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            <title xml:lang="en">Signaling mediated by the dopamine D2 receptor potentiates circadian regulation by CLOCK:BMAL1.</title>
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              <persName>
                <forename type="first">Irene</forename>
                <surname>Yujnovsky</surname>
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                <forename type="first">Jun</forename>
                <surname>Hirayama</surname>
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            <author role="aut">
              <persName>
                <forename type="first">Masao</forename>
                <surname>Doi</surname>
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                <forename type="first">Emiliana</forename>
                <surname>Borrelli</surname>
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              <date type="whenSubmitted">2007-11-16 10:08:32</date>
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            <idno type="halRefHtml">&lt;i&gt;Proceedings of the National Academy of Sciences of the United States of America&lt;/i&gt;, 2006, 103 (16), pp.6386-91. &lt;a target="_blank" href="https://dx.doi.org/10.1073/pnas.0510691103"&gt;&amp;#x27E8;10.1073/pnas.0510691103&amp;#x27E9;&lt;/a&gt;</idno>
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            <idno type="stamp" n="UNIV-STRASBG">Université de Strasbourg</idno>
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                <title xml:lang="en">Signaling mediated by the dopamine D2 receptor potentiates circadian regulation by CLOCK:BMAL1.</title>
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                    <forename type="first">Jun</forename>
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                </author>
                <author role="aut">
                  <persName>
                    <forename type="first">Masao</forename>
                    <surname>Doi</surname>
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                  <idno type="halauthorid">240773-0</idno>
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                <author role="aut">
                  <persName>
                    <forename type="first">Emiliana</forename>
                    <surname>Borrelli</surname>
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                <idno type="eissn">1091-6490</idno>
                <title level="j">Proceedings of the National Academy of Sciences of the United States of America</title>
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                  <publisher>National Academy of Sciences</publisher>
                  <biblScope unit="volume">103</biblScope>
                  <biblScope unit="issue">16</biblScope>
                  <biblScope unit="pp">6386-91</biblScope>
                  <date type="datePub">2006-04-18</date>
                  <date type="dateEpub">2006-04-10</date>
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              <classCode scheme="mesh">Animals</classCode>
              <classCode scheme="mesh">Basic Helix-Loop-Helix Transcription Factors</classCode>
              <classCode scheme="mesh">Mice</classCode>
              <classCode scheme="mesh">Mitogen-Activated Protein Kinase Kinases</classCode>
              <classCode scheme="mesh">Nuclear Proteins</classCode>
              <classCode scheme="mesh">Phosphorylation</classCode>
              <classCode scheme="mesh">Promoter Regions (Genetics)</classCode>
              <classCode scheme="mesh">Receptors, Dopamine D2</classCode>
              <classCode scheme="mesh">Retina</classCode>
              <classCode scheme="mesh">Signal Transduction</classCode>
              <classCode scheme="mesh">Trans-Activation (Genetics)</classCode>
              <classCode scheme="mesh">Trans-Activators</classCode>
              <classCode scheme="mesh">CREB-Binding Protein</classCode>
              <classCode scheme="mesh">Transcription, Genetic</classCode>
              <classCode scheme="mesh">Cell Cycle Proteins</classCode>
              <classCode scheme="mesh">Circadian Rhythm</classCode>
              <classCode scheme="mesh">Dopamine</classCode>
              <classCode scheme="mesh">Down-Regulation</classCode>
              <classCode scheme="mesh">Flavoproteins</classCode>
              <classCode scheme="mesh">Gene Expression Regulation</classCode>
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            <abstract xml:lang="en">
              <p>Environmental cues modulate a variety of intracellular pathways whose signaling is integrated by the molecular mechanism that constitutes the circadian clock. Although the essential gears of the circadian machinery have been elucidated, very little is known about the signaling systems regulating it. Here, we report that signaling mediated by the dopamine D2 receptor (D2R) enhances the transcriptional capacity of the CLOCK:BMAL1 complex. This effect involves the mitogen-activated protein kinase transduction cascade and is associated with a D2R-induced increase in the recruiting and phosphorylation of the transcriptional coactivator cAMP-responsive element-binding protein (CREB) binding protein. Importantly, CLOCK:BMAL1-dependent activation and light-inducibility of mPer1 gene transcription is drastically dampened in retinas of D2R-null mice. Because dopamine is the major catecholamine in the retina, central for the neural adaptation to light, our findings establish a physiological link among photic input, dopamine signaling, and the molecular clock machinery.</p>
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