Tmem100 Is a Regulator of TRPA1-TRPV1 Complex and Contributes to Persistent Pain
TRPA1 and TRPV1 are crucial pain mediators, but how their interaction contributes to persistent pain is unknown. Here, we identify Tmem100 as a potentiating modulator of TRPA1-V1 complexes. Tmem100 is coexpressed and forms a complex with TRPA1 and TRPV1 in DRG neurons. Tmem100-deficient mice show a...
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| Veröffentlicht in: | Neuron (Cambridge, Mass.) Mass.), 2015-02, Vol.85 (4), p.833-846 |
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| creator | Weng, Hao-Jui Patel, Kush N. Jeske, Nathaniel A. Bierbower, Sonya M. Zou, Wangyuan Tiwari, Vinod Zheng, Qin Tang, Zongxiang Mo, Gary C.H. Wang, Yan Geng, Yixun Zhang, Jin Guan, Yun Akopian, Armen N. Dong, Xinzhong |
| description | TRPA1 and TRPV1 are crucial pain mediators, but how their interaction contributes to persistent pain is unknown. Here, we identify Tmem100 as a potentiating modulator of TRPA1-V1 complexes. Tmem100 is coexpressed and forms a complex with TRPA1 and TRPV1 in DRG neurons. Tmem100-deficient mice show a reduction in inflammatory mechanical hyperalgesia and TRPA1- but not TRPV1-mediated pain. Single-channel recording in a heterologous system reveals that Tmem100 selectively potentiates TRPA1 activity in a TRPV1-dependent manner. Mechanistically, Tmem100 weakens the association of TRPA1 and TRPV1, thereby releasing the inhibition of TRPA1 by TRPV1. A Tmem100 mutant, Tmem100-3Q, exerts the opposite effect; i.e., it enhances the association of TRPA1 and TRPV1 and strongly inhibits TRPA1. Strikingly, a cell-permeable peptide (CPP) containing the C-terminal sequence of Tmem100-3Q mimics its effect and inhibits persistent pain. Our study unveils a context-dependent modulation of the TRPA1-V1 complex, and Tmem100-3Q CPP is a promising pain therapy.
•A unique context-dependent TRP channel regulation by disinhibitory mechanism•Tmem100 as a potentiating modulator of TRPA1 in the TRPA1-TRPV1 complex•Tmem100-mutant-derived cell-permeable peptide as novel pain therapeutics•The first mechanistic study of Tmem100, an important gene implicated in diseases
TRPA1 and TRPV1 are crucial pain mediators, but how their interaction contributes to persistent pain is unknown. Weng et al. identify Tmem100 as a potentiating modulator of TRPA1-V1 complexes. Targeting this modulation, they developed a strategy for blocking persistent pain. |
| doi_str_mv | 10.1016/j.neuron.2014.12.065 |
| format | Article |
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•A unique context-dependent TRP channel regulation by disinhibitory mechanism•Tmem100 as a potentiating modulator of TRPA1 in the TRPA1-TRPV1 complex•Tmem100-mutant-derived cell-permeable peptide as novel pain therapeutics•The first mechanistic study of Tmem100, an important gene implicated in diseases
TRPA1 and TRPV1 are crucial pain mediators, but how their interaction contributes to persistent pain is unknown. Weng et al. identify Tmem100 as a potentiating modulator of TRPA1-V1 complexes. Targeting this modulation, they developed a strategy for blocking persistent pain.</description><identifier>ISSN: 0896-6273</identifier><identifier>EISSN: 1097-4199</identifier><identifier>DOI: 10.1016/j.neuron.2014.12.065</identifier><identifier>PMID: 25640077</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Action Potentials - drug effects ; Action Potentials - genetics ; Animals ; Biophysical Phenomena - drug effects ; Biophysical Phenomena - genetics ; Capsaicin - toxicity ; Cells, Cultured ; CHO Cells ; Cricetulus ; Disease Models, Animal ; Electric Stimulation ; Ganglia, Spinal - cytology ; Ganglia, Spinal - metabolism ; HEK293 Cells ; Humans ; Hyperalgesia - genetics ; Hyperalgesia - metabolism ; Male ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neurons ; Neurons - drug effects ; Neurons - physiology ; Pain ; Pain - chemically induced ; Pain - metabolism ; Pain - pathology ; Pain Measurement ; Peptides ; Physical Stimulation ; Proteins ; Studies ; Transient Receptor Potential Channels - metabolism ; TRPA1 Cation Channel ; TRPV Cation Channels - metabolism</subject><ispartof>Neuron (Cambridge, Mass.), 2015-02, Vol.85 (4), p.833-846</ispartof><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited Feb 18, 2015</rights><rights>2014 Elsevier Inc. All rights reserved 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c660t-793028d6ba62a3c6504dc337e196b69b0168b1b473b2afbd6bcb6455fd9ed5363</citedby><cites>FETCH-LOGICAL-c660t-793028d6ba62a3c6504dc337e196b69b0168b1b473b2afbd6bcb6455fd9ed5363</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S089662731401174X$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25640077$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Weng, Hao-Jui</creatorcontrib><creatorcontrib>Patel, Kush N.</creatorcontrib><creatorcontrib>Jeske, Nathaniel A.</creatorcontrib><creatorcontrib>Bierbower, Sonya M.</creatorcontrib><creatorcontrib>Zou, Wangyuan</creatorcontrib><creatorcontrib>Tiwari, Vinod</creatorcontrib><creatorcontrib>Zheng, Qin</creatorcontrib><creatorcontrib>Tang, Zongxiang</creatorcontrib><creatorcontrib>Mo, Gary C.H.</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Geng, Yixun</creatorcontrib><creatorcontrib>Zhang, Jin</creatorcontrib><creatorcontrib>Guan, Yun</creatorcontrib><creatorcontrib>Akopian, Armen N.</creatorcontrib><creatorcontrib>Dong, Xinzhong</creatorcontrib><title>Tmem100 Is a Regulator of TRPA1-TRPV1 Complex and Contributes to Persistent Pain</title><title>Neuron (Cambridge, Mass.)</title><addtitle>Neuron</addtitle><description>TRPA1 and TRPV1 are crucial pain mediators, but how their interaction contributes to persistent pain is unknown. Here, we identify Tmem100 as a potentiating modulator of TRPA1-V1 complexes. Tmem100 is coexpressed and forms a complex with TRPA1 and TRPV1 in DRG neurons. Tmem100-deficient mice show a reduction in inflammatory mechanical hyperalgesia and TRPA1- but not TRPV1-mediated pain. Single-channel recording in a heterologous system reveals that Tmem100 selectively potentiates TRPA1 activity in a TRPV1-dependent manner. Mechanistically, Tmem100 weakens the association of TRPA1 and TRPV1, thereby releasing the inhibition of TRPA1 by TRPV1. A Tmem100 mutant, Tmem100-3Q, exerts the opposite effect; i.e., it enhances the association of TRPA1 and TRPV1 and strongly inhibits TRPA1. Strikingly, a cell-permeable peptide (CPP) containing the C-terminal sequence of Tmem100-3Q mimics its effect and inhibits persistent pain. Our study unveils a context-dependent modulation of the TRPA1-V1 complex, and Tmem100-3Q CPP is a promising pain therapy.
•A unique context-dependent TRP channel regulation by disinhibitory mechanism•Tmem100 as a potentiating modulator of TRPA1 in the TRPA1-TRPV1 complex•Tmem100-mutant-derived cell-permeable peptide as novel pain therapeutics•The first mechanistic study of Tmem100, an important gene implicated in diseases
TRPA1 and TRPV1 are crucial pain mediators, but how their interaction contributes to persistent pain is unknown. Weng et al. identify Tmem100 as a potentiating modulator of TRPA1-V1 complexes. Targeting this modulation, they developed a strategy for blocking persistent pain.</description><subject>Action Potentials - drug effects</subject><subject>Action Potentials - genetics</subject><subject>Animals</subject><subject>Biophysical Phenomena - drug effects</subject><subject>Biophysical Phenomena - genetics</subject><subject>Capsaicin - toxicity</subject><subject>Cells, Cultured</subject><subject>CHO Cells</subject><subject>Cricetulus</subject><subject>Disease Models, Animal</subject><subject>Electric Stimulation</subject><subject>Ganglia, Spinal - cytology</subject><subject>Ganglia, Spinal - metabolism</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Hyperalgesia - genetics</subject><subject>Hyperalgesia - metabolism</subject><subject>Male</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - physiology</subject><subject>Pain</subject><subject>Pain - chemically induced</subject><subject>Pain - metabolism</subject><subject>Pain - pathology</subject><subject>Pain Measurement</subject><subject>Peptides</subject><subject>Physical Stimulation</subject><subject>Proteins</subject><subject>Studies</subject><subject>Transient Receptor Potential Channels - metabolism</subject><subject>TRPA1 Cation Channel</subject><subject>TRPV Cation Channels - metabolism</subject><issn>0896-6273</issn><issn>1097-4199</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUuLFDEUhYMoTjv6D0QCbtxUmVclnY0wND4GBmyG1m1IUrfGNFVJm1QN-u9N0-P4WIibJJDvnnvvOQg9p6SlhMrX-zbCklNsGaGipawlsnuAVpRo1Qiq9UO0ImstG8kUP0NPStmTCnaaPkZnrJOCEKVWaLubYKKE4MuCLb6Gm2W0c8o4DXh3vb2gTT0_U7xJ02GEb9jGvr7jnINbZih4TngLuYQyQ5zx1ob4FD0a7Fjg2d19jj69e7vbfGiuPr6_3FxcNV5KMjdKc8LWvXRWMsu97IjoPecKqJZOalc3XDvqhOKO2cFV0Dspum7oNfQdl_wcvTnpHhY3Qe9r_2xHc8hhsvm7STaYP39i-GJu0q0RnEvG1lXg1Z1ATl8XKLOZQvEwjjZCWoqhUgpGGJHsP9BO8RoDVRV9-Re6T0uO1YkjJYkgWh-HFyfK51RKhuF-bkrMMV2zN6d0zTFdQ5mp6dayF7_vfF_0M85fpkB1_jZANsUHiB76kMHPpk_h3x1-ACYita0</recordid><startdate>20150218</startdate><enddate>20150218</enddate><creator>Weng, Hao-Jui</creator><creator>Patel, Kush N.</creator><creator>Jeske, Nathaniel A.</creator><creator>Bierbower, Sonya M.</creator><creator>Zou, Wangyuan</creator><creator>Tiwari, Vinod</creator><creator>Zheng, Qin</creator><creator>Tang, Zongxiang</creator><creator>Mo, Gary C.H.</creator><creator>Wang, Yan</creator><creator>Geng, Yixun</creator><creator>Zhang, Jin</creator><creator>Guan, Yun</creator><creator>Akopian, Armen N.</creator><creator>Dong, Xinzhong</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150218</creationdate><title>Tmem100 Is a Regulator of TRPA1-TRPV1 Complex and Contributes to Persistent Pain</title><author>Weng, Hao-Jui ; Patel, Kush N. ; Jeske, Nathaniel A. ; Bierbower, Sonya M. ; Zou, Wangyuan ; Tiwari, Vinod ; Zheng, Qin ; Tang, Zongxiang ; Mo, Gary C.H. ; Wang, Yan ; Geng, Yixun ; Zhang, Jin ; Guan, Yun ; Akopian, Armen N. ; Dong, Xinzhong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c660t-793028d6ba62a3c6504dc337e196b69b0168b1b473b2afbd6bcb6455fd9ed5363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Action Potentials - drug effects</topic><topic>Action Potentials - genetics</topic><topic>Animals</topic><topic>Biophysical Phenomena - drug effects</topic><topic>Biophysical Phenomena - genetics</topic><topic>Capsaicin - toxicity</topic><topic>Cells, Cultured</topic><topic>CHO Cells</topic><topic>Cricetulus</topic><topic>Disease Models, Animal</topic><topic>Electric Stimulation</topic><topic>Ganglia, Spinal - cytology</topic><topic>Ganglia, Spinal - metabolism</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Hyperalgesia - genetics</topic><topic>Hyperalgesia - metabolism</topic><topic>Male</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Neurons</topic><topic>Neurons - drug effects</topic><topic>Neurons - physiology</topic><topic>Pain</topic><topic>Pain - chemically induced</topic><topic>Pain - metabolism</topic><topic>Pain - pathology</topic><topic>Pain Measurement</topic><topic>Peptides</topic><topic>Physical Stimulation</topic><topic>Proteins</topic><topic>Studies</topic><topic>Transient Receptor Potential Channels - metabolism</topic><topic>TRPA1 Cation Channel</topic><topic>TRPV Cation Channels - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weng, Hao-Jui</creatorcontrib><creatorcontrib>Patel, Kush N.</creatorcontrib><creatorcontrib>Jeske, Nathaniel A.</creatorcontrib><creatorcontrib>Bierbower, Sonya M.</creatorcontrib><creatorcontrib>Zou, Wangyuan</creatorcontrib><creatorcontrib>Tiwari, Vinod</creatorcontrib><creatorcontrib>Zheng, Qin</creatorcontrib><creatorcontrib>Tang, Zongxiang</creatorcontrib><creatorcontrib>Mo, Gary C.H.</creatorcontrib><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Geng, Yixun</creatorcontrib><creatorcontrib>Zhang, Jin</creatorcontrib><creatorcontrib>Guan, Yun</creatorcontrib><creatorcontrib>Akopian, Armen N.</creatorcontrib><creatorcontrib>Dong, Xinzhong</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Neuron (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weng, Hao-Jui</au><au>Patel, Kush N.</au><au>Jeske, Nathaniel A.</au><au>Bierbower, Sonya M.</au><au>Zou, Wangyuan</au><au>Tiwari, Vinod</au><au>Zheng, Qin</au><au>Tang, Zongxiang</au><au>Mo, Gary C.H.</au><au>Wang, Yan</au><au>Geng, Yixun</au><au>Zhang, Jin</au><au>Guan, Yun</au><au>Akopian, Armen N.</au><au>Dong, Xinzhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tmem100 Is a Regulator of TRPA1-TRPV1 Complex and Contributes to Persistent Pain</atitle><jtitle>Neuron (Cambridge, Mass.)</jtitle><addtitle>Neuron</addtitle><date>2015-02-18</date><risdate>2015</risdate><volume>85</volume><issue>4</issue><spage>833</spage><epage>846</epage><pages>833-846</pages><issn>0896-6273</issn><eissn>1097-4199</eissn><abstract>TRPA1 and TRPV1 are crucial pain mediators, but how their interaction contributes to persistent pain is unknown. Here, we identify Tmem100 as a potentiating modulator of TRPA1-V1 complexes. Tmem100 is coexpressed and forms a complex with TRPA1 and TRPV1 in DRG neurons. Tmem100-deficient mice show a reduction in inflammatory mechanical hyperalgesia and TRPA1- but not TRPV1-mediated pain. Single-channel recording in a heterologous system reveals that Tmem100 selectively potentiates TRPA1 activity in a TRPV1-dependent manner. Mechanistically, Tmem100 weakens the association of TRPA1 and TRPV1, thereby releasing the inhibition of TRPA1 by TRPV1. A Tmem100 mutant, Tmem100-3Q, exerts the opposite effect; i.e., it enhances the association of TRPA1 and TRPV1 and strongly inhibits TRPA1. Strikingly, a cell-permeable peptide (CPP) containing the C-terminal sequence of Tmem100-3Q mimics its effect and inhibits persistent pain. Our study unveils a context-dependent modulation of the TRPA1-V1 complex, and Tmem100-3Q CPP is a promising pain therapy.
•A unique context-dependent TRP channel regulation by disinhibitory mechanism•Tmem100 as a potentiating modulator of TRPA1 in the TRPA1-TRPV1 complex•Tmem100-mutant-derived cell-permeable peptide as novel pain therapeutics•The first mechanistic study of Tmem100, an important gene implicated in diseases
TRPA1 and TRPV1 are crucial pain mediators, but how their interaction contributes to persistent pain is unknown. Weng et al. identify Tmem100 as a potentiating modulator of TRPA1-V1 complexes. Targeting this modulation, they developed a strategy for blocking persistent pain.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>25640077</pmid><doi>10.1016/j.neuron.2014.12.065</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Action Potentials - drug effects Action Potentials - genetics Animals Biophysical Phenomena - drug effects Biophysical Phenomena - genetics Capsaicin - toxicity Cells, Cultured CHO Cells Cricetulus Disease Models, Animal Electric Stimulation Ganglia, Spinal - cytology Ganglia, Spinal - metabolism HEK293 Cells Humans Hyperalgesia - genetics Hyperalgesia - metabolism Male Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mice, Transgenic Neurons Neurons - drug effects Neurons - physiology Pain Pain - chemically induced Pain - metabolism Pain - pathology Pain Measurement Peptides Physical Stimulation Proteins Studies Transient Receptor Potential Channels - metabolism TRPA1 Cation Channel TRPV Cation Channels - metabolism |
| title | Tmem100 Is a Regulator of TRPA1-TRPV1 Complex and Contributes to Persistent Pain |
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