iPSC model of CHRFAM7A effect on α7 nicotinic acetylcholine receptor function in the human context
The α7 nicotinic acetylcholine receptor (α7nAChR) has been a promising target for diseases affecting cognition and higher cortical functions; however, the effect observed in animal models failed to translate into human clinical trials identifying a translational gap. CHRFAM7A is a human-specific fus...
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| Veröffentlicht in: | Translational psychiatry 2019-02, Vol.9 (1), p.59-59, Article 59 |
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| creator | Ihnatovych, Ivanna Nayak, Tapan K. Ouf, Aya Sule, Norbert Birkaya, Barbara Chaves, Lee Auerbach, Anthony Szigeti, Kinga |
| description | The α7 nicotinic acetylcholine receptor (α7nAChR) has been a promising target for diseases affecting cognition and higher cortical functions; however, the effect observed in animal models failed to translate into human clinical trials identifying a translational gap.
CHRFAM7A
is a human-specific fusion gene with properties that enable incorporation into the α7nAChR and, being human specific,
CHRFAM7A
effect was not accounted for in preclinical studies. We hypothesized that
CHRFAM7A
may account for this translational gap and understanding its function may offer novel insights when exploring α7nAChR as a drug target.
CHRFAM7A
is present in different copy number variations (CNV) in the human genome with high frequency. To study the functional consequences of the presence of the
CHRFAM7A
, two induced pluripotent stem cell (iPSC) lines (0 copy and 1 copy direct) were developed. The 0 copy line was rescued with
CHRFAM7A
transfection to control for genetic heterogeneity. As readouts for genotype–phenotype correlation, α7nAChR synaptic transmission and amyloid beta 1–42 (Aβ
1–42
) uptake were tested. Synaptic transmission in the presence of
CHRFAM7A
demonstrated that PNU-modulated desensitization of α7nAChR currents increased as a function of
CHRFAM7A
dosage.
CHRFAM7A
mitigated the dose response of Aβ
1–42
uptake suggesting a protective effect beyond physiological concentrations. Furthermore, in the presence of CHRFAM7A Aβ
1–42
uptake activated neuronal interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) without activating the canonical inflammasome pathway. Lead optimization may identify more potent molecules when the screen has a model harboring
CHRFAM7A
. Incorporating pharmacogenetics into clinical trials may enhance signals in efficacy measures. |
| doi_str_mv | 10.1038/s41398-019-0375-z |
| format | Article |
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CHRFAM7A
is a human-specific fusion gene with properties that enable incorporation into the α7nAChR and, being human specific,
CHRFAM7A
effect was not accounted for in preclinical studies. We hypothesized that
CHRFAM7A
may account for this translational gap and understanding its function may offer novel insights when exploring α7nAChR as a drug target.
CHRFAM7A
is present in different copy number variations (CNV) in the human genome with high frequency. To study the functional consequences of the presence of the
CHRFAM7A
, two induced pluripotent stem cell (iPSC) lines (0 copy and 1 copy direct) were developed. The 0 copy line was rescued with
CHRFAM7A
transfection to control for genetic heterogeneity. As readouts for genotype–phenotype correlation, α7nAChR synaptic transmission and amyloid beta 1–42 (Aβ
1–42
) uptake were tested. Synaptic transmission in the presence of
CHRFAM7A
demonstrated that PNU-modulated desensitization of α7nAChR currents increased as a function of
CHRFAM7A
dosage.
CHRFAM7A
mitigated the dose response of Aβ
1–42
uptake suggesting a protective effect beyond physiological concentrations. Furthermore, in the presence of CHRFAM7A Aβ
1–42
uptake activated neuronal interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) without activating the canonical inflammasome pathway. Lead optimization may identify more potent molecules when the screen has a model harboring
CHRFAM7A
. Incorporating pharmacogenetics into clinical trials may enhance signals in efficacy measures.</description><identifier>ISSN: 2158-3188</identifier><identifier>EISSN: 2158-3188</identifier><identifier>DOI: 10.1038/s41398-019-0375-z</identifier><identifier>PMID: 30710073</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>101/1 ; 13/95 ; 14/19 ; 45/77 ; 631/378 ; 631/532 ; 9/74 ; 96/100 ; 96/31 ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Amyloid beta-Peptides - administration & dosage ; Amyloid beta-Peptides - metabolism ; Behavioral Sciences ; Biological Psychology ; Cell Differentiation ; Cells, Cultured ; Clinical trials ; Gene Expression ; HEK293 Cells ; Humans ; Induced Pluripotent Stem Cells - metabolism ; Inflammation - metabolism ; Medicine ; Medicine & Public Health ; Neurons - metabolism ; Neurosciences ; Peptide Fragments - administration & dosage ; Peptide Fragments - metabolism ; Pharmacotherapy ; Psychiatry ; Synaptic Transmission ; Tumor necrosis factor-TNF</subject><ispartof>Translational psychiatry, 2019-02, Vol.9 (1), p.59-59, Article 59</ispartof><rights>The Author(s) 2019</rights><rights>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><citedby>FETCH-LOGICAL-c385z-28d8c0abd870c5bb0b45cff4e1508ce37c17c60532175f589fef5e83d36406973</citedby><cites>FETCH-LOGICAL-c385z-28d8c0abd870c5bb0b45cff4e1508ce37c17c60532175f589fef5e83d36406973</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6358606/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6358606/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27922,27923,41118,42187,51574,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30710073$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ihnatovych, Ivanna</creatorcontrib><creatorcontrib>Nayak, Tapan K.</creatorcontrib><creatorcontrib>Ouf, Aya</creatorcontrib><creatorcontrib>Sule, Norbert</creatorcontrib><creatorcontrib>Birkaya, Barbara</creatorcontrib><creatorcontrib>Chaves, Lee</creatorcontrib><creatorcontrib>Auerbach, Anthony</creatorcontrib><creatorcontrib>Szigeti, Kinga</creatorcontrib><title>iPSC model of CHRFAM7A effect on α7 nicotinic acetylcholine receptor function in the human context</title><title>Translational psychiatry</title><addtitle>Transl Psychiatry</addtitle><addtitle>Transl Psychiatry</addtitle><description>The α7 nicotinic acetylcholine receptor (α7nAChR) has been a promising target for diseases affecting cognition and higher cortical functions; however, the effect observed in animal models failed to translate into human clinical trials identifying a translational gap.
CHRFAM7A
is a human-specific fusion gene with properties that enable incorporation into the α7nAChR and, being human specific,
CHRFAM7A
effect was not accounted for in preclinical studies. We hypothesized that
CHRFAM7A
may account for this translational gap and understanding its function may offer novel insights when exploring α7nAChR as a drug target.
CHRFAM7A
is present in different copy number variations (CNV) in the human genome with high frequency. To study the functional consequences of the presence of the
CHRFAM7A
, two induced pluripotent stem cell (iPSC) lines (0 copy and 1 copy direct) were developed. The 0 copy line was rescued with
CHRFAM7A
transfection to control for genetic heterogeneity. As readouts for genotype–phenotype correlation, α7nAChR synaptic transmission and amyloid beta 1–42 (Aβ
1–42
) uptake were tested. Synaptic transmission in the presence of
CHRFAM7A
demonstrated that PNU-modulated desensitization of α7nAChR currents increased as a function of
CHRFAM7A
dosage.
CHRFAM7A
mitigated the dose response of Aβ
1–42
uptake suggesting a protective effect beyond physiological concentrations. Furthermore, in the presence of CHRFAM7A Aβ
1–42
uptake activated neuronal interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) without activating the canonical inflammasome pathway. Lead optimization may identify more potent molecules when the screen has a model harboring
CHRFAM7A
. Incorporating pharmacogenetics into clinical trials may enhance signals in efficacy measures.</description><subject>101/1</subject><subject>13/95</subject><subject>14/19</subject><subject>45/77</subject><subject>631/378</subject><subject>631/532</subject><subject>9/74</subject><subject>96/100</subject><subject>96/31</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Amyloid beta-Peptides - administration & dosage</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Behavioral Sciences</subject><subject>Biological Psychology</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Clinical trials</subject><subject>Gene Expression</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Induced Pluripotent Stem Cells - metabolism</subject><subject>Inflammation - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurons - metabolism</subject><subject>Neurosciences</subject><subject>Peptide Fragments - administration & dosage</subject><subject>Peptide Fragments - metabolism</subject><subject>Pharmacotherapy</subject><subject>Psychiatry</subject><subject>Synaptic Transmission</subject><subject>Tumor necrosis factor-TNF</subject><issn>2158-3188</issn><issn>2158-3188</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1kc9u1DAQxiMEolXpA3BBlrhwCYxjO3YuSKtVS5GKQPw5W4kz7rpK7MV2EN234kV4JrzaUgoSc_CMNL_5xqOvqp5SeEmBqVeJU9apGmhXA5Oi3j2ojhsqVM2oUg_v1UfVaUrXUEJwRSV9XB0xkBRAsuPKuA-f1mQOI04kWLK--Hi-eidXBK1Fk0nw5OcPSbwzIbvykt5gvpnMJkzOI4locJtDJHbxJrtCO0_yBslmmXtPTPAZv-cn1SPbTwlPb_NJ9eX87PP6or58_-btenVZG6bErm7UqAz0w6gkGDEMMHBhrOVIBSiDTBoqTQuCNVQKK1Rn0QpUbGQth7aT7KR6fdDdLsOMo0GfYz_pbXRzH2906J3-u-PdRl-Fb7plQrXQFoEXtwIxfF0wZT27ZHCaeo9hSbos7gTwDpqCPv8HvQ5L9OW8PcUl522zp-iBMjGkFNHefYaC3ruoDy7q4qLeu6h3ZebZ_SvuJn57VoDmAKTS8lcY_6z-v-ovezmopw</recordid><startdate>20190201</startdate><enddate>20190201</enddate><creator>Ihnatovych, Ivanna</creator><creator>Nayak, Tapan K.</creator><creator>Ouf, Aya</creator><creator>Sule, Norbert</creator><creator>Birkaya, Barbara</creator><creator>Chaves, Lee</creator><creator>Auerbach, Anthony</creator><creator>Szigeti, Kinga</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190201</creationdate><title>iPSC model of CHRFAM7A effect on α7 nicotinic acetylcholine receptor function in the human context</title><author>Ihnatovych, Ivanna ; Nayak, Tapan K. ; Ouf, Aya ; Sule, Norbert ; Birkaya, Barbara ; Chaves, Lee ; Auerbach, Anthony ; Szigeti, Kinga</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385z-28d8c0abd870c5bb0b45cff4e1508ce37c17c60532175f589fef5e83d36406973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>101/1</topic><topic>13/95</topic><topic>14/19</topic><topic>45/77</topic><topic>631/378</topic><topic>631/532</topic><topic>9/74</topic><topic>96/100</topic><topic>96/31</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>Amyloid beta-Peptides - administration & dosage</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Behavioral Sciences</topic><topic>Biological Psychology</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>Clinical trials</topic><topic>Gene Expression</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Induced Pluripotent Stem Cells - metabolism</topic><topic>Inflammation - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neurons - metabolism</topic><topic>Neurosciences</topic><topic>Peptide Fragments - administration & dosage</topic><topic>Peptide Fragments - metabolism</topic><topic>Pharmacotherapy</topic><topic>Psychiatry</topic><topic>Synaptic Transmission</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ihnatovych, Ivanna</creatorcontrib><creatorcontrib>Nayak, Tapan K.</creatorcontrib><creatorcontrib>Ouf, Aya</creatorcontrib><creatorcontrib>Sule, Norbert</creatorcontrib><creatorcontrib>Birkaya, Barbara</creatorcontrib><creatorcontrib>Chaves, Lee</creatorcontrib><creatorcontrib>Auerbach, Anthony</creatorcontrib><creatorcontrib>Szigeti, Kinga</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>Translational psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ihnatovych, Ivanna</au><au>Nayak, Tapan K.</au><au>Ouf, Aya</au><au>Sule, Norbert</au><au>Birkaya, Barbara</au><au>Chaves, Lee</au><au>Auerbach, Anthony</au><au>Szigeti, Kinga</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>iPSC model of CHRFAM7A effect on α7 nicotinic acetylcholine receptor function in the human context</atitle><jtitle>Translational psychiatry</jtitle><stitle>Transl Psychiatry</stitle><addtitle>Transl Psychiatry</addtitle><date>2019-02-01</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>59</spage><epage>59</epage><pages>59-59</pages><artnum>59</artnum><issn>2158-3188</issn><eissn>2158-3188</eissn><abstract>The α7 nicotinic acetylcholine receptor (α7nAChR) has been a promising target for diseases affecting cognition and higher cortical functions; however, the effect observed in animal models failed to translate into human clinical trials identifying a translational gap.
CHRFAM7A
is a human-specific fusion gene with properties that enable incorporation into the α7nAChR and, being human specific,
CHRFAM7A
effect was not accounted for in preclinical studies. We hypothesized that
CHRFAM7A
may account for this translational gap and understanding its function may offer novel insights when exploring α7nAChR as a drug target.
CHRFAM7A
is present in different copy number variations (CNV) in the human genome with high frequency. To study the functional consequences of the presence of the
CHRFAM7A
, two induced pluripotent stem cell (iPSC) lines (0 copy and 1 copy direct) were developed. The 0 copy line was rescued with
CHRFAM7A
transfection to control for genetic heterogeneity. As readouts for genotype–phenotype correlation, α7nAChR synaptic transmission and amyloid beta 1–42 (Aβ
1–42
) uptake were tested. Synaptic transmission in the presence of
CHRFAM7A
demonstrated that PNU-modulated desensitization of α7nAChR currents increased as a function of
CHRFAM7A
dosage.
CHRFAM7A
mitigated the dose response of Aβ
1–42
uptake suggesting a protective effect beyond physiological concentrations. Furthermore, in the presence of CHRFAM7A Aβ
1–42
uptake activated neuronal interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) without activating the canonical inflammasome pathway. Lead optimization may identify more potent molecules when the screen has a model harboring
CHRFAM7A
. Incorporating pharmacogenetics into clinical trials may enhance signals in efficacy measures.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30710073</pmid><doi>10.1038/s41398-019-0375-z</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Translational psychiatry, 2019-02, Vol.9 (1), p.59-59, Article 59 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | 101/1 13/95 14/19 45/77 631/378 631/532 9/74 96/100 96/31 alpha7 Nicotinic Acetylcholine Receptor - metabolism Amyloid beta-Peptides - administration & dosage Amyloid beta-Peptides - metabolism Behavioral Sciences Biological Psychology Cell Differentiation Cells, Cultured Clinical trials Gene Expression HEK293 Cells Humans Induced Pluripotent Stem Cells - metabolism Inflammation - metabolism Medicine Medicine & Public Health Neurons - metabolism Neurosciences Peptide Fragments - administration & dosage Peptide Fragments - metabolism Pharmacotherapy Psychiatry Synaptic Transmission Tumor necrosis factor-TNF |
| title | iPSC model of CHRFAM7A effect on α7 nicotinic acetylcholine receptor function in the human context |
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