Links to Exploration step
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Molecular basis of crosstalk between oncogenic Ras and the master regulator of hematopoiesis GATA-2</title>
<author><name sortKey="Katsumura, Koichi R" sort="Katsumura, Koichi R" uniqKey="Katsumura K" first="Koichi R" last="Katsumura">Koichi R. Katsumura</name>
<affiliation><nlm:aff id="au1"><institution>UW-Madison Blood Research Program, Department of Cell and Regenerative Biology, Carbone Cancer Center, Wisconsin Institutes for Medical Research, University of Wisconsin School of Medicine and Public Health</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Yang, Chenxi" sort="Yang, Chenxi" uniqKey="Yang C" first="Chenxi" last="Yang">Chenxi Yang</name>
<affiliation><nlm:aff id="au2"><institution>Department of Chemistry, University of Wisconsin</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Boyer, Meghan E" sort="Boyer, Meghan E" uniqKey="Boyer M" first="Meghan E" last="Boyer">Meghan E. Boyer</name>
<affiliation><nlm:aff id="au1"><institution>UW-Madison Blood Research Program, Department of Cell and Regenerative Biology, Carbone Cancer Center, Wisconsin Institutes for Medical Research, University of Wisconsin School of Medicine and Public Health</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Li, Lingjun" sort="Li, Lingjun" uniqKey="Li L" first="Lingjun" last="Li">Lingjun Li</name>
<affiliation><nlm:aff id="au2"><institution>Department of Chemistry, University of Wisconsin</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="au3"><institution>University of Wisconsin School of Pharmacy</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Bresnick, Emery H" sort="Bresnick, Emery H" uniqKey="Bresnick E" first="Emery H" last="Bresnick">Emery H. Bresnick</name>
<affiliation><nlm:aff id="au1"><institution>UW-Madison Blood Research Program, Department of Cell and Regenerative Biology, Carbone Cancer Center, Wisconsin Institutes for Medical Research, University of Wisconsin School of Medicine and Public Health</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">25056917</idno>
<idno type="pmc">4198037</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4198037</idno>
<idno type="RBID">PMC:4198037</idno>
<idno type="doi">10.15252/embr.201438808</idno>
<date when="2014">2014</date>
<idno type="wicri:Area/Pmc/Corpus">002D94</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002D94</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Molecular basis of crosstalk between oncogenic Ras and the master regulator of hematopoiesis GATA-2</title>
<author><name sortKey="Katsumura, Koichi R" sort="Katsumura, Koichi R" uniqKey="Katsumura K" first="Koichi R" last="Katsumura">Koichi R. Katsumura</name>
<affiliation><nlm:aff id="au1"><institution>UW-Madison Blood Research Program, Department of Cell and Regenerative Biology, Carbone Cancer Center, Wisconsin Institutes for Medical Research, University of Wisconsin School of Medicine and Public Health</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Yang, Chenxi" sort="Yang, Chenxi" uniqKey="Yang C" first="Chenxi" last="Yang">Chenxi Yang</name>
<affiliation><nlm:aff id="au2"><institution>Department of Chemistry, University of Wisconsin</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Boyer, Meghan E" sort="Boyer, Meghan E" uniqKey="Boyer M" first="Meghan E" last="Boyer">Meghan E. Boyer</name>
<affiliation><nlm:aff id="au1"><institution>UW-Madison Blood Research Program, Department of Cell and Regenerative Biology, Carbone Cancer Center, Wisconsin Institutes for Medical Research, University of Wisconsin School of Medicine and Public Health</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Li, Lingjun" sort="Li, Lingjun" uniqKey="Li L" first="Lingjun" last="Li">Lingjun Li</name>
<affiliation><nlm:aff id="au2"><institution>Department of Chemistry, University of Wisconsin</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
<affiliation><nlm:aff id="au3"><institution>University of Wisconsin School of Pharmacy</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Bresnick, Emery H" sort="Bresnick, Emery H" uniqKey="Bresnick E" first="Emery H" last="Bresnick">Emery H. Bresnick</name>
<affiliation><nlm:aff id="au1"><institution>UW-Madison Blood Research Program, Department of Cell and Regenerative Biology, Carbone Cancer Center, Wisconsin Institutes for Medical Research, University of Wisconsin School of Medicine and Public Health</institution>
<addr-line>Madison, WI, USA</addr-line>
</nlm:aff>
</affiliation>
</author>
</analytic>
<series><title level="j">EMBO Reports</title>
<idno type="ISSN">1469-221X</idno>
<idno type="eISSN">1469-3178</idno>
<imprint><date when="2014">2014</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>Disease mutations provide unique opportunities to decipher protein and cell function. Mutations in the master regulator of hematopoiesis GATA-2 underlie an immunodeficiency associated with myelodysplastic syndrome and leukemia. We discovered that a GATA-2 disease mutant (T354M) defective in chromatin binding was hyperphosphorylated by p38 mitogen-activated protein kinase. p38 also induced multisite phosphorylation of wild-type GATA-2, which required a single phosphorylated residue (S192). Phosphorylation of GATA-2, but not T354M, stimulated target gene expression. While crosstalk between oncogenic Ras and GATA-2 has been implicated as an important axis in cancer biology, its mechanistic underpinnings are unclear. Oncogenic Ras enhanced S192-dependent GATA-2 phosphorylation, nuclear foci localization, and transcriptional activation. These studies define a mechanism that controls a key regulator of hematopoiesis and a dual mode of impairing GATA-2-dependent genetic networks: mutational disruption of chromatin occupancy yielding insufficient GATA-2, and oncogenic Ras-mediated amplification of GATA-2 activity.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">EMBO Rep</journal-id>
<journal-id journal-id-type="iso-abbrev">EMBO Rep</journal-id>
<journal-id journal-id-type="publisher-id">embr</journal-id>
<journal-title-group><journal-title>EMBO Reports</journal-title>
</journal-title-group>
<issn pub-type="ppub">1469-221X</issn>
<issn pub-type="epub">1469-3178</issn>
<publisher><publisher-name>BlackWell Publishing Ltd</publisher-name>
<publisher-loc>Oxford, UK</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">25056917</article-id>
<article-id pub-id-type="pmc">4198037</article-id>
<article-id pub-id-type="doi">10.15252/embr.201438808</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Scientific Reports</subject>
</subj-group>
</article-categories>
<title-group><article-title>Molecular basis of crosstalk between oncogenic Ras and the master regulator of hematopoiesis GATA-2</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Katsumura</surname>
<given-names>Koichi R</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Yang</surname>
<given-names>Chenxi</given-names>
</name>
<xref ref-type="aff" rid="au2">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Boyer</surname>
<given-names>Meghan E</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Lingjun</given-names>
</name>
<xref ref-type="aff" rid="au2">2</xref>
<xref ref-type="aff" rid="au3">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bresnick</surname>
<given-names>Emery H</given-names>
</name>
<xref ref-type="aff" rid="au1">1</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
<aff id="au1"><label>1</label>
<institution>UW-Madison Blood Research Program, Department of Cell and Regenerative Biology, Carbone Cancer Center, Wisconsin Institutes for Medical Research, University of Wisconsin School of Medicine and Public Health</institution>
<addr-line>Madison, WI, USA</addr-line>
</aff>
<aff id="au2"><label>2</label>
<institution>Department of Chemistry, University of Wisconsin</institution>
<addr-line>Madison, WI, USA</addr-line>
</aff>
<aff id="au3"><label>3</label>
<institution>University of Wisconsin School of Pharmacy</institution>
<addr-line>Madison, WI, USA</addr-line>
</aff>
</contrib-group>
<author-notes><corresp id="cor1">*Corresponding author. Tel: +1 608 265 6446; E-mail: <email>ehbresni@wisc.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>9</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>23</day>
<month>7</month>
<year>2014</year>
</pub-date>
<volume>15</volume>
<issue>9</issue>
<fpage>938</fpage>
<lpage>947</lpage>
<history><date date-type="received"><day>21</day>
<month>3</month>
<year>2014</year>
</date>
<date date-type="rev-recd"><day>19</day>
<month>6</month>
<year>2014</year>
</date>
<date date-type="accepted"><day>23</day>
<month>6</month>
<year>2014</year>
</date>
</history>
<permissions><copyright-statement>© 2014 The Authors</copyright-statement>
<copyright-year>2014</copyright-year>
</permissions>
<abstract><p>Disease mutations provide unique opportunities to decipher protein and cell function. Mutations in the master regulator of hematopoiesis GATA-2 underlie an immunodeficiency associated with myelodysplastic syndrome and leukemia. We discovered that a GATA-2 disease mutant (T354M) defective in chromatin binding was hyperphosphorylated by p38 mitogen-activated protein kinase. p38 also induced multisite phosphorylation of wild-type GATA-2, which required a single phosphorylated residue (S192). Phosphorylation of GATA-2, but not T354M, stimulated target gene expression. While crosstalk between oncogenic Ras and GATA-2 has been implicated as an important axis in cancer biology, its mechanistic underpinnings are unclear. Oncogenic Ras enhanced S192-dependent GATA-2 phosphorylation, nuclear foci localization, and transcriptional activation. These studies define a mechanism that controls a key regulator of hematopoiesis and a dual mode of impairing GATA-2-dependent genetic networks: mutational disruption of chromatin occupancy yielding insufficient GATA-2, and oncogenic Ras-mediated amplification of GATA-2 activity.</p>
</abstract>
<kwd-group><kwd>GATA factor</kwd>
<kwd>GATA-2</kwd>
<kwd>p38</kwd>
<kwd>Ras</kwd>
<kwd>transcription</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/LymphedemaV1/Data/Pmc/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002D94 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Corpus/biblio.hfd -nk 002D94 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= LymphedemaV1 |flux= Pmc |étape= Corpus |type= RBID |clé= |texte= }}
This area was generated with Dilib version V0.6.31. |