RGS3 and RGS4 are GTPase Activating Proteins in the Heart
RGS family members are regulatory molecules that act as GTPase activating proteins (GAPs) for Gαsubunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Giα, Goαand Gqαsubtypes when testedin vitroandin vivo. Although the function of RGS proteins in cardiac...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 1998-02, Vol.30 (2), p.269-276 |
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| container_title | Journal of molecular and cellular cardiology |
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| creator | Zhang, Shaosong Watson, Ned Zahner, Joseph Rottman, Jeffrey N. Blumer, Kendall J. Muslin, Anthony J. |
| description | RGS family members are regulatory molecules that act as GTPase activating proteins (GAPs) for Gαsubunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Giα, Goαand Gqαsubtypes when testedin vitroandin vivo. Although the function of RGS proteins in cardiac physiology is unknown, their ability to deactivate Gαsubunits suggests that they may inhibit the action of muscarinic, α-adrenergic, endothelin, and other agonists. To evaluate the role of RGS family members in the regulation of cardiac physiology, we investigated the expression pattern of two RGS genes in normal and diseased rat heart tissue. RGS3 and RGS4 mRNAs and proteins were detected in adult myocardium. RGS3 and RGS4 gene expression was markedly enhanced in two model systems of cardiac hypertrophy: growth factor-stimulated cultured neonatal rat cardiomyocytes and pulmonary artery-banded (PAB) mice. RGS3 and RGS4 mRNA levels were reduced in failing myocardium obtained from SHHF/Mcc-facp(SHHF) rats. These findings support the hypothesis that RGS gene expression is highly regulated in myocardium and imply that RGS family members play an important role in the regulation of cardiac function. |
| doi_str_mv | 10.1006/jmcc.1997.0591 |
| format | Article |
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RGS proteins are able to deactivate G protein subunits of the Giα, Goαand Gqαsubtypes when testedin vitroandin vivo. Although the function of RGS proteins in cardiac physiology is unknown, their ability to deactivate Gαsubunits suggests that they may inhibit the action of muscarinic, α-adrenergic, endothelin, and other agonists. To evaluate the role of RGS family members in the regulation of cardiac physiology, we investigated the expression pattern of two RGS genes in normal and diseased rat heart tissue. RGS3 and RGS4 mRNAs and proteins were detected in adult myocardium. RGS3 and RGS4 gene expression was markedly enhanced in two model systems of cardiac hypertrophy: growth factor-stimulated cultured neonatal rat cardiomyocytes and pulmonary artery-banded (PAB) mice. RGS3 and RGS4 mRNA levels were reduced in failing myocardium obtained from SHHF/Mcc-facp(SHHF) rats. These findings support the hypothesis that RGS gene expression is highly regulated in myocardium and imply that RGS family members play an important role in the regulation of cardiac function.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1006/jmcc.1997.0591</identifier><identifier>PMID: 9515003</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Amino Acid Sequence ; Animals ; Cardiomegaly - etiology ; Cardiomegaly - genetics ; Cardiomegaly - metabolism ; Cells, Cultured ; Disease Models, Animal ; Enzyme Activation ; G protein ; Gene Expression ; GTP Phosphohydrolases - metabolism ; GTP-Binding Proteins - metabolism ; GTPase activating protein ; GTPase-Activating Proteins ; Heart Failure - genetics ; Heart Failure - metabolism ; Humans ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myocardium - metabolism ; Neonatal cardiomyocyte ; Proteins - genetics ; Proteins - metabolism ; Rats ; Rats, Mutant Strains ; Repressor Proteins ; RGS ; RGS Proteins ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Signal transduction</subject><ispartof>Journal of molecular and cellular cardiology, 1998-02, Vol.30 (2), p.269-276</ispartof><rights>1998 Academic Press</rights><rights>Copyright 1998 Academic Press Limited.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-89d7877c0812bcf41deeea3198a51be24864a807add7349ce2e5d6080a9d3d7b3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0022282897905915$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9515003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Shaosong</creatorcontrib><creatorcontrib>Watson, Ned</creatorcontrib><creatorcontrib>Zahner, Joseph</creatorcontrib><creatorcontrib>Rottman, Jeffrey N.</creatorcontrib><creatorcontrib>Blumer, Kendall J.</creatorcontrib><creatorcontrib>Muslin, Anthony J.</creatorcontrib><title>RGS3 and RGS4 are GTPase Activating Proteins in the Heart</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>RGS family members are regulatory molecules that act as GTPase activating proteins (GAPs) for Gαsubunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Giα, Goαand Gqαsubtypes when testedin vitroandin vivo. Although the function of RGS proteins in cardiac physiology is unknown, their ability to deactivate Gαsubunits suggests that they may inhibit the action of muscarinic, α-adrenergic, endothelin, and other agonists. To evaluate the role of RGS family members in the regulation of cardiac physiology, we investigated the expression pattern of two RGS genes in normal and diseased rat heart tissue. RGS3 and RGS4 mRNAs and proteins were detected in adult myocardium. RGS3 and RGS4 gene expression was markedly enhanced in two model systems of cardiac hypertrophy: growth factor-stimulated cultured neonatal rat cardiomyocytes and pulmonary artery-banded (PAB) mice. RGS3 and RGS4 mRNA levels were reduced in failing myocardium obtained from SHHF/Mcc-facp(SHHF) rats. These findings support the hypothesis that RGS gene expression is highly regulated in myocardium and imply that RGS family members play an important role in the regulation of cardiac function.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Cardiomegaly - etiology</subject><subject>Cardiomegaly - genetics</subject><subject>Cardiomegaly - metabolism</subject><subject>Cells, Cultured</subject><subject>Disease Models, Animal</subject><subject>Enzyme Activation</subject><subject>G protein</subject><subject>Gene Expression</subject><subject>GTP Phosphohydrolases - metabolism</subject><subject>GTP-Binding Proteins - metabolism</subject><subject>GTPase activating protein</subject><subject>GTPase-Activating Proteins</subject><subject>Heart Failure - genetics</subject><subject>Heart Failure - metabolism</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular Sequence Data</subject><subject>Myocardium - metabolism</subject><subject>Neonatal cardiomyocyte</subject><subject>Proteins - genetics</subject><subject>Proteins - metabolism</subject><subject>Rats</subject><subject>Rats, Mutant Strains</subject><subject>Repressor Proteins</subject><subject>RGS</subject><subject>RGS Proteins</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal transduction</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFLAzEQRoMotVav3oScvG2d7CZNciyirVCwaD2HbDLVlO5uTbYF_727tHjzNAPfmw_mEXLLYMwAJg-byrkx01qOQWh2RoYMtMiUUPycDAHyPMtVri7JVUobANC8KAZkoAUTAMWQ6LfZe0Ft7Wm3cGoj0tlqaRPSqWvDwbah_qTL2LQY6kRDTdsvpHO0sb0mF2u7TXhzmiPy8fy0epxni9fZy-N0kTkOos2U9lJJ6UCxvHRrzjwi2oJpZQUrMedqwq0Cab2XBdcOcxR-Agqs9oWXZTEi98feXWy-95haU4XkcLu1NTb7ZKSWXAnGOnB8BF1sUoq4NrsYKht_DAPTuzK9K9O7Mr2r7uDu1LwvK_R_-ElOl6tjjt17h4DRJBewduhDRNca34T_qn8BS5l1uw</recordid><startdate>19980201</startdate><enddate>19980201</enddate><creator>Zhang, Shaosong</creator><creator>Watson, Ned</creator><creator>Zahner, Joseph</creator><creator>Rottman, Jeffrey N.</creator><creator>Blumer, Kendall J.</creator><creator>Muslin, Anthony J.</creator><general>Elsevier Ltd</general><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>7X8</scope></search><sort><creationdate>19980201</creationdate><title>RGS3 and RGS4 are GTPase Activating Proteins in the Heart</title><author>Zhang, Shaosong ; Watson, Ned ; Zahner, Joseph ; Rottman, Jeffrey N. ; Blumer, Kendall J. ; Muslin, Anthony J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-89d7877c0812bcf41deeea3198a51be24864a807add7349ce2e5d6080a9d3d7b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Cardiomegaly - etiology</topic><topic>Cardiomegaly - genetics</topic><topic>Cardiomegaly - metabolism</topic><topic>Cells, Cultured</topic><topic>Disease Models, Animal</topic><topic>Enzyme Activation</topic><topic>G protein</topic><topic>Gene Expression</topic><topic>GTP Phosphohydrolases - metabolism</topic><topic>GTP-Binding Proteins - metabolism</topic><topic>GTPase activating protein</topic><topic>GTPase-Activating Proteins</topic><topic>Heart Failure - genetics</topic><topic>Heart Failure - metabolism</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular Sequence Data</topic><topic>Myocardium - metabolism</topic><topic>Neonatal cardiomyocyte</topic><topic>Proteins - genetics</topic><topic>Proteins - metabolism</topic><topic>Rats</topic><topic>Rats, Mutant Strains</topic><topic>Repressor Proteins</topic><topic>RGS</topic><topic>RGS Proteins</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Shaosong</creatorcontrib><creatorcontrib>Watson, Ned</creatorcontrib><creatorcontrib>Zahner, Joseph</creatorcontrib><creatorcontrib>Rottman, Jeffrey N.</creatorcontrib><creatorcontrib>Blumer, Kendall J.</creatorcontrib><creatorcontrib>Muslin, Anthony J.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Shaosong</au><au>Watson, Ned</au><au>Zahner, Joseph</au><au>Rottman, Jeffrey N.</au><au>Blumer, Kendall J.</au><au>Muslin, Anthony J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RGS3 and RGS4 are GTPase Activating Proteins in the Heart</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>1998-02-01</date><risdate>1998</risdate><volume>30</volume><issue>2</issue><spage>269</spage><epage>276</epage><pages>269-276</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>RGS family members are regulatory molecules that act as GTPase activating proteins (GAPs) for Gαsubunits of heterotrimeric G proteins. RGS proteins are able to deactivate G protein subunits of the Giα, Goαand Gqαsubtypes when testedin vitroandin vivo. Although the function of RGS proteins in cardiac physiology is unknown, their ability to deactivate Gαsubunits suggests that they may inhibit the action of muscarinic, α-adrenergic, endothelin, and other agonists. To evaluate the role of RGS family members in the regulation of cardiac physiology, we investigated the expression pattern of two RGS genes in normal and diseased rat heart tissue. RGS3 and RGS4 mRNAs and proteins were detected in adult myocardium. RGS3 and RGS4 gene expression was markedly enhanced in two model systems of cardiac hypertrophy: growth factor-stimulated cultured neonatal rat cardiomyocytes and pulmonary artery-banded (PAB) mice. RGS3 and RGS4 mRNA levels were reduced in failing myocardium obtained from SHHF/Mcc-facp(SHHF) rats. These findings support the hypothesis that RGS gene expression is highly regulated in myocardium and imply that RGS family members play an important role in the regulation of cardiac function.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>9515003</pmid><doi>10.1006/jmcc.1997.0591</doi><tpages>8</tpages></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Amino Acid Sequence Animals Cardiomegaly - etiology Cardiomegaly - genetics Cardiomegaly - metabolism Cells, Cultured Disease Models, Animal Enzyme Activation G protein Gene Expression GTP Phosphohydrolases - metabolism GTP-Binding Proteins - metabolism GTPase activating protein GTPase-Activating Proteins Heart Failure - genetics Heart Failure - metabolism Humans Mice Mice, Inbred C57BL Molecular Sequence Data Myocardium - metabolism Neonatal cardiomyocyte Proteins - genetics Proteins - metabolism Rats Rats, Mutant Strains Repressor Proteins RGS RGS Proteins RNA, Messenger - genetics RNA, Messenger - metabolism Signal transduction |
| title | RGS3 and RGS4 are GTPase Activating Proteins in the Heart |
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