Reticulon 4: Difference between revisions

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{{Infobox_gene}}
{{Infobox_gene}}
'''Reticulon-4''', also known as '''Neurite outgrowth inhibitor''' or '''Nogo''',  is a [[protein]] that in humans is encoded by the ''RTN4'' [[gene]]<ref name="pmid10667797">{{cite journal | vauthors = GrandPré T, Nakamura F, Vartanian T, Strittmatter SM | title = Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein | journal = Nature | volume = 403 | issue = 6768 | pages = 439–44 | date = Jan 2000 | pmid = 10667797 | pmc =  | doi = 10.1038/35000226 }}</ref><ref name="pmid10773680">{{cite journal | vauthors = Yang J, Yu L, Bi AD, Zhao SY | title = Assignment of the human reticulon 4 gene (RTN4) to chromosome 2p14-->2p13 by radiation hybrid mapping | journal = Cytogenetics and Cell Genetics | volume = 88 | issue = 1-2 | pages = 101–2 | date = June 2000 | pmid = 10773680 | pmc =  | doi = 10.1159/000015499 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: RTN4 reticulon 4| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=57142| accessdate = }}</ref> that has been identified as an [[Enzyme inhibitor|inhibitor]] of [[neurite]] outgrowth specific to the [[central nervous system]]. During neural development Nogo is expressed mainly by neurons and provides an inhibitory signal for the migration and sprouting of CNS endothelial (tip) cells, thereby restricting blood vessel density.
'''Reticulon 4''', also known as '''Neurite outgrowth inhibitor''' or '''Nogo''',  is a [[protein]] that in humans is encoded by the ''RTN4'' [[gene]]<ref name="pmid10667797">{{cite journal | vauthors = GrandPré T, Nakamura F, Vartanian T, Strittmatter SM | title = Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein | journal = Nature | volume = 403 | issue = 6768 | pages = 439–44 | date = Jan 2000 | pmid = 10667797 | pmc =  | doi = 10.1038/35000226 }}</ref><ref name="pmid10773680">{{cite journal | vauthors = Yang J, Yu L, Bi AD, Zhao SY | title = Assignment of the human reticulon 4 gene (RTN4) to chromosome 2p14-->2p13 by radiation hybrid mapping | journal = Cytogenetics and Cell Genetics | volume = 88 | issue = 1-2 | pages = 101–2 | date = June 2000 | pmid = 10773680 | pmc =  | doi = 10.1159/000015499 }}</ref><ref name="entrez">{{cite web | title = Entrez Gene: RTN4 reticulon 4| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=57142| accessdate = }}</ref> that has been identified as an [[Enzyme inhibitor|inhibitor]] of [[neurite]] outgrowth specific to the [[central nervous system]]. During neural development Nogo is expressed mainly by neurons and provides an inhibitory signal for the migration and sprouting of CNS endothelial (tip) cells, thereby restricting blood vessel density.


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 that 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.<ref name="entrez"/> There are three [[isoforms]]: Nogo A, B and C. Nogo-A has two known inhibitory domains including amino-Nogo, at the N-terminus and Nogo-66, which makes up the molecules extracellular loop. Both amino-Nogo and Nogo-66 are involved in inhibitory responses, where amino-Nogo is a strong inhibitor of neurite outgrowth, and Nogo-66 is involved in [[growth cone]] destruction.<ref name=Karnezis2004/>
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 that 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.<ref name="entrez"/> There are three [[isoforms]]: Nogo A, B and C. Nogo-A has two known inhibitory domains including amino-Nogo, at the N-terminus and Nogo-66, which makes up the molecules extracellular loop. Both amino-Nogo and Nogo-66 are involved in inhibitory responses, where amino-Nogo is a strong inhibitor of neurite outgrowth, and Nogo-66 is involved in [[growth cone]] destruction.<ref name=Karnezis2004/>


Research suggests that blocking Nogo-A during neuronal damage (from diseases such as [[Multiple Sclerosis]]) will help to protect or restore the damaged neurons.<ref name=Karnezis2004>{{cite journal | vauthors = Karnezis T, Mandemakers W, McQualter JL, Zheng B, Ho PP, Jordan KA, Murray BM, Barres B, Tessier-Lavigne M, Bernard CC | title = The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination | journal = Nature Neuroscience | volume = 7 | issue = 7 | pages = 736–44 | date = Jul 2004 | pmid = 15184901 | doi = 10.1038/nn1261 }}</ref><ref>{{cite journal|last1=Sozmen|first1=EG et al|title=Nogo receptor blockade overcomes remyelination failure after white matter stroke and stimulates functional recovery in aged mice|journal=PNAS USA|date=2016|volume=113|pages=E8453–E8462|doi=10.1073/pnas.1615322113}}</ref> The investigation into the mechanisms of this protein presents a great potential for the treatment of [[Autoimmune disease|auto-immune]] mediated [[demyelinating diseases]] and [[spinal cord injury]] [[Neuroregeneration|regeneration]]. It has also been found to be a key player in the process whereby physical exercise enhances learning and memory processes in the brain.<ref>[http://www.eurekalert.org/pub_releases/2008-03/uorm-sar031808.php Stopping a receptor called 'nogo' boosts the synapses]</ref>
Research suggests that blocking Nogo-A during neuronal damage (from diseases such as [[Multiple Sclerosis]]) will help to protect or restore the damaged neurons.<ref name=Karnezis2004>{{cite journal | vauthors = Karnezis T, Mandemakers W, McQualter JL, Zheng B, Ho PP, Jordan KA, Murray BM, Barres B, Tessier-Lavigne M, Bernard CC | title = The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination | journal = Nature Neuroscience | volume = 7 | issue = 7 | pages = 736–44 | date = Jul 2004 | pmid = 15184901 | doi = 10.1038/nn1261 }}</ref><ref>{{cite journal|last1=Sozmen|first1=EG et al|title=Nogo receptor blockade overcomes remyelination failure after white matter stroke and stimulates functional recovery in aged mice|journal=PNAS USA|date=2016|volume=113|pages=E8453–E8462|doi=10.1073/pnas.1615322113|pmc=5206535}}</ref> The investigation into the mechanisms of this protein presents a great potential for the treatment of [[Autoimmune disease|auto-immune]] mediated [[demyelinating diseases]] and [[spinal cord injury]] [[Neuroregeneration|regeneration]]. It has also been found to be a key player in the process whereby physical exercise enhances learning and memory processes in the brain.<ref>[http://www.eurekalert.org/pub_releases/2008-03/uorm-sar031808.php Stopping a receptor called 'nogo' boosts the synapses]</ref>


== Interactions ==
== Interactions ==

Latest revision as of 07:29, 23 May 2018

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Identifiers
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External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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View/Edit Human

Reticulon 4, also known as Neurite outgrowth inhibitor or Nogo, is a protein that in humans is encoded by the RTN4 gene[1][2][3] that has been identified as an inhibitor of neurite outgrowth specific to the central nervous system. During neural development Nogo is expressed mainly by neurons and provides an inhibitory signal for the migration and sprouting of CNS endothelial (tip) cells, thereby restricting blood vessel density.

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 that 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.[3] There are three isoforms: Nogo A, B and C. Nogo-A has two known inhibitory domains including amino-Nogo, at the N-terminus and Nogo-66, which makes up the molecules extracellular loop. Both amino-Nogo and Nogo-66 are involved in inhibitory responses, where amino-Nogo is a strong inhibitor of neurite outgrowth, and Nogo-66 is involved in growth cone destruction.[4]

Research suggests that blocking Nogo-A during neuronal damage (from diseases such as Multiple Sclerosis) will help to protect or restore the damaged neurons.[4][5] The investigation into the mechanisms of this protein presents a great potential for the treatment of auto-immune mediated demyelinating diseases and spinal cord injury regeneration. It has also been found to be a key player in the process whereby physical exercise enhances learning and memory processes in the brain.[6]

Interactions

Reticulon 4 has been shown to interact with WWP1,[7] BCL2-like 1[8] and Bcl-2.[8]

See also

References

  1. ↑ GrandPré T, Nakamura F, Vartanian T, Strittmatter SM (Jan 2000). "Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein". Nature. 403 (6768): 439–44. doi:10.1038/35000226. PMID 10667797.
  2. ↑ Yang J, Yu L, Bi AD, Zhao SY (June 2000). "Assignment of the human reticulon 4 gene (RTN4) to chromosome 2p14-->2p13 by radiation hybrid mapping". Cytogenetics and Cell Genetics. 88 (1–2): 101–2. doi:10.1159/000015499. PMID 10773680.
  3. ↑ 3.0 3.1 "Entrez Gene: RTN4 reticulon 4".
  4. ↑ 4.0 4.1 Karnezis T, Mandemakers W, McQualter JL, Zheng B, Ho PP, Jordan KA, Murray BM, Barres B, Tessier-Lavigne M, Bernard CC (Jul 2004). "The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination". Nature Neuroscience. 7 (7): 736–44. doi:10.1038/nn1261. PMID 15184901.
  5. ↑ Sozmen, EG; et al. (2016). "Nogo receptor blockade overcomes remyelination failure after white matter stroke and stimulates functional recovery in aged mice". PNAS USA. 113: E8453–E8462. doi:10.1073/pnas.1615322113. PMC 5206535.
  6. ↑ Stopping a receptor called 'nogo' boosts the synapses
  7. ↑ Qin H, Pu HX, Li M, Ahmed S, Song J (Dec 2008). "Identification and structural mechanism for a novel interaction between a ubiquitin ligase WWP1 and Nogo-A, a key inhibitor for central nervous system regeneration". Biochemistry. 47 (51): 13647–58. doi:10.1021/bi8017976. PMID 19035836.
  8. ↑ 8.0 8.1 Tagami S, Eguchi Y, Kinoshita M, Takeda M, Tsujimoto Y (Nov 2000). "A novel protein, RTN-XS, interacts with both Bcl-XL and Bcl-2 on endoplasmic reticulum and reduces their anti-apoptotic activity". Oncogene. 19 (50): 5736–46. doi:10.1038/sj.onc.1203948. PMID 11126360.

Further reading

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