<?xml version="1.0" encoding="UTF-8"?>
<rss version="2.0"
  xmlns:trackback="http://madskills.com/public/xml/rss/module/trackback/">
  <channel>
    <title>Current Opinion in Pharmacology</title>
    <link>http://barf.jcowboy.org</link>
    <description>Current Opinion in Pharmacology recent publications</description>
    <language>en-us</language>
    <image>
      <url>http://barf.jcowboy.org/pubmed.gif</url>
      <title>the data for this feed is provided by PubMed</title>
      <link>http://barf.jcowboy.org</link>
    </image>
    <item>
      <title>Glucocorticoid receptor cofactors as therapeutic targets.</title>
      <link>http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&amp;db=PubMed&amp;dopt=Abstract&amp;list_uids=20801081</link>
      <description>Publication Date: 2010 Aug 26 PMID: 20801081&lt;br/&gt;Authors: Simons Jr, S. S.&lt;br/&gt;Journal: Curr Opin Pharmacol&lt;br/&gt;&lt;br/&gt;Numerous transcriptional cofactors (e.g. coactivators, corepressors, and comodulators) are known to alter the maximal transcriptional activity (A(max)) in gene induction and repression by steroid receptors in general and glucocorticoid receptors (GRs) in particular. However, recent data advance the earlier reports that these same factors also modify other parameters of glucocorticoid receptor transcriptional activity: the potency of agonists (or EC(50)) and the partial agonist activity of antisteroids (or PAA). In several instances, factors modulate the EC(50) and/or PAA without changing A(max). Thus, studies of all three parameters reveal new factors acting at various stages of receptor action, thereby increasing the potential therapeutic targets for adjusting GR actions in pathological situations.&lt;br/&gt;&lt;br/&gt;post to: &lt;a href = &quot;http://www.citeulike.org/posturl?url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Fcmd%3DRetrieve%26db%3DPubMed%26dopt%3DAbstract%26list_uids%3D20801081&amp;title=Entrez+Pubmed&quot;&gt;CiteULike&lt;/a&gt;</description>
    </item>
  </channel>
</rss>
