Inhibition of Alanyl Aminopeptidase Induces MAP-Kinase p42/ERK2 in the Human T Cell Line KARPAS-299
Identifieur interne : 001970 ( Main/Exploration ); précédent : 001969; suivant : 001971Inhibition of Alanyl Aminopeptidase Induces MAP-Kinase p42/ERK2 in the Human T Cell Line KARPAS-299
Auteurs : Uwe Lendeckel [Allemagne] ; Thilo K Hne [Allemagne] ; Marco Arndt [Allemagne] ; Karin Frank [Allemagne] ; Siegfried Ansorge [Allemagne]Source :
- Biochemical and Biophysical Research Communications [ 0006-291X ] ; 1998.
English descriptors
- KwdEn :
- Teeft :
- Academic press, Actinonin, Alanyl, Alanyl aminopeptidase, Aminopeptidase, Aminopeptidase inhibitors, Ansorge, Atlas cdna expression array, Biophysical research communications, Boehringer mannheim, Cdna, Cell line, Cell number, Cell proliferation, Clontech, Densitometry scanning, Erk2, Erk2 mrna, Erk2 mrna content, Febs letters, Gene expression, Idaho technology, Inhibitor, Inhibitor administration, Kinase, Kinase pathway, Lendeckel, Membrane alanyl aminopeptidase activity, Molecular components, Mrna, Probestin, Prominent changes, Protein kinase, Reaction mixture, Strand cdna, Surface expression.
Abstract
Abstract: Inhibition of alanyl aminopeptidase (EC 3.4.11.2, aminopeptidase N, CD13) expression, or activity compromise cell proliferation in a number of cell systems [1,2,3,4,5,6]. The underlying mechanisms and the molecular components involved have not been identified as yet. In this study we show that inhibition of alanyl aminopeptidase enzymatic activity decreases the proliferation rate of the CD13-positive T cell line Karpas-299. By using the ATLAS cDNA expression array (Clontech) we identified the p42/ERK2 MAP kinase as one downstream target of probestin, a potent inhibitor of alanyl aminopeptidase. Probestin and another specific aminopeptidase inhibitor, actinonin, in addition to their capability of inducing erk-2 mRNA levels, significantly increase p42 phosphorylation state. This is the first report on signal transduction components possibly mediating the growth-modulatory effects of alanyl aminopeptidase inhibitors.
Url:
DOI: 10.1006/bbrc.1998.9585
Affiliations:
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proliferation</term><term>Clontech</term><term>Densitometry scanning</term><term>Erk2</term><term>Erk2 mrna</term><term>Erk2 mrna content</term><term>Febs letters</term><term>Gene expression</term><term>Idaho technology</term><term>Inhibitor</term><term>Inhibitor administration</term><term>Kinase</term><term>Kinase pathway</term><term>Lendeckel</term><term>Membrane alanyl aminopeptidase activity</term><term>Molecular components</term><term>Mrna</term><term>Probestin</term><term>Prominent changes</term><term>Protein kinase</term><term>Reaction mixture</term><term>Strand cdna</term><term>Surface expression</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Inhibition of alanyl aminopeptidase (EC 3.4.11.2, aminopeptidase N, CD13) expression, or activity compromise cell proliferation in a number of cell systems [1,2,3,4,5,6]. The underlying mechanisms and the molecular components involved have not been identified as yet. In this study we show that inhibition of alanyl aminopeptidase enzymatic activity decreases the proliferation rate of the CD13-positive T cell line Karpas-299. By using the ATLAS cDNA expression array (Clontech) we identified the p42/ERK2 MAP kinase as one downstream target of probestin, a potent inhibitor of alanyl aminopeptidase. Probestin and another specific aminopeptidase inhibitor, actinonin, in addition to their capability of inducing erk-2 mRNA levels, significantly increase p42 phosphorylation state. This is the first report on signal transduction components possibly mediating the growth-modulatory effects of alanyl aminopeptidase inhibitors.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Saxe-Anhalt</li></region><settlement><li>Magdebourg</li></settlement></list><tree><country name="Allemagne"><region name="Saxe-Anhalt"><name sortKey="Lendeckel, Uwe" sort="Lendeckel, Uwe" uniqKey="Lendeckel U" first="Uwe" last="Lendeckel">Uwe Lendeckel</name></region><name sortKey="Ansorge, Siegfried" sort="Ansorge, Siegfried" uniqKey="Ansorge S" first="Siegfried" last="Ansorge">Siegfried Ansorge</name><name sortKey="Arndt, Marco" sort="Arndt, Marco" uniqKey="Arndt M" first="Marco" last="Arndt">Marco Arndt</name><name sortKey="Frank, Karin" sort="Frank, Karin" uniqKey="Frank K" first="Karin" last="Frank">Karin Frank</name><name sortKey="K Hne, Thilo" sort="K Hne, Thilo" uniqKey="K Hne T" first="Thilo" last="K Hne">Thilo K Hne</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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