The trafficking of NaV1.8
▶ The β3 subunit masks the ER retention signal of NaV1.8 and release the channel from the ER. ▶ p11 directly binds to NaV1.8 and help its translocation to the plasma membrane. ▶ PDZD2 is responsible for the functional expression of NaV1.8 on the plasma membrane. ▶ Contactin KO mice exhibit a reducti...
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| Veröffentlicht in: | Neuroscience letters 2010-12, Vol.486 (2), p.78-83 |
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| container_title | Neuroscience letters |
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| creator | Swanwick, Richard S. Pristerá, Alessandro Okuse, Kenji |
| description | ▶ The β3 subunit masks the ER retention signal of NaV1.8 and release the channel from the ER. ▶ p11 directly binds to NaV1.8 and help its translocation to the plasma membrane. ▶ PDZD2 is responsible for the functional expression of NaV1.8 on the plasma membrane. ▶ Contactin KO mice exhibit a reduction of NaV1.8 along unmyelinated axons in the sciatic nerve. ▶ PKA activation increases the NaV1.8 density on the membrane through direct phosphorylation.
The α-subunit of tetrodotoxin-resistant voltage-gated sodium channel NaV1.8 is selectively expressed in sensory neurons. It has been reported that NaV1.8 is involved in the transmission of nociceptive information from sensory neurons to the central nervous system in nociceptive [1] and neuropathic [24] pain conditions. Thus NaV1.8 has been a promising target to treat chronic pain. Here we discuss the recent advances in the study of trafficking mechanism of NaV1.8. These pieces of information are particularly important as such trafficking machinery could be new targets for painkillers. |
| doi_str_mv | 10.1016/j.neulet.2010.08.074 |
| format | Article |
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The α-subunit of tetrodotoxin-resistant voltage-gated sodium channel NaV1.8 is selectively expressed in sensory neurons. It has been reported that NaV1.8 is involved in the transmission of nociceptive information from sensory neurons to the central nervous system in nociceptive [1] and neuropathic [24] pain conditions. Thus NaV1.8 has been a promising target to treat chronic pain. Here we discuss the recent advances in the study of trafficking mechanism of NaV1.8. These pieces of information are particularly important as such trafficking machinery could be new targets for painkillers.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2010.08.074</identifier><identifier>PMID: 20816723</identifier><language>eng</language><publisher>Elsevier Ireland Ltd</publisher><subject>Pain ; Review ; Sensory Neuron ; Sodium Channel ; Trafficking</subject><ispartof>Neuroscience letters, 2010-12, Vol.486 (2), p.78-83</ispartof><rights>2010 Elsevier Ireland Ltd</rights><rights>2010 Elsevier Ireland Ltd. 2010 Elsevier Ireland Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3224-58ae0a1c297edab9b5cf29141a5c6fdb1d8d7a69dead99e5efbe1d8efffd4c753</citedby><cites>FETCH-LOGICAL-c3224-58ae0a1c297edab9b5cf29141a5c6fdb1d8d7a69dead99e5efbe1d8efffd4c753</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0304394010011547$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids></links><search><creatorcontrib>Swanwick, Richard S.</creatorcontrib><creatorcontrib>Pristerá, Alessandro</creatorcontrib><creatorcontrib>Okuse, Kenji</creatorcontrib><title>The trafficking of NaV1.8</title><title>Neuroscience letters</title><description>▶ The β3 subunit masks the ER retention signal of NaV1.8 and release the channel from the ER. ▶ p11 directly binds to NaV1.8 and help its translocation to the plasma membrane. ▶ PDZD2 is responsible for the functional expression of NaV1.8 on the plasma membrane. ▶ Contactin KO mice exhibit a reduction of NaV1.8 along unmyelinated axons in the sciatic nerve. ▶ PKA activation increases the NaV1.8 density on the membrane through direct phosphorylation.
The α-subunit of tetrodotoxin-resistant voltage-gated sodium channel NaV1.8 is selectively expressed in sensory neurons. It has been reported that NaV1.8 is involved in the transmission of nociceptive information from sensory neurons to the central nervous system in nociceptive [1] and neuropathic [24] pain conditions. Thus NaV1.8 has been a promising target to treat chronic pain. Here we discuss the recent advances in the study of trafficking mechanism of NaV1.8. These pieces of information are particularly important as such trafficking machinery could be new targets for painkillers.</description><subject>Pain</subject><subject>Review</subject><subject>Sensory Neuron</subject><subject>Sodium Channel</subject><subject>Trafficking</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNp9kM9KAzEQh4MotlYfQPDQF9h1kk02yUWQ4j8oeqleQzaZtKntbsm2gm9vSkXx4mngN8w3Mx8hVxRKCrS-XpYt7la4LRnkCFQJkh-RIVWSFVJLdkyGUAEvKs1hQM76fgkAggp-SgYMFK0lq4bkcrbA8TbZEKJ7j-183IXxs32jpTonJ8Guerz4riPyen83mzwW05eHp8nttHAVY7wQyiJY6piW6G2jG-EC05RTK1wdfEO98tLW2qP1WqPA0GDOMITguZOiGpGbA3eza9boHbb5nJXZpLi26dN0Npq_nTYuzLz7MHmjVFxlAD8AXOr6PmH4maVg9qrM0hxUmb0qA8pkVb97MT_3ETGZ3kVsHfqY0G2N7-L_gC-yFnNV</recordid><startdate>20101210</startdate><enddate>20101210</enddate><creator>Swanwick, Richard S.</creator><creator>Pristerá, Alessandro</creator><creator>Okuse, Kenji</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Scientific Publishers Ireland</general><scope>6I.</scope><scope>AAFTH</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20101210</creationdate><title>The trafficking of NaV1.8</title><author>Swanwick, Richard S. ; Pristerá, Alessandro ; Okuse, Kenji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3224-58ae0a1c297edab9b5cf29141a5c6fdb1d8d7a69dead99e5efbe1d8efffd4c753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Pain</topic><topic>Review</topic><topic>Sensory Neuron</topic><topic>Sodium Channel</topic><topic>Trafficking</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Swanwick, Richard S.</creatorcontrib><creatorcontrib>Pristerá, Alessandro</creatorcontrib><creatorcontrib>Okuse, Kenji</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Swanwick, Richard S.</au><au>Pristerá, Alessandro</au><au>Okuse, Kenji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The trafficking of NaV1.8</atitle><jtitle>Neuroscience letters</jtitle><date>2010-12-10</date><risdate>2010</risdate><volume>486</volume><issue>2</issue><spage>78</spage><epage>83</epage><pages>78-83</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><abstract>▶ The β3 subunit masks the ER retention signal of NaV1.8 and release the channel from the ER. ▶ p11 directly binds to NaV1.8 and help its translocation to the plasma membrane. ▶ PDZD2 is responsible for the functional expression of NaV1.8 on the plasma membrane. ▶ Contactin KO mice exhibit a reduction of NaV1.8 along unmyelinated axons in the sciatic nerve. ▶ PKA activation increases the NaV1.8 density on the membrane through direct phosphorylation.
The α-subunit of tetrodotoxin-resistant voltage-gated sodium channel NaV1.8 is selectively expressed in sensory neurons. It has been reported that NaV1.8 is involved in the transmission of nociceptive information from sensory neurons to the central nervous system in nociceptive [1] and neuropathic [24] pain conditions. Thus NaV1.8 has been a promising target to treat chronic pain. Here we discuss the recent advances in the study of trafficking mechanism of NaV1.8. These pieces of information are particularly important as such trafficking machinery could be new targets for painkillers.</abstract><pub>Elsevier Ireland Ltd</pub><pmid>20816723</pmid><doi>10.1016/j.neulet.2010.08.074</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Neuroscience letters, 2010-12, Vol.486 (2), p.78-83 |
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| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2977848 |
| source | Elsevier ScienceDirect Journals |
| subjects | Pain Review Sensory Neuron Sodium Channel Trafficking |
| title | The trafficking of NaV1.8 |
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