<?xml version="1.0" encoding="UTF-8"?>
<collection xmlns="http://www.loc.gov/MARC21/slim">
 <record>
  <leader>     caa a22        4500</leader>
  <controlfield tag="001">378858858</controlfield>
  <controlfield tag="003">CHVBK</controlfield>
  <controlfield tag="005">20180305123341.0</controlfield>
  <controlfield tag="007">cr unu---uuuuu</controlfield>
  <controlfield tag="008">161128e20031107xx      s     000 0 eng  </controlfield>
  <datafield tag="024" ind1="7" ind2="0">
   <subfield code="a">10.1515/BC.2003.153</subfield>
   <subfield code="2">doi</subfield>
  </datafield>
  <datafield tag="035" ind1=" " ind2=" ">
   <subfield code="a">(NATIONALLICENCE)gruyter-10.1515/BC.2003.153</subfield>
  </datafield>
  <datafield tag="100" ind1="1" ind2=" ">
   <subfield code="a">Kröncke</subfield>
   <subfield code="D">K.-D</subfield>
  </datafield>
  <datafield tag="245" ind1="1" ind2="0">
   <subfield code="a">Nitrosative Stress and Transcription</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[K.-D. Kröncke]</subfield>
  </datafield>
  <datafield tag="520" ind1="3" ind2=" ">
   <subfield code="a">Low NO concentrations synthesized by constitutively expressed NO synthases act on several signaling pathways activating transcription factors (TF), such as NF-κB or AP-1, and thereby influence gene expression. In contrast, during inflammatory reactions the inducible NO synthase produces NO for prolonged periods of time. The resulting nitrosative stress directly affects redoxsensitive TF like NF-κB, AP-1, Oct-1, c-Myb, or zinc fingercontaining TF, but also additional mechanisms have been identified. Nitrosative stress in some cases induces expression of TF (AP-1, p53), indirectly modulates activity or stability of TF (HIF-1, p53) or their inhibitors (NF-κB), or modulates accessibility of promoters via increased DNA methylation or histone deacetylation. Depending on the promoter the result is induced, increased, decreased or even totally inhibited expression of various target genes. In unstimulated cells nitrosative stress increases NF-κB or AP-1-dependent transcription, while in activated cells nitrosative stress rather abolishes NF-κB or AP-1-dependent transcription. Sometimes the oxygen concentration also is of prime importance, since under normoxic conditions nitrosative stress activates HIF-1-dependent transcription, while under hypoxic conditions nitrosative stress leads to inhibition of HIF-1-dependent transcription. This review summarizes what is known about effects of physiological NO levels as well as of nitrosative stress on transcription.</subfield>
  </datafield>
  <datafield tag="540" ind1=" " ind2=" ">
   <subfield code="a">Copyright © 2003 by Walter de Gruyter GmbH &amp; Co. KG</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Biochemistry</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Molecular biology</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Cellular biology</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="773" ind1="0" ind2=" ">
   <subfield code="t">Biological Chemistry</subfield>
   <subfield code="d">Walter de Gruyter</subfield>
   <subfield code="g">384/10-11(2003-11-07), 1365-1377</subfield>
   <subfield code="x">1431-6730</subfield>
   <subfield code="q">384:10-11&lt;1365</subfield>
   <subfield code="1">2003</subfield>
   <subfield code="2">384</subfield>
   <subfield code="o">bchm</subfield>
  </datafield>
  <datafield tag="856" ind1="4" ind2="0">
   <subfield code="u">https://doi.org/10.1515/BC.2003.153</subfield>
   <subfield code="q">text/html</subfield>
   <subfield code="z">Onlinezugriff via DOI</subfield>
  </datafield>
  <datafield tag="908" ind1=" " ind2=" ">
   <subfield code="D">1</subfield>
   <subfield code="a">research article</subfield>
   <subfield code="2">jats</subfield>
  </datafield>
  <datafield tag="950" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">856</subfield>
   <subfield code="E">40</subfield>
   <subfield code="u">https://doi.org/10.1515/BC.2003.153</subfield>
   <subfield code="q">text/html</subfield>
   <subfield code="z">Onlinezugriff via DOI</subfield>
  </datafield>
  <datafield tag="950" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">100</subfield>
   <subfield code="E">1-</subfield>
   <subfield code="a">Kröncke</subfield>
   <subfield code="D">K.-D</subfield>
  </datafield>
  <datafield tag="950" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">773</subfield>
   <subfield code="E">0-</subfield>
   <subfield code="t">Biological Chemistry</subfield>
   <subfield code="d">Walter de Gruyter</subfield>
   <subfield code="g">384/10-11(2003-11-07), 1365-1377</subfield>
   <subfield code="x">1431-6730</subfield>
   <subfield code="q">384:10-11&lt;1365</subfield>
   <subfield code="1">2003</subfield>
   <subfield code="2">384</subfield>
   <subfield code="o">bchm</subfield>
  </datafield>
  <datafield tag="900" ind1=" " ind2="7">
   <subfield code="b">CC0</subfield>
   <subfield code="u">http://creativecommons.org/publicdomain/zero/1.0</subfield>
   <subfield code="2">nationallicence</subfield>
  </datafield>
  <datafield tag="898" ind1=" " ind2=" ">
   <subfield code="a">BK010053</subfield>
   <subfield code="b">XK010053</subfield>
   <subfield code="c">XK010000</subfield>
  </datafield>
  <datafield tag="949" ind1=" " ind2=" ">
   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="F">NATIONALLICENCE</subfield>
   <subfield code="b">NL-gruyter</subfield>
  </datafield>
 </record>
</collection>
