DARPP-32, Jack of All Trades… Master of Which?
Identifieur interne : 000921 ( Pmc/Curation ); précédent : 000920; suivant : 000922DARPP-32, Jack of All Trades… Master of Which?
Auteurs : Marion Yger [France] ; Jean-Antoine Girault [France]Source :
- Frontiers in Behavioral Neuroscience [ 1662-5153 ] ; 2011.
Abstract
DARPP-32 (PPP1R1B) was discovered as a substrate of cAMP-dependent protein kinase (PKA) enriched in dopamine-innervated brain areas. It is one of three related, PKA-regulated inhibitors of protein phosphatase-1 (PP1). These inhibitors seem to have appeared in early vertebrate ancestors, possibly Gnathostomes. DARPP-32 has additional important biochemical properties including inhibition of PKA when phosphorylated by Cdk5 and regulation by casein kinases 1 and 2. It is highly enriched in specific neuronal populations, especially striatal medium-size spiny neurons. As PP1 inhibitor DARPP-32 amplifies and/or mediates many actions of PKA at the plasma membrane and in the cytoplasm, with a broad spectrum of potential targets and functions. DARPP-32 also undergoes a continuous and tightly regulated cytonuclear shuttling. This trafficking is controlled by phosphorylation of Ser-97, which is necessary for nuclear export. When phosphorylated on Thr-34 and dephosphorylated on Ser-97, DARPP-32 can inhibit PP1 in the nucleus and modulate signaling pathways involved in the regulation of chromatin response. Recent work with multiple transgenic and knockout mutant mice has allowed the dissection of DARPP-32 function in striato-nigral and striato-pallidal neurons. It is implicated in the action of therapeutic and abused psychoactive drugs, in prefrontal cortex function, and in sexual behavior. However, the contribution of DARPP-32 in human behavior remains poorly understood. Post-mortem studies in humans suggest possible alterations of DARPP-32 levels in schizophrenia and bipolar disorder. Genetic studies have revealed a polymorphism with possible association with psychological and psychopathological traits. In addition, a short isoform of DARPP-32, t-DARPP, plays a role in cancer, indicating additional signaling properties. Thus, DARPP-32 is a non-essential but tightly regulated signaling hub molecule which may improve the general performance of the neuronal circuits in which it is expressed.
Url:
DOI: 10.3389/fnbeh.2011.00056
PubMed: 21927600
PubMed Central: 3168893
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<front><div type="abstract" xml:lang="en"><p>DARPP-32 (PPP1R1B) was discovered as a substrate of cAMP-dependent protein kinase (PKA) enriched in dopamine-innervated brain areas. It is one of three related, PKA-regulated inhibitors of protein phosphatase-1 (PP1). These inhibitors seem to have appeared in early vertebrate ancestors, possibly Gnathostomes. DARPP-32 has additional important biochemical properties including inhibition of PKA when phosphorylated by Cdk5 and regulation by casein kinases 1 and 2. It is highly enriched in specific neuronal populations, especially striatal medium-size spiny neurons. As PP1 inhibitor DARPP-32 amplifies and/or mediates many actions of PKA at the plasma membrane and in the cytoplasm, with a broad spectrum of potential targets and functions. DARPP-32 also undergoes a continuous and tightly regulated cytonuclear shuttling. This trafficking is controlled by phosphorylation of Ser-97, which is necessary for nuclear export. When phosphorylated on Thr-34 and dephosphorylated on Ser-97, DARPP-32 can inhibit PP1 in the nucleus and modulate signaling pathways involved in the regulation of chromatin response. Recent work with multiple transgenic and knockout mutant mice has allowed the dissection of DARPP-32 function in striato-nigral and striato-pallidal neurons. It is implicated in the action of therapeutic and abused psychoactive drugs, in prefrontal cortex function, and in sexual behavior. However, the contribution of DARPP-32 in human behavior remains poorly understood. Post-mortem studies in humans suggest possible alterations of DARPP-32 levels in schizophrenia and bipolar disorder. Genetic studies have revealed a polymorphism with possible association with psychological and psychopathological traits. In addition, a short isoform of DARPP-32, t-DARPP, plays a role in cancer, indicating additional signaling properties. Thus, DARPP-32 is a non-essential but tightly regulated signaling hub molecule which may improve the general performance of the neuronal circuits in which it is expressed.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Behav Neurosci</journal-id>
<journal-id journal-id-type="publisher-id">Front. Behav. Neurosci.</journal-id>
<journal-title-group><journal-title>Frontiers in Behavioral Neuroscience</journal-title>
</journal-title-group>
<issn pub-type="epub">1662-5153</issn>
<publisher><publisher-name>Frontiers Research Foundation</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">21927600</article-id>
<article-id pub-id-type="pmc">3168893</article-id>
<article-id pub-id-type="doi">10.3389/fnbeh.2011.00056</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Neuroscience</subject>
<subj-group><subject>Review Article</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>DARPP-32, Jack of All Trades… Master of Which?</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Yger</surname>
<given-names>Marion</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Girault</surname>
<given-names>Jean-Antoine</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<xref ref-type="author-notes" rid="fn001">*</xref>
</contrib>
</contrib-group>
<aff id="aff1"><sup>1</sup>
<institution>INSERM UMR-S 839</institution>
<country>Paris, France</country>
</aff>
<aff id="aff2"><sup>2</sup>
<institution>Université Pierre et Marie Curie</institution>
<country>Paris, France</country>
</aff>
<aff id="aff3"><sup>3</sup>
<institution>Institut du Fer à Moulin</institution>
<country>Paris, France</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Riccardo Brambilla, San Raffaele Scientific Institute and University, Italy</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Rosario Moratalla, Cajal Institute, Consejo Superior de Investigaciones Científicas, Spain; Serge N. Schiffmann, Université Libre de Bruxelles, Belgium</p>
</fn>
<corresp id="fn001">*Correspondence: Jean-Antoine Girault, INSERM UMR-S 839, Institut du Fer à Moulin, Université Pierre et Marie Curie, 17 rue du Fer à Moulin, 75005 Paris, France. e-mail: <email>jean-antoine.girault@inserm.fr</email>
</corresp>
</author-notes>
<pub-date pub-type="epub"><day>08</day>
<month>9</month>
<year>2011</year>
</pub-date>
<pub-date pub-type="collection"><year>2011</year>
</pub-date>
<volume>5</volume>
<elocation-id>56</elocation-id>
<history><date date-type="received"><day>16</day>
<month>7</month>
<year>2011</year>
</date>
<date date-type="accepted"><day>16</day>
<month>8</month>
<year>2011</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2011 Yger and Girault.</copyright-statement>
<copyright-year>2011</copyright-year>
<license license-type="open-access" xlink:href="http://www.frontiersin.org/licenseagreement"><license-p>This is an open-access article subject to a non-exclusive license between the authors and Frontiers Media SA, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and other Frontiers conditions are complied with.</license-p>
</license>
</permissions>
<abstract><p>DARPP-32 (PPP1R1B) was discovered as a substrate of cAMP-dependent protein kinase (PKA) enriched in dopamine-innervated brain areas. It is one of three related, PKA-regulated inhibitors of protein phosphatase-1 (PP1). These inhibitors seem to have appeared in early vertebrate ancestors, possibly Gnathostomes. DARPP-32 has additional important biochemical properties including inhibition of PKA when phosphorylated by Cdk5 and regulation by casein kinases 1 and 2. It is highly enriched in specific neuronal populations, especially striatal medium-size spiny neurons. As PP1 inhibitor DARPP-32 amplifies and/or mediates many actions of PKA at the plasma membrane and in the cytoplasm, with a broad spectrum of potential targets and functions. DARPP-32 also undergoes a continuous and tightly regulated cytonuclear shuttling. This trafficking is controlled by phosphorylation of Ser-97, which is necessary for nuclear export. When phosphorylated on Thr-34 and dephosphorylated on Ser-97, DARPP-32 can inhibit PP1 in the nucleus and modulate signaling pathways involved in the regulation of chromatin response. Recent work with multiple transgenic and knockout mutant mice has allowed the dissection of DARPP-32 function in striato-nigral and striato-pallidal neurons. It is implicated in the action of therapeutic and abused psychoactive drugs, in prefrontal cortex function, and in sexual behavior. However, the contribution of DARPP-32 in human behavior remains poorly understood. Post-mortem studies in humans suggest possible alterations of DARPP-32 levels in schizophrenia and bipolar disorder. Genetic studies have revealed a polymorphism with possible association with psychological and psychopathological traits. In addition, a short isoform of DARPP-32, t-DARPP, plays a role in cancer, indicating additional signaling properties. Thus, DARPP-32 is a non-essential but tightly regulated signaling hub molecule which may improve the general performance of the neuronal circuits in which it is expressed.</p>
</abstract>
<kwd-group><kwd>dopamine</kwd>
<kwd>glutamate</kwd>
<kwd>cAMP</kwd>
<kwd>protein-phosphatase 1</kwd>
<kwd>CDK5</kwd>
<kwd>behavior</kwd>
<kwd>addiction</kwd>
<kwd>Parkinson’s disease</kwd>
</kwd-group>
<counts><fig-count count="4"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="161"></ref-count>
<page-count count="14"></page-count>
<word-count count="14156"></word-count>
</counts>
</article-meta>
</front>
</pmc>
</record>
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