Nogos and the Nogo‐66 receptor: Factors inhibiting CNS neuron regeneration

Ng, C. M.; Tang, Bor Luen

doi:10.1002/jnr.10134

Cited by 35 publications

(24 citation statements)

References 31 publications

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“…In an in vitro assay of axonal outgrowth, a synthetic peptide corresponding to NEP 1-40 functions as an antagonist [25]. The interaction between the Nogo-66 loop and NgR evidently transduces signals from oligodendrocytes to neurons for inhibiting axonal regeneration (for reviews see [26][27][28][29]). In addition to the signaling pathway that is initiated from Nogo-66, the interaction of the Nogo-66 loop in oligodendrocytes with Caspr in axons underscores an additional importance of RTN4 in the control of K + channel localization at axonal paranodes [10].…”

Section: The Loop Regionmentioning

confidence: 99%

Reticulon proteins: emerging players in neurodegenerative diseases

Yan

Shi

et al. 2006

Cell. Mol. Life Sci.

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Reticulons (RTNs) are a group of integral membrane proteins that have a uniquely conserved C-terminal domain named RHD. In mammalian genomes, transcripts are produced from four genes, rtn1 to rtn4, under the regulation of tissue or cell-type-specific expression. The presence of alternative promoters for gene expression and multiple cryptic splicing sites have resulted in large numbers of genes/proteins that are classified among the reticulon family. Although this family exists in almost all eukaryotes, only the rtn4 gene product, Nogo (RTN4), has gained relatively more in-depth attention. Despite predominant localization in the endoplasmic reticulum, Nogo on the cell surface appears to play a critical role as an inhibitory molecule for axonal growth and regeneration in humans and rodents. Recently, studies have expanded the biological functions of RTNs to other facets including modulating the enzymatic activity of beta-secretase in Alzheimer's disease. In this review, we summarize the accumulated findings concerning the structural and functional aspects of RTNs and speculate on their linkage to the pathogenesis of neurodegenerative diseases.

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Section: The Loop Regionmentioning

confidence: 99%

Reticulon proteins: emerging players in neurodegenerative diseases

Yan

Shi

et al. 2006

Cell. Mol. Life Sci.

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“…Previous studies have proposed differing orientations of the molecule in the plasma membrane. Specifically, the intracellular or extracellular location of the N-terminal domain that contains a putative functional site, has been a matter of debate (GrandPre et al, 2000;Huber and Schwab, 2000;Ng and Tang, 2002). The Nterminus contains an active region of Nogo that can collapse axons and inhibit fibroblast spreading, although it seems to evoke such response only when substrate bound (Fournier et al, 2001).…”

Section: N-terminal Domain Of Nogo-a Is Primarily Intracellularmentioning

confidence: 99%

Nogo and Nogo‐66 receptor in human and chick: Implications for development and regeneration

O’Neill¹,

Whalley²,

Ferretti³

2004

Developmental Dynamics

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Antibodies to the myelin protein Nogo increase axonal regrowth after central nervous system injury. We have investigated whether Nogo expression contributes to loss of regenerative potential during development by using chick embryos, which regenerate their spinal cord until embryonic day (E) 13, when myelination begins. We show that Nogo-A and the Nogo receptor (NgR) are developmentally regulated both in chick and human embryos, are first detected at developmental stages when the chick spinal cord regenerates, and are not down-regulated after injury at permissive stages for regeneration. Therefore, expression of Nogo-A and NgR in pre-E13 chick spinal cords is not sufficient to inhibit regeneration. Nogo-A expression in the chick early embryo is primarily observed in axons, whereas NgR is mainly located on neuronal cell bodies, both in spinal cord and eye, and in striated muscle including the heart. With the onset of myelination, there is down-regulation of Nogo-A expression in neurons. Therefore, loss of regenerative potential might be linked to changes in its cellular localization. The possibility that only Nogo expressed in mature oligodendrocytes can exercise inhibitory effects would reconcile the lack of inhibition we observe in developing chick spinal cords before the onset of myelination with evidence from other laboratories on the inhibitory effects of Nogo in mature central nervous system. The distinctive and complementary patterns of Nogo-A and NgR expression and their conservation throughout evolution support the view that Nogo signaling represents a key pathway in nervous system and striated muscle development. Its putative role in target innervation and establishment of neural circuitry is discussed.

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“…Nogo-A (RTN4A), Nogo-B (RTN4B) and Nogo-C (RTN4C) are the three main isoforms of RTN4 [44]. They are encoded by the same gene, and their variants, generated by alternative splicing or alternative promoter usage, are diVerentially distributed in various tissues [25,32,44]. RTNs are especially abundant in the endoplasmic reticulum [32,44].…”

Section: Introductionmentioning

confidence: 99%