Systems genetics analysis reveals the common genetic basis for pain sensitivity and cognitive function
Background There is growing evidence of a strong correlation between pain sensitivity and cognitive function under both physiological and pathological conditions. However, the detailed mechanisms remain largely unknown. In the current study, we sought to explore candidate genes and common molecular...
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| Veröffentlicht in: | CNS neuroscience & therapeutics 2024-02, Vol.30 (2), p.e14557-n/a |
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| creator | Xu, Fuyi Chen, Anran Pan, Shuijing Wu, Yingying He, Hongjie Han, Zhe Lu, Lu Orgil, Buyan‐Ochir Chi, XiaoDong Yang, Cunhua Jia, Shushan Yu, Cuicui Mi, Jia |
| description | Background
There is growing evidence of a strong correlation between pain sensitivity and cognitive function under both physiological and pathological conditions. However, the detailed mechanisms remain largely unknown. In the current study, we sought to explore candidate genes and common molecular mechanisms underlying pain sensitivity and cognitive function with a transcriptome‐wide association study using recombinant inbred mice from the BXD family.
Methods
The pain sensitivity determined by Hargreaves' paw withdrawal test and cognition‐related phenotypes were systematically analyzed in 60 strains of BXD mice and correlated with hippocampus transcriptomes, followed by quantitative trait locus (QTL) mapping and systems genetics analysis.
Results
The pain sensitivity showed significant variability across the BXD strains and co‐varies with cognitive traits. Pain sensitivity correlated hippocampual genes showed a significant involvement in cognition‐related pathways, including glutamatergic synapse, and PI3K‐Akt signaling pathway. Moreover, QTL mapping identified a genomic region on chromosome 4, potentially regulating the variation of pain sensitivity. Integrative analysis of expression QTL mapping, correlation analysis, and Bayesian network modeling identified Ring finger protein 20 (Rnf20) as the best candidate. Further pathway analysis indicated that Rnf20 may regulate the expression of pain sensitivity and cognitive function through the PI3K‐Akt signaling pathway, particularly through interactions with genes Ppp2r2b, Ppp2r5c, Col9a3, Met, Rps6, Tnc, and Kras.
Conclusions
Our study demonstrated that pain sensitivity is associated with genetic background and Rnf20‐mediated PI3K‐Akt signaling may involve in the regulation of pain sensitivity and cognitive functions.
Pain sensitivity is associated with genetic background and Rnf20‐mediated PI3K‐Akt signaling may involve in the regulation of pain sensitivity and cognitive functions. |
| doi_str_mv | 10.1111/cns.14557 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_10850811</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A800016349</galeid><sourcerecordid>A800016349</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4717-63fc2fc8df813ec2da9f9e0b230c5365b9a122f9873c55343403fc5c1c8f91b93</originalsourceid><addsrcrecordid>eNp1kU1v1DAQhi0EomXhwB9AlrjQw279ESf2CVUrCkgVHApny3HGW1eJvdjJovx7vKRdARL2wV_PvOOZF6HXlGxoGZc25A2thGieoHPaCLEWqlJPT3tOztCLnO8JqZlU8jk647JilHJ2jtztnEcYMt5BgNHbjE0w_Zx9xgkOYPqMxzvANg5DDI8Qbs0RcDHhvfEBZwjZj_7gx7mEd4XeheMZsJuCHX0ML9EzV7Tg1cO6Qt-vP3zbflrffP34eXt1s7ZVQ5t1zZ1lzsrOScrBss4op4C0jBMreC1aZShjTsmGWyF4xStSIoSlVjpFW8VX6P2iu5_aAToLYUym1_vkB5NmHY3Xf78Ef6d38aApkYLI0pMVevegkOKPCfKoB58t9L0JEKesmeK8qmnNWUHf_oPexymV9i0UZ6xislCbhdqZHrQPLpbEtswOBm9jAOfL_ZUkhBTV6ljDxRJgU8w5gTt9nxJ99FsXv_Vvvwv75s96T-SjwQW4XICfJcv8fyW9_XK7SP4CvWK2Mg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2933322428</pqid></control><display><type>article</type><title>Systems genetics analysis reveals the common genetic basis for pain sensitivity and cognitive function</title><source>DOAJ Directory of Open Access Journals</source><source>Wiley-Blackwell Open Access Titles</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library All Journals</source><source>PubMed Central</source><creator>Xu, Fuyi ; Chen, Anran ; Pan, Shuijing ; Wu, Yingying ; He, Hongjie ; Han, Zhe ; Lu, Lu ; Orgil, Buyan‐Ochir ; Chi, XiaoDong ; Yang, Cunhua ; Jia, Shushan ; Yu, Cuicui ; Mi, Jia</creator><creatorcontrib>Xu, Fuyi ; Chen, Anran ; Pan, Shuijing ; Wu, Yingying ; He, Hongjie ; Han, Zhe ; Lu, Lu ; Orgil, Buyan‐Ochir ; Chi, XiaoDong ; Yang, Cunhua ; Jia, Shushan ; Yu, Cuicui ; Mi, Jia</creatorcontrib><description>Background
There is growing evidence of a strong correlation between pain sensitivity and cognitive function under both physiological and pathological conditions. However, the detailed mechanisms remain largely unknown. In the current study, we sought to explore candidate genes and common molecular mechanisms underlying pain sensitivity and cognitive function with a transcriptome‐wide association study using recombinant inbred mice from the BXD family.
Methods
The pain sensitivity determined by Hargreaves' paw withdrawal test and cognition‐related phenotypes were systematically analyzed in 60 strains of BXD mice and correlated with hippocampus transcriptomes, followed by quantitative trait locus (QTL) mapping and systems genetics analysis.
Results
The pain sensitivity showed significant variability across the BXD strains and co‐varies with cognitive traits. Pain sensitivity correlated hippocampual genes showed a significant involvement in cognition‐related pathways, including glutamatergic synapse, and PI3K‐Akt signaling pathway. Moreover, QTL mapping identified a genomic region on chromosome 4, potentially regulating the variation of pain sensitivity. Integrative analysis of expression QTL mapping, correlation analysis, and Bayesian network modeling identified Ring finger protein 20 (Rnf20) as the best candidate. Further pathway analysis indicated that Rnf20 may regulate the expression of pain sensitivity and cognitive function through the PI3K‐Akt signaling pathway, particularly through interactions with genes Ppp2r2b, Ppp2r5c, Col9a3, Met, Rps6, Tnc, and Kras.
Conclusions
Our study demonstrated that pain sensitivity is associated with genetic background and Rnf20‐mediated PI3K‐Akt signaling may involve in the regulation of pain sensitivity and cognitive functions.
Pain sensitivity is associated with genetic background and Rnf20‐mediated PI3K‐Akt signaling may involve in the regulation of pain sensitivity and cognitive functions.</description><identifier>ISSN: 1755-5930</identifier><identifier>ISSN: 1755-5949</identifier><identifier>EISSN: 1755-5949</identifier><identifier>DOI: 10.1111/cns.14557</identifier><identifier>PMID: 38421132</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Animal cognition ; Bayesian analysis ; Brain ; BXD mice ; Chromosome 4 ; Cognition ; Cognitive ability ; Collagen (type IX) ; Correlation analysis ; Gene expression ; Gene mapping ; Genes ; Genetic aspects ; Genetic research ; Genetics ; Genomes ; Genotype & phenotype ; Glutamatergic transmission ; hippocampus ; Inbreeding ; Memory ; Molecular modelling ; Original ; Pain ; pain sensitivity ; Peptide mapping ; Phenotypes ; Physiological aspects ; Quantitative genetics ; Quantitative trait loci ; RING finger proteins ; Rnf20 ; Signal transduction ; Synapses ; Transcriptomes</subject><ispartof>CNS neuroscience & therapeutics, 2024-02, Vol.30 (2), p.e14557-n/a</ispartof><rights>2023 The Authors. published by John Wiley & Sons Ltd.</rights><rights>2023 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.</rights><rights>COPYRIGHT 2024 John Wiley & Sons, Inc.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4717-63fc2fc8df813ec2da9f9e0b230c5365b9a122f9873c55343403fc5c1c8f91b93</cites><orcidid>0000-0002-5952-5771</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10850811/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10850811/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1416,11561,27923,27924,45573,45574,46051,46475,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38421132$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xu, Fuyi</creatorcontrib><creatorcontrib>Chen, Anran</creatorcontrib><creatorcontrib>Pan, Shuijing</creatorcontrib><creatorcontrib>Wu, Yingying</creatorcontrib><creatorcontrib>He, Hongjie</creatorcontrib><creatorcontrib>Han, Zhe</creatorcontrib><creatorcontrib>Lu, Lu</creatorcontrib><creatorcontrib>Orgil, Buyan‐Ochir</creatorcontrib><creatorcontrib>Chi, XiaoDong</creatorcontrib><creatorcontrib>Yang, Cunhua</creatorcontrib><creatorcontrib>Jia, Shushan</creatorcontrib><creatorcontrib>Yu, Cuicui</creatorcontrib><creatorcontrib>Mi, Jia</creatorcontrib><title>Systems genetics analysis reveals the common genetic basis for pain sensitivity and cognitive function</title><title>CNS neuroscience & therapeutics</title><addtitle>CNS Neurosci Ther</addtitle><description>Background
There is growing evidence of a strong correlation between pain sensitivity and cognitive function under both physiological and pathological conditions. However, the detailed mechanisms remain largely unknown. In the current study, we sought to explore candidate genes and common molecular mechanisms underlying pain sensitivity and cognitive function with a transcriptome‐wide association study using recombinant inbred mice from the BXD family.
Methods
The pain sensitivity determined by Hargreaves' paw withdrawal test and cognition‐related phenotypes were systematically analyzed in 60 strains of BXD mice and correlated with hippocampus transcriptomes, followed by quantitative trait locus (QTL) mapping and systems genetics analysis.
Results
The pain sensitivity showed significant variability across the BXD strains and co‐varies with cognitive traits. Pain sensitivity correlated hippocampual genes showed a significant involvement in cognition‐related pathways, including glutamatergic synapse, and PI3K‐Akt signaling pathway. Moreover, QTL mapping identified a genomic region on chromosome 4, potentially regulating the variation of pain sensitivity. Integrative analysis of expression QTL mapping, correlation analysis, and Bayesian network modeling identified Ring finger protein 20 (Rnf20) as the best candidate. Further pathway analysis indicated that Rnf20 may regulate the expression of pain sensitivity and cognitive function through the PI3K‐Akt signaling pathway, particularly through interactions with genes Ppp2r2b, Ppp2r5c, Col9a3, Met, Rps6, Tnc, and Kras.
Conclusions
Our study demonstrated that pain sensitivity is associated with genetic background and Rnf20‐mediated PI3K‐Akt signaling may involve in the regulation of pain sensitivity and cognitive functions.
Pain sensitivity is associated with genetic background and Rnf20‐mediated PI3K‐Akt signaling may involve in the regulation of pain sensitivity and cognitive functions.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Animal cognition</subject><subject>Bayesian analysis</subject><subject>Brain</subject><subject>BXD mice</subject><subject>Chromosome 4</subject><subject>Cognition</subject><subject>Cognitive ability</subject><subject>Collagen (type IX)</subject><subject>Correlation analysis</subject><subject>Gene expression</subject><subject>Gene mapping</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic research</subject><subject>Genetics</subject><subject>Genomes</subject><subject>Genotype & phenotype</subject><subject>Glutamatergic transmission</subject><subject>hippocampus</subject><subject>Inbreeding</subject><subject>Memory</subject><subject>Molecular modelling</subject><subject>Original</subject><subject>Pain</subject><subject>pain sensitivity</subject><subject>Peptide mapping</subject><subject>Phenotypes</subject><subject>Physiological aspects</subject><subject>Quantitative genetics</subject><subject>Quantitative trait loci</subject><subject>RING finger proteins</subject><subject>Rnf20</subject><subject>Signal transduction</subject><subject>Synapses</subject><subject>Transcriptomes</subject><issn>1755-5930</issn><issn>1755-5949</issn><issn>1755-5949</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kU1v1DAQhi0EomXhwB9AlrjQw279ESf2CVUrCkgVHApny3HGW1eJvdjJovx7vKRdARL2wV_PvOOZF6HXlGxoGZc25A2thGieoHPaCLEWqlJPT3tOztCLnO8JqZlU8jk647JilHJ2jtztnEcYMt5BgNHbjE0w_Zx9xgkOYPqMxzvANg5DDI8Qbs0RcDHhvfEBZwjZj_7gx7mEd4XeheMZsJuCHX0ML9EzV7Tg1cO6Qt-vP3zbflrffP34eXt1s7ZVQ5t1zZ1lzsrOScrBss4op4C0jBMreC1aZShjTsmGWyF4xStSIoSlVjpFW8VX6P2iu5_aAToLYUym1_vkB5NmHY3Xf78Ef6d38aApkYLI0pMVevegkOKPCfKoB58t9L0JEKesmeK8qmnNWUHf_oPexymV9i0UZ6xislCbhdqZHrQPLpbEtswOBm9jAOfL_ZUkhBTV6ljDxRJgU8w5gTt9nxJ99FsXv_Vvvwv75s96T-SjwQW4XICfJcv8fyW9_XK7SP4CvWK2Mg</recordid><startdate>202402</startdate><enddate>202402</enddate><creator>Xu, Fuyi</creator><creator>Chen, Anran</creator><creator>Pan, Shuijing</creator><creator>Wu, Yingying</creator><creator>He, Hongjie</creator><creator>Han, Zhe</creator><creator>Lu, Lu</creator><creator>Orgil, Buyan‐Ochir</creator><creator>Chi, XiaoDong</creator><creator>Yang, Cunhua</creator><creator>Jia, Shushan</creator><creator>Yu, Cuicui</creator><creator>Mi, Jia</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IAO</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5952-5771</orcidid></search><sort><creationdate>202402</creationdate><title>Systems genetics analysis reveals the common genetic basis for pain sensitivity and cognitive function</title><author>Xu, Fuyi ; Chen, Anran ; Pan, Shuijing ; Wu, Yingying ; He, Hongjie ; Han, Zhe ; Lu, Lu ; Orgil, Buyan‐Ochir ; Chi, XiaoDong ; Yang, Cunhua ; Jia, Shushan ; Yu, Cuicui ; Mi, Jia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4717-63fc2fc8df813ec2da9f9e0b230c5365b9a122f9873c55343403fc5c1c8f91b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Animal cognition</topic><topic>Bayesian analysis</topic><topic>Brain</topic><topic>BXD mice</topic><topic>Chromosome 4</topic><topic>Cognition</topic><topic>Cognitive ability</topic><topic>Collagen (type IX)</topic><topic>Correlation analysis</topic><topic>Gene expression</topic><topic>Gene mapping</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic research</topic><topic>Genetics</topic><topic>Genomes</topic><topic>Genotype & phenotype</topic><topic>Glutamatergic transmission</topic><topic>hippocampus</topic><topic>Inbreeding</topic><topic>Memory</topic><topic>Molecular modelling</topic><topic>Original</topic><topic>Pain</topic><topic>pain sensitivity</topic><topic>Peptide mapping</topic><topic>Phenotypes</topic><topic>Physiological aspects</topic><topic>Quantitative genetics</topic><topic>Quantitative trait loci</topic><topic>RING finger proteins</topic><topic>Rnf20</topic><topic>Signal transduction</topic><topic>Synapses</topic><topic>Transcriptomes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xu, Fuyi</creatorcontrib><creatorcontrib>Chen, Anran</creatorcontrib><creatorcontrib>Pan, Shuijing</creatorcontrib><creatorcontrib>Wu, Yingying</creatorcontrib><creatorcontrib>He, Hongjie</creatorcontrib><creatorcontrib>Han, Zhe</creatorcontrib><creatorcontrib>Lu, Lu</creatorcontrib><creatorcontrib>Orgil, Buyan‐Ochir</creatorcontrib><creatorcontrib>Chi, XiaoDong</creatorcontrib><creatorcontrib>Yang, Cunhua</creatorcontrib><creatorcontrib>Jia, Shushan</creatorcontrib><creatorcontrib>Yu, Cuicui</creatorcontrib><creatorcontrib>Mi, Jia</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Wiley Free Content</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale Academic OneFile</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>CNS neuroscience & therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xu, Fuyi</au><au>Chen, Anran</au><au>Pan, Shuijing</au><au>Wu, Yingying</au><au>He, Hongjie</au><au>Han, Zhe</au><au>Lu, Lu</au><au>Orgil, Buyan‐Ochir</au><au>Chi, XiaoDong</au><au>Yang, Cunhua</au><au>Jia, Shushan</au><au>Yu, Cuicui</au><au>Mi, Jia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Systems genetics analysis reveals the common genetic basis for pain sensitivity and cognitive function</atitle><jtitle>CNS neuroscience & therapeutics</jtitle><addtitle>CNS Neurosci Ther</addtitle><date>2024-02</date><risdate>2024</risdate><volume>30</volume><issue>2</issue><spage>e14557</spage><epage>n/a</epage><pages>e14557-n/a</pages><issn>1755-5930</issn><issn>1755-5949</issn><eissn>1755-5949</eissn><abstract>Background
There is growing evidence of a strong correlation between pain sensitivity and cognitive function under both physiological and pathological conditions. However, the detailed mechanisms remain largely unknown. In the current study, we sought to explore candidate genes and common molecular mechanisms underlying pain sensitivity and cognitive function with a transcriptome‐wide association study using recombinant inbred mice from the BXD family.
Methods
The pain sensitivity determined by Hargreaves' paw withdrawal test and cognition‐related phenotypes were systematically analyzed in 60 strains of BXD mice and correlated with hippocampus transcriptomes, followed by quantitative trait locus (QTL) mapping and systems genetics analysis.
Results
The pain sensitivity showed significant variability across the BXD strains and co‐varies with cognitive traits. Pain sensitivity correlated hippocampual genes showed a significant involvement in cognition‐related pathways, including glutamatergic synapse, and PI3K‐Akt signaling pathway. Moreover, QTL mapping identified a genomic region on chromosome 4, potentially regulating the variation of pain sensitivity. Integrative analysis of expression QTL mapping, correlation analysis, and Bayesian network modeling identified Ring finger protein 20 (Rnf20) as the best candidate. Further pathway analysis indicated that Rnf20 may regulate the expression of pain sensitivity and cognitive function through the PI3K‐Akt signaling pathway, particularly through interactions with genes Ppp2r2b, Ppp2r5c, Col9a3, Met, Rps6, Tnc, and Kras.
Conclusions
Our study demonstrated that pain sensitivity is associated with genetic background and Rnf20‐mediated PI3K‐Akt signaling may involve in the regulation of pain sensitivity and cognitive functions.
Pain sensitivity is associated with genetic background and Rnf20‐mediated PI3K‐Akt signaling may involve in the regulation of pain sensitivity and cognitive functions.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>38421132</pmid><doi>10.1111/cns.14557</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-5952-5771</orcidid><oa>free_for_read</oa></addata></record> |
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| source | DOAJ Directory of Open Access Journals; Wiley-Blackwell Open Access Titles; EZB-FREE-00999 freely available EZB journals; Wiley Online Library All Journals; PubMed Central |
| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Animal cognition Bayesian analysis Brain BXD mice Chromosome 4 Cognition Cognitive ability Collagen (type IX) Correlation analysis Gene expression Gene mapping Genes Genetic aspects Genetic research Genetics Genomes Genotype & phenotype Glutamatergic transmission hippocampus Inbreeding Memory Molecular modelling Original Pain pain sensitivity Peptide mapping Phenotypes Physiological aspects Quantitative genetics Quantitative trait loci RING finger proteins Rnf20 Signal transduction Synapses Transcriptomes |
| title | Systems genetics analysis reveals the common genetic basis for pain sensitivity and cognitive function |
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