phage. Inhibiting the ischemia‐induced SNO‐Dexras1 by AAV vector‐mediated knockdown of Dexras1 or over‐expression of dominant negative Dexras1 (Dexras1‐C11S) produced sustained recovery of motor function from stroke. In contrast, up‐regulation of SNO‐Dexras1 by over‐expressing Dexras1 worsened stroke outcome. Using electrophysiology recordings, we also observed that silence of Dexras1 in the peri‐infarct cortex increased the spike number and the miniature excitatory postsynaptic currents (mEPSCs) frequency, suggesting enhancement of neuronal excitability. In addition, silence of Dexras1 increased dendritic complexity in cultured neuron and more importantly enhanced dendritic spine density in the peri‐infarct cortex, implying dendritic remodeling.ConclusionThus, inhibition of SNO‐Dexras1 positively regulates post‐stroke functional recovery via enhanced neuronal excitability and dendritic remodeling. Our results identify that SNO‐Dexras1 may serve as a novel target for promoting motor functional restoration from stroke in the delayed phase, shedding light on stroke treatment.

01 Jan 2025·American Journal of Rhinology & Allergy

Soluble Guanylate Cyclase Dysfunction and Nitric Oxide Pathway in Chronic Rhinosinusitis With Nasal Polyps: Predictive Markers for Postoperative Recurrence

Article

Author: Tong, MD, Zongjing ; Xie, MD, Zhihai ; Zhang, MD, Hua ; Zhang, MD, Caixia ; Xie, PhD, Shaobing ; Jiang, MD, Weihong ; Jiang, MD, Sijie

Background Elevated nitric oxide (NO) levels have been linked to a heightened risk of recurrence in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). However, the precise influence of NO on CRSwNP recurrence remains unclear. Objective This study seeks to elucidate the relationship between NO levels and the risk of CRSwNP recurrence. Methods A protein chip array analysis was conducted to identify differentially expressed inflammatory mediators in the nasal tissues between patients with CRSwNP and healthy controls (HC). Differentially expressed proteins were analyzed, and bioinformatics analysis was used to predict the potential functions and pathways of these proteins. Western blotting (WB) and immunohistochemistry were employed to validate the candidate proteins in 2 independent cohorts. Receiver-operating characteristic (ROC) curves were employed to assess the abilities of target proteins for predicting the postoperative recurrence of CRSwNP. Results Twelve differentially expressed proteins were identified between the CRSwNP and HC groups. Notably, differentially expressed proteins exhibited high expression of the biological process term “positive regulation of nitric oxide-mediated signal transduction” ( P < .05). WB and immunohistochemistry results demonstrated that guanylate cyclase 1 soluble subunit alpha 1 (GUCY1A1), GUCY1A2, nitric oxide synthase 1 adaptor protein, epidermal growth factor receptor, and insulin were found to be upregulated in the CRSwNP group compared to the HC group ( P < .05). Moreover, elevated levels of GUCY1A2 and GUCY1A1 were observed to be associated with an increased risk of CRSwNP recurrence ( P < .05), and ROC curve analysis confirmed their effectiveness as predictors for postoperative recurrence ( P < .05). Conclusion Our findings revealed that CRSwNP exhibited a distinct tissue protein profile, with soluble guanylate cyclase dysfunction and the nitric oxide pathway implicated in the underlying pathological mechanisms. The discovery-validation results suggested that GUCY1A1 and GUCY1A2 were promising predictors for postoperative recurrence in patients with CRSwNP.

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NOS1AP

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