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Cardiac function modulation depends on the A‐kinase anchoring protein complex
The A‐kinase anchoring proteins (AKAPs) are a group of structurally diverse proteins identified in various species and tissues. These proteins are able to anchor protein kinase and other signalling proteins to regulate cardiac function. Acting as a scaffold protein, AKAPs ensure specificity in signa...
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| Published in: | Journal of cellular and molecular medicine 2019-11, Vol.23 (11), p.7170-7179 |
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| container_issue | 11 |
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| container_title | Journal of cellular and molecular medicine |
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| creator | Zhu, Yan‐Rong Jiang, Xiao‐Xin Zheng, Yaguo Xiong, Jing Wei, Dongping Zhang, Dai‐Min |
| description | The A‐kinase anchoring proteins (AKAPs) are a group of structurally diverse proteins identified in various species and tissues. These proteins are able to anchor protein kinase and other signalling proteins to regulate cardiac function. Acting as a scaffold protein, AKAPs ensure specificity in signal transduction by enzymes close to their appropriate effectors and substrates. Over the decades, more than 70 different AKAPs have been discovered. Accumulative evidence indicates that AKAPs play crucial roles in the functional regulation of cardiac diseases, including cardiac hypertrophy, myofibre contractility dysfunction and arrhythmias. By anchoring different partner proteins (PKA, PKC, PKD and LTCCs), AKAPs take part in different regulatory pathways to function as regulators in the heart, and a damaged structure can influence the activities of these complexes. In this review, we highlight recent advances in AKAP‐associated protein complexes, focusing on local signalling events that are perturbed in cardiac diseases and their roles in interacting with ion channels and their regulatory molecules. These new findings suggest that AKAPs might have potential therapeutic value in patients with cardiac diseases, particularly malignant rhythm. |
| doi_str_mv | 10.1111/jcmm.14659 |
| format | article |
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These proteins are able to anchor protein kinase and other signalling proteins to regulate cardiac function. Acting as a scaffold protein, AKAPs ensure specificity in signal transduction by enzymes close to their appropriate effectors and substrates. Over the decades, more than 70 different AKAPs have been discovered. Accumulative evidence indicates that AKAPs play crucial roles in the functional regulation of cardiac diseases, including cardiac hypertrophy, myofibre contractility dysfunction and arrhythmias. By anchoring different partner proteins (PKA, PKC, PKD and LTCCs), AKAPs take part in different regulatory pathways to function as regulators in the heart, and a damaged structure can influence the activities of these complexes. In this review, we highlight recent advances in AKAP‐associated protein complexes, focusing on local signalling events that are perturbed in cardiac diseases and their roles in interacting with ion channels and their regulatory molecules. These new findings suggest that AKAPs might have potential therapeutic value in patients with cardiac diseases, particularly malignant rhythm.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.14659</identifier><identifier>PMID: 31512389</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>A Kinase Anchor Proteins - metabolism ; A kinase-anchoring protein ; Anchoring ; Animals ; arrhythmia ; A‐kinase anchoring proteins ; Binding sites ; calmodulin ; Cardiac arrhythmia ; Cardiac function ; Cardiomyocytes ; Coronary artery disease ; Genes ; Heart ; Heart diseases ; Heart Diseases - metabolism ; Heart Diseases - physiopathology ; Humans ; Hypertrophy ; Ion channels ; Kinases ; large‐conductance Ca2+‐activated K+ channels ; Ligands ; Muscle contraction ; Physiology ; Protein kinase A ; Protein kinase C ; Proteins ; Review ; Reviews ; Signal Transduction ; sudden cardiac death</subject><ispartof>Journal of cellular and molecular medicine, 2019-11, Vol.23 (11), p.7170-7179</ispartof><rights>2019 The Authors. published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2019. 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-c4489-cba9e3dd69b256d030390579e0503e0dd81d35e781e30e112d185c1b7f0f3fa53</citedby><cites>FETCH-LOGICAL-c4489-cba9e3dd69b256d030390579e0503e0dd81d35e781e30e112d185c1b7f0f3fa53</cites><orcidid>0000-0001-5251-3113</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2309210380/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2309210380?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,11562,25753,27924,27925,37012,37013,44590,46052,46476,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31512389$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Yan‐Rong</creatorcontrib><creatorcontrib>Jiang, Xiao‐Xin</creatorcontrib><creatorcontrib>Zheng, Yaguo</creatorcontrib><creatorcontrib>Xiong, Jing</creatorcontrib><creatorcontrib>Wei, Dongping</creatorcontrib><creatorcontrib>Zhang, Dai‐Min</creatorcontrib><title>Cardiac function modulation depends on the A‐kinase anchoring protein complex</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>The A‐kinase anchoring proteins (AKAPs) are a group of structurally diverse proteins identified in various species and tissues. These proteins are able to anchor protein kinase and other signalling proteins to regulate cardiac function. Acting as a scaffold protein, AKAPs ensure specificity in signal transduction by enzymes close to their appropriate effectors and substrates. Over the decades, more than 70 different AKAPs have been discovered. Accumulative evidence indicates that AKAPs play crucial roles in the functional regulation of cardiac diseases, including cardiac hypertrophy, myofibre contractility dysfunction and arrhythmias. By anchoring different partner proteins (PKA, PKC, PKD and LTCCs), AKAPs take part in different regulatory pathways to function as regulators in the heart, and a damaged structure can influence the activities of these complexes. In this review, we highlight recent advances in AKAP‐associated protein complexes, focusing on local signalling events that are perturbed in cardiac diseases and their roles in interacting with ion channels and their regulatory molecules. These new findings suggest that AKAPs might have potential therapeutic value in patients with cardiac diseases, particularly malignant rhythm.</description><subject>A Kinase Anchor Proteins - metabolism</subject><subject>A kinase-anchoring protein</subject><subject>Anchoring</subject><subject>Animals</subject><subject>arrhythmia</subject><subject>A‐kinase anchoring proteins</subject><subject>Binding sites</subject><subject>calmodulin</subject><subject>Cardiac arrhythmia</subject><subject>Cardiac function</subject><subject>Cardiomyocytes</subject><subject>Coronary artery disease</subject><subject>Genes</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart Diseases - metabolism</subject><subject>Heart Diseases - physiopathology</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Ion channels</subject><subject>Kinases</subject><subject>large‐conductance Ca2+‐activated K+ channels</subject><subject>Ligands</subject><subject>Muscle contraction</subject><subject>Physiology</subject><subject>Protein kinase A</subject><subject>Protein kinase C</subject><subject>Proteins</subject><subject>Review</subject><subject>Reviews</subject><subject>Signal Transduction</subject><subject>sudden cardiac death</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><recordid>eNp9kc1u1DAURi1E1T-64QFQJDao0hRfO07sDVI1otCqVTdlbXnsm46HxA52AnTHI_QZeRIynWkFLOqNP8lHR_f6I-Q10BOYzvuV7boTKCuhXpB9EJLNSsXLl9sMkss9cpDzilJeAVe7ZI-DAMal2ifXc5OcN7ZoxmAHH0PRRTe25iE67DG4XExxWGJx-vvX_VcfTMbCBLuMyYfbok9xQB8KG7u-xZ-vyE5j2oxH2_uQfDn7eDP_PLu8_nQ-P72c2bKUamYXRiF3rlILJipHOeWKilohFZQjdU6C4wJrCcgpAjAHUlhY1A1teGMEPyQfNt5-XHToLIYhmVb3yXcm3elovP73Jfilvo3fdSXXv1JPgndbQYrfRsyD7ny22LYmYByzZkwqUZeMsQl9-x-6imMK03qacaoYUC7pRB1vKJtizgmbp2GA6nVPet2Tfuhpgt_8Pf4T-ljMBMAG-OFbvHtGpS_mV1cb6R_3v58T</recordid><startdate>201911</startdate><enddate>201911</enddate><creator>Zhu, Yan‐Rong</creator><creator>Jiang, Xiao‐Xin</creator><creator>Zheng, Yaguo</creator><creator>Xiong, Jing</creator><creator>Wei, Dongping</creator><creator>Zhang, Dai‐Min</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5251-3113</orcidid></search><sort><creationdate>201911</creationdate><title>Cardiac function modulation depends on the A‐kinase anchoring protein complex</title><author>Zhu, Yan‐Rong ; Jiang, Xiao‐Xin ; Zheng, Yaguo ; Xiong, Jing ; Wei, Dongping ; Zhang, Dai‐Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4489-cba9e3dd69b256d030390579e0503e0dd81d35e781e30e112d185c1b7f0f3fa53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>A Kinase Anchor Proteins - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Yan‐Rong</au><au>Jiang, Xiao‐Xin</au><au>Zheng, Yaguo</au><au>Xiong, Jing</au><au>Wei, Dongping</au><au>Zhang, Dai‐Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiac function modulation depends on the A‐kinase anchoring protein complex</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2019-11</date><risdate>2019</risdate><volume>23</volume><issue>11</issue><spage>7170</spage><epage>7179</epage><pages>7170-7179</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>The A‐kinase anchoring proteins (AKAPs) are a group of structurally diverse proteins identified in various species and tissues. These proteins are able to anchor protein kinase and other signalling proteins to regulate cardiac function. Acting as a scaffold protein, AKAPs ensure specificity in signal transduction by enzymes close to their appropriate effectors and substrates. Over the decades, more than 70 different AKAPs have been discovered. Accumulative evidence indicates that AKAPs play crucial roles in the functional regulation of cardiac diseases, including cardiac hypertrophy, myofibre contractility dysfunction and arrhythmias. By anchoring different partner proteins (PKA, PKC, PKD and LTCCs), AKAPs take part in different regulatory pathways to function as regulators in the heart, and a damaged structure can influence the activities of these complexes. In this review, we highlight recent advances in AKAP‐associated protein complexes, focusing on local signalling events that are perturbed in cardiac diseases and their roles in interacting with ion channels and their regulatory molecules. These new findings suggest that AKAPs might have potential therapeutic value in patients with cardiac diseases, particularly malignant rhythm.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>31512389</pmid><doi>10.1111/jcmm.14659</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-5251-3113</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | A Kinase Anchor Proteins - metabolism A kinase-anchoring protein Anchoring Animals arrhythmia A‐kinase anchoring proteins Binding sites calmodulin Cardiac arrhythmia Cardiac function Cardiomyocytes Coronary artery disease Genes Heart Heart diseases Heart Diseases - metabolism Heart Diseases - physiopathology Humans Hypertrophy Ion channels Kinases large‐conductance Ca2+‐activated K+ channels Ligands Muscle contraction Physiology Protein kinase A Protein kinase C Proteins Review Reviews Signal Transduction sudden cardiac death |
| title | Cardiac function modulation depends on the A‐kinase anchoring protein complex |
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