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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Reticulon 4

Nogo, Nogo-A, NSP
This gene belongs to the family of reticulon encoding genes. Reticulons are associated with the endoplasmic reticulum, and are involved in neuroendocrine secretion or in membrane trafficking in neuroendocrine cells. The product of this gene is a potent neurite outgrowth inhibitor which may also help block the regeneration of the central nervous system in higher vertebrates. Alternatively spliced transcript variants derived both from differential splicing and differential promoter usage and encoding different isoforms have been identified. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, NgR, HAD, CD45, V1a
Papers using Nogo antibodies
Inhibitor of neurite outgrowth in humans.
Cookson Mark R., In PLoS ONE, 1999
... Nogo-R (Catalog #: sc-25659, Santa Cruz Biotechnology); GFAP (Catalog #: ab929, ...
Papers on Nogo
Formation of stable nanodiscs by bihelical apolipoprotein A-I mimetic peptide.
Saito et al., Tokushima, Japan. In J Pept Sci, Feb 2016
In this study, we designed a novel nanodisc scaffold peptide (NSP) that has proline-punctuated bihelical amphipathic structure based on apoA-I mimetic peptides.
Foot-and-mouth disease vaccines: progress and problems.
Liu et al., Lanzhou, China. In Expert Rev Vaccines, Feb 2016
Vaccines may sometimes contain traces of FMD viral non-structural proteins (NSPs), therefore, interfering with the NSP-based serological differentiation infected from vaccinated animals (DIVA).
NgBR is essential for endothelial cell glycosylation and vascular development.
Sessa et al., New Haven, United States. In Embo Rep, Feb 2016
UNASSIGNED: NgBR is a transmembrane protein identified as a Nogo-B-interacting protein and recently has been shown to be a subunit required for cis-prenyltransferase (cisPTase) activity.
Nogo-A controls structural plasticity at dendritic spines by rapidly modulating actin dynamics.
Zagrebelsky et al., Braunschweig, Germany. In Hippocampus, Feb 2016
UNASSIGNED: Nogo-A and its receptors have been shown to control synaptic plasticity, including negatively regulating long-term potentiation (LTP) in the cortex and hippocampus at a fast time scale and restraining experience-dependent turnover of dendritic spines over days.
[Axonal Regeneration-related Molecules as Biomarkers for Multiple Sclerosis].
Takei et al., Yokohama, Japan. In Brain Nerve, Jan 2016
Nogo protein and its receptor (Nogo receptor-1; NgR1) are well known representative molecules that prevent axonal regeneration, and we identified lateral olfactory tract usher substance (LOTUS) as an endogenous antagonist of NgR1.
Reaching the brain: Advances in optic nerve regeneration.
Goldberg et al., In Exp Neurol, Jan 2016
More recently, some degree of regeneration has been achieved through the optic nerve itself by factors associated with intraocular inflammation (oncomodulin) or by altering levels of particular transcription factors (Klf-4, -9, c-myc), cell-intrinsic suppressors of axon growth (PTEN, SOCS3), receptors to cell-extrinsic inhibitors of axon growth (Nogo receptor, LAR, PTP-σ) or the intracellular signaling pathway activated by these receptors (RhoA).
Experimental and Clinical Advances in Immunotherapy Strategies for Spinal Cord Injury Target on MAIs and Their Receptors.
Wang et al., Chongqing, China. In Curr Pharm Des, Jan 2016
UNASSIGNED: In the injured adult mammalian central nervous system (CNS), the failure of axonal regeneration is thought to be attributed, at least in part, to various myelin-associated inhibitors (MAIs), such as Nogo, myelin-associated glycoprotein (MAG), and oligodendrocyte-myelin glycoprotein (OMgp) around the damaged site.
X-ray therapy promotes structural regeneration after spinal cord injury in a rat model.
Zhang et al., Suzhou, China. In J Orthop Surg Res, Dec 2015
The glial fibrillary acidic protein (GFAP) and Nogo-A counts at 14 weeks were higher than those at 6 weeks in all the groups (P < 0.05), and there was no statistical significance with kinology and electrophysiology tests in all groups.
Multiple Roles for Nogo Receptor 1 in Visual System Plasticity.
McGee et al., Los Angeles, United States. In Neuroscientist, Dec 2015
The nogo-66 receptor 1 (ngr1) is one of only a small number of genes identified thus far that is essential to closing the critical period.
Nogo-B regulates endothelial sphingolipid homeostasis to control vascular function and blood pressure.
Di Lorenzo et al., New York City, United States. In Nat Med, Sep 2015
Here we report that Nogo-B, a membrane protein of the endoplasmic reticulum, regulates endothelial sphingolipid biosynthesis with direct effects on vascular function and blood pressure.
Axon regeneration impediment: the role of paired immunoglobulin-like receptor B.
Fu et al., Beijing, China. In Neural Regen Res, Aug 2015
In addition to the Nogo receptor (NgR), the paired immunoglobulin-like receptor B (PirB) is a recently discovered coreceptor of Nogo, myelin-associated glycoprotein, and myelin oligodendrocyte glycoprotein.
NIK1-mediated translation suppression functions as a plant antiviral immunity mechanism.
Fontes et al., Viçosa, Brazil. In Nature, May 2015
Here we demonstrate in Arabidopsis that the constitutive activation of NIK1, a leucine-rich repeat receptor-like kinase (LRR-RLK) identified as a virulence target of the begomovirus nuclear shuttle protein (NSP), leads to global translation suppression and translocation of the downstream component RPL10 to the nucleus, where it interacts with a newly identified MYB-like protein, L10-INTERACTING MYB DOMAIN-CONTAINING PROTEIN (LIMYB), to downregulate translational machinery genes fully.
Mutation of Nogo-B receptor, a subunit of cis-prenyltransferase, causes a congenital disorder of glycosylation.
Sessa et al., United States. In Cell Metab, 2014
Here we show that Nogo-B receptor (NgBR) is a subunit required for dolichol synthesis in yeast, mice, and man.
Neuronal Nogo-A upregulation does not contribute to ER stress-associated apoptosis but participates in the regenerative response in the axotomized adult retina.
Schwab et al., Zürich, Switzerland. In Cell Death Differ, 2012
Nogo-A overexpression in RGCs in vivo or in the neuronal cell line F11 in vitro promoted regeneration, demonstrating a positive, cell-autonomous role for neuronal Nogo-A in the modulation of axonal regeneration.
Amino-Nogo-A antagonizes reactive oxygen species generation and protects immature primary cortical neurons from oxidative toxicity.
Jin et al., Shanghai, China. In Cell Death Differ, 2012
Interacting with peroxiredoxin 2 (Prdx2), amino-Nogo-A reduces reactive oxygen species (ROS) generation and extracellular signal-regulated kinase phosphorylation to exert neuroprotective effects.
RNT4 3'-UTR insertion/deletion polymorphisms are not associated with atrial septal defect in Chinese Han population: a brief communication.
Rao et al., Chengdu, China. In Dna Cell Biol, 2012
CAA and TATC insertion/deletion polymorphisms of RNT4 gene may not be a useful marker to predict the susceptibility of ASD in Chinese Han population
Genetic variation in RTN4 3'-UTR and susceptibility to cervical squamous cell carcinoma.
Zhang et al., Chengdu, China. In Dna Cell Biol, 2012
genetic variation in RTN4 3'-UTR contributes to the susceptibility to CSCC
A metal-binding site in the RTN1-C protein: new perspectives on the physiological role of a neuronal protein.
Melino et al., Roma, Italy. In Metallomics, 2012
In the present study a potential metal ion binding motif (HxE/D) at the C-terminal of the RTN1-C has been identified and its capability to bind metals investigated by UV-vis, CD, multidimensional NMR spectroscopy and biological assays.
Cartilage acidic protein-1B (LOTUS), an endogenous Nogo receptor antagonist for axon tract formation.
Takei et al., Yokohama, Japan. In Science, 2011
We further identified Nogo receptor-1 (NgR1) as a LOTUS-binding protein.
Functions of Nogo proteins and their receptors in the nervous system.
Schwab, Zürich, Switzerland. In Nat Rev Neurosci, 2010
The membrane protein Nogo-A was initially characterized as a CNS-specific inhibitor of axonal regeneration.
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