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Study provide evidence for the first time that the TATC insertion/deletion polymorphism in RTN4 3'-UTR may contributes to clear cell renal cell carcinoma risk in Chinese Han population.
This review aims at presenting our current knowledge on the role of Nogo-A in the visual system and to discuss how its therapeutic targeting may promote visual improvement in ophthalmic diseases.
CAA and TATC Insertion/Deletion Genetic Polymorphisms of RTN4 3'-UTR are associated with Hepatocellular Carcinoma
Nogo-B was shown to play an important negative role in apoptotic signaling through its interaction with c-FLIP in colorectal cancer cells.
NOGO-B/RTN4B and NOGO-A/RTN4A are simultaneously expressed in cultured epithelial, fibroblast and neuronal cells. Morphological analysis of cells with manipulated levels of NOGO-B/RTN4B revealed that it is required for maintenance of normal endoplasmic reticulum shape.
Nogo-B is expressed aberrantly in HCCs and plays an oncogenic role. These findings support that Nogo-B may be a novel anti-HCC therapeutic target.
observations suggest that Rtn4A counteracts the Nrdp1-mediated degradation of ErbB3 by sequestering the ubiquitin ligase into ER tubules.
NOGO-A/B may be a negative prognostic factor of malignant melanoma.
LILRA3 significantly reversed Nogo-66-mediated inhibition of neurite outgrowth and promoted synapse formation in primary cortical neurons through regulation of the ERK/MEK pathway.
Nogo-B expression is down-regulated in intrahepatic cholangiocarcinoma, the implication of which, however, remains to be investigated.
Data show that the mean peak serum neuroglobin and Nogo-A concentrations were both significantly higher in patients with an unfavorable outcome at 6 months after traumatic brain injury (TBI).
RTN4-C knockdown blocks cell cycle progression and cell growth in colorectal cancer cell lines.
Epithelial RTN-4B/NOGO-B was downregulated in human and experimental inflammatory bowel disease
The Nogo-B-PirB axis controls macrophage-mediated vascular remodeling.
a novel mechanism that functionally couples cAMP signaling with the proteolytic turnover of NOGO-A, positively impacting on neurite outgrowth in mammalian brain.
The RTN4 del allele could significantly increase NSCLC risk.
Identify Nogo-C as a tumor suppressor gene in hepatocellular carcinoma and B-raf as a novel interacting protein.
the present study found that Nogo-A depletion was capable of inhibiting HCC SMMC-7721 cell proliferation by promoting G2/M cell cycle arrest and apoptosis.
The expression of Nogo-B, in arterial intima, is impeded in the early stages of atherosclerosis. Macrophage infiltration is not accompanied by Nogo-B expression in atherosclerotic arteries.
Nogo-A/B expression decreased with increasing squamous cell carcinoma malignancy grade (p=0.026).
The steady-state level of reticulon 4-B mRNA was shown to be up-regulated by pressure, but not by mechanical stretch; close association with endoplasmic reticulum
Loss of Nogo-A, encoded by the schizophrenia risk gene Rtn4, reduces mGlu3 expression and causes hyperexcitability in hippocampal CA3 circuits
Nogo-A and NgR1 interactions may contribute to axonal branching in lateral olfactory tract development
The results of this study showed the Nogo-B is expressed in the floor plate of mouse embryo, which probably mediates axon crossing in the spinal cord by repelling axons out of the midline when they start upregulate NgR.
induction of hepatic NgBR expression by atorvastatin mainly depended on inactivation of extracellular signal-regulated kinases 1/2 (ERK1/2) and protein kinase B (Akt). Taken together, our study demonstrates that statins inhibit NAFLD mainly through activation of NgBR expression.
We show here that Nogo-A is highly expressed not only in excitatory, but also in inhibitory, Parvalbumin positive neurons in the adult hippocampus. By this means our current and previous data indicate that Nogo-A loss-of-function positively influences spatial learning by priming the neuronal structure to a higher plasticity level.
Nogo-A signaling in the adult nervous system modulates the spine actin cytoskeleton within minutes to control structural plasticity at dendritic spines of CA3 pyramidal neurons. Acute Nogo-A loss-of-function transiently increases F-actin stability and results in an increase in dendritic spine density and length. Nogo-A acutely restricts AMPAR insertion and membrane potential amplitude at hippocampal synaptic sites.
deregulation of Nogo-C by miRNA may be a potential therapeutic target for ischemia-related heart diseases.
stimulated angiogenesis upon Nogo-A gene deletion results in the insertion of complete capillary micro-networks and not just single vessels into existing vascular networks.
The increase of Nogo-A expression can selectively influence the distribution of inwardly rectifying potassium channel 4.1 in glia but is not essential for inwardly rectifying potassium channel 4.1-mediated potassium conductance at the plasma membrane in physiological conditions.
Nogo-A restricts visual experience-driven plasticity of the optokinetic response and plays a role in the segregation and maintenance of retinal projections to the brain.
The Ad-Nogo-B-treated mice also had less severe lung injury, less alveolar protein exudation, and a higher number of macrophages but less neutrophil infiltration compared with Ad-RFP-treated mice.
Nogo knockdown (KD) in non-transformed and Ras-transformed cells both enhanced virus-induced IFN response, suggesting that both cleaved and uncleaved Nogo can suppress IFN response.
the Nogo/NgR signal might be involved in multiple processes in various inflammation-associated CNS diseases.
identifies Nogo-B as a key inhibitor of local sphingolipid synthesis
The findings indicate a critical role of Nogo-B and GRAMD4 in trafficking of TLR9.
study represents the first side-by-side comparison between PTEN deletion and Nogo deletion on Corticospinal tract regeneration and sprouting.
the downregulation of Nogo-A protein might have a role in the altered synaptic plasticity during aging.
Nogo receptor inhibition enhances functional recovery following lysolecithin-induced demyelination in mouse optic chiasm.
rtn4a is essential for embryonic development and patterning of the nervous system.
data demonstrates that zebrafish Rtn4/Nogo transcripts might be generated by coupling mechanisms of alternative first exons and alternative promoter usage.
The present results have uncovered new factors underlying successful axon regeneration in the fish CNS: Binding of Nogo-66 of fish RTN-4 to NgR is growth promoting on fish retinal ganglion cell axon growth
Data suggest that localized Nogo/Nogo66 expression defines inhibitory territories that through repulsion restrict axon growth to permissive regions.
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.
, My043 protein
, neurite growth inhibitor 220
, neurite outgrowth inhibitor
, neuroendocrine-specific protein C homolog
, reticulon 5
, reticulon 4
, GLUT4 vesicle 20kDa protein
, glut4 vesicle 20 kDa protein
, nogo protein