Neuritin Inhibits Notch Signaling through Interacted with Neuralized to Promote the Neurite Growth

Zhang, Pan; Guo, Zheng; Xiong, Anying; Dong, Hongchang; Qiao, Zhihua; Liu, Chunyan; Zhu, Jingling; Wang, Haiyan; Yu, Na; Zhang, Jinli; Yu, Hong; Yang, Lei; Huang, Jin

doi:10.3389/fnmol.2017.00179

Cited by 20 publications

(19 citation statements)

References 32 publications

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“…Naeve et al found that treatment of primary cultured rat hippocampal and cortical neurons with recombinant neuritin over 4 days produced extensive neuritogenesis compared with control cultures [2] . Other groups have found similar neuritogenesis effects in PC12 cells and in motor neurons [21][22][23] . Moreover, Picard et al indicated that the absence of neuritin by global knock-out of cpg15 induced aberrant development and plasticity of excitatory visual cortical networks [24] .…”

Section: Neuritin Promotes Neuritogenesis and Neuronal Regenerationsupporting

confidence: 57%

“…Using yeast two-hybrid and co-immunoprecipitation assays, they discovered an interaction between neuritin and Neuralized E3 Ubiquitin Protein Ligase 1 (NEURL1), an important regulator of Notch. Notably, recombinant neuritin restored the retraction of neurites caused by activation of Notch, and neurite growth stimulated by neuritin was partially blocked by NEURL1; suggesting that neuritin is an upstream and negative regulator of NEURL1 that inhibits Notch signaling to promote neurite growth [23] . This mechanism provides a valuable foundation for further investigation into the role of neuritin in neurodevelopment and neural plasticity.…”

Section: Other Possible Signaling Pathwaysmentioning

confidence: 95%

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Functions and the related signaling pathways of the neurotrophic factor neuritin

Yao

Zhao

et al. 2018

Acta Pharmacol Sin

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Neuritin is a member of the neurotrophic factor family, which is activated by neural activity and neurotrophins, and promotes neurite growth and branching. It has shown to play an important role in neuronal plasticity and regeneration. It is also involved in other biological processes such as angiogenesis, tumorigenesis and immunomodulation. Thus far, however, the primary mechanisms of neuritin, including whether or not it acts through a receptor or which downstream signals might be activated following binding, are not fully understood. Recent evidence suggests that neuritin may be a potential therapeutic target in several neurodegenerative diseases. This review focuses on the recent advances in studies regarding the newly identified functions of neuritin and the signaling pathways related to these functions. We also discuss current hot topics and difficulties in neuritin research.

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Section: Neuritin Promotes Neuritogenesis and Neuronal Regenerationsupporting

confidence: 57%

Section: Other Possible Signaling Pathwaysmentioning

confidence: 95%

Functions and the related signaling pathways of the neurotrophic factor neuritin

Yao

Zhao

et al. 2018

Acta Pharmacol Sin

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“…Additionally, it is necessary for the survival of neurons [34]. A previous study by our group has shown that a recombinant NRN1 induced extensive neuritogenesis from PC12 cells [35]. Picard et al have observed that knocking out NRN1 impairs the development and plasticity of excitatory visual cortical networks in mice [36].…”

Section: Discussionmentioning

confidence: 98%

NRN1 and CAT Gene Polymorphisms, Complex Noise, and Lifestyles Interactively Affect the Risk of Noise-Induced Hearing Loss

LIU

Xin

Zheng

et al. 2020

Preprint

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Background: Multiple genetic and environmental factors influence the severity of NIHL. However, few studies have reported interactions among such factors in modulating the risk of NIHL. This study aimed to assess for interactions among gene polymorphisms, noise metrics, and lifestyles on the risk of NIHL.Methods: A case-control study was conducted using 307 patients with NIHL and 307 matched healthy individuals from five manufacturing industries. General demographic data, lifestyle details, and noise exposure levels were recorded. The kompetitive allele-specific polymerase chain reaction (KASP) was used to analyze the genotypes of 18 single nucleotide polymorphisms (SNPs). The generalized multifactor dimensionality reduction (GMDR) method was used to examine the effects of all possible interactions. Results: The proportion of people with complex noise exposure, high CNE, high adj-CNE, smoking, propensity to watch loud videos, or sedentary lifestyle was significantly greater in the NIHL group than in the healthy group (P < 0.05). The GMDR model demonstrated a relevant interaction between NRN1 rs3805789 and CAT rs7943316. Subjects with the SNP pair of NRN1 rs3805789-CC and CAT rs7943316-AT, NRN1 rs3805789-CT and CAT rs7943316-AA, NRN1 rs3805789-CT and CAT rs7943316-TT, NRN1 rs3805789-CT/TT and CAT rs7943316-AA, or NRN1 rs3805789-CC and CAT rs7943316-AT/TT had higher risks of NIHL than those with NRN1 rs3805789-CC and CAT rs7943316-AA (P < 0.05). There was an interaction among NRN1 rs3805789, CAT rs7943316, and kurtosis. Subjects exposed to complex noise and carrying both NRN1 rs3805789-CT and CAT rs7943316-TT or NRN1 rs3805789-CT/TT and CAT rs7943316-AA had higher risks of NIHL than those exposed to steady noise and carrying both NRN1 rs3805789-CC and CAT rs7943316-AA (P < 0.05). The best six‐locus model involving NRN1 rs3805789, CAT rs7943316, smoking, video volume, physical exercise, and working pressure for the risk of NIHL was found to be the interaction (P = 0.0010). An interaction was also found among smoking, video volume, physical exercise, working pressure, and kurtosis (P = 0.0107).Conclusions: Complex noise, high CNE, high adj-CNE, smoking, high video volume, and sedentary lifestyle are environmental risk factors for NIHL. Concurrence of NRN1 rs3805789 and CAT rs7943316 constitutes a genetic risk factor for NIHL. Complex noise exposure significantly increases the risk of NIHL in subjects with a high genetic risk score. Interactions between genes and lifestyle as well as noise metrics and lifestyle affect the risk of NIHL. These results provide a theoretical basis for screening genetic and environmental risk factors to prevent NIHL.

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“…During development, Notch receptors can regulate gross neuronal morphology and fine synaptic architecture through both canonical and non-canonical signaling in diverse species. This includes regulation of neuronal migration [ 144 , 145 , 146 , 147 ], neurite outgrowth and morphogenesis [ 148 , 149 , 150 , 151 , 152 , 153 , 154 , 155 , 156 , 157 , 158 ], axon guidance and targeting [ 159 , 160 , 161 , 162 , 163 , 164 ], dendrite morphogenesis [ 165 , 166 , 167 , 168 , 169 , 170 , 171 , 172 ], synaptogenesis [ 173 , 174 ], and synaptic growth [ 121 , 175 ]. Hence, one may consider that Notch signaling may regulate neuronal and synaptic physiology by fine-tuning cellular mechanisms that lead to structural alterations in the post-developmental brain.…”

Section: Mechanisms By Which Post-developmental Notch Signaling Rementioning

confidence: 99%

Post-Developmental Roles of Notch Signaling in the Nervous System

2020

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Since its discovery in Drosophila, the Notch signaling pathway has been studied in numerous developmental contexts in diverse multicellular organisms. The role of Notch signaling in nervous system development has been extensively investigated by numerous scientists, partially because many of the core Notch signaling components were initially identified through their dramatic ‘neurogenic’ phenotype of developing fruit fly embryos. Components of the Notch signaling pathway continue to be expressed in mature neurons and glia cells, which is suggestive of a role in the post-developmental nervous system. The Notch pathway has been, so far, implicated in learning and memory, social behavior, addiction, and other complex behaviors using genetic model organisms including Drosophila and mice. Additionally, Notch signaling has been shown to play a modulatory role in several neurodegenerative disease model animals and in mediating neural toxicity of several environmental factors. In this paper, we summarize the knowledge pertaining to the post-developmental roles of Notch signaling in the nervous system with a focus on discoveries made using the fruit fly as a model system as well as relevant studies in C elegans, mouse, rat, and cellular models. Since components of this pathway have been implicated in the pathogenesis of numerous psychiatric and neurodegenerative disorders in human, understanding the role of Notch signaling in the mature brain using model organisms will likely provide novel insights into the mechanisms underlying these diseases.

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Neuritin Inhibits Notch Signaling through Interacted with Neuralized to Promote the Neurite Growth

Cited by 20 publications

References 32 publications

Functions and the related signaling pathways of the neurotrophic factor neuritin

Functions and the related signaling pathways of the neurotrophic factor neuritin

NRN1 and CAT Gene Polymorphisms, Complex Noise, and Lifestyles Interactively Affect the Risk of Noise-Induced Hearing Loss

Post-Developmental Roles of Notch Signaling in the Nervous System

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