Title : Induced ATF-2 represses CDK4 transcription through dimerization with JunD inhibiting intestinal epithelial cell growth after polyamine depletion.

Pub. Date : 2010 May

PMID : 20181929






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1 Induced ATF-2 represses CDK4 transcription through dimerization with JunD inhibiting intestinal epithelial cell growth after polyamine depletion. Polyamines activating transcription factor 2 Homo sapiens
2 Decreased levels of cellular polyamines increase activating transcription factor (ATF)-2, but the exact role and mechanism of induced ATF-2 in the regulation of intestinal epithelial cell (IEC) growth remain elusive. Polyamines activating transcription factor 2 Homo sapiens
3 Here, we reported that induced ATF-2 following polyamine depletion repressed CDK4 gene transcription in IECs by increasing formation of the ATF-2/JunD heterodimers. Polyamines activating transcription factor 2 Homo sapiens
4 Here, we reported that induced ATF-2 following polyamine depletion repressed CDK4 gene transcription in IECs by increasing formation of the ATF-2/JunD heterodimers. Polyamines activating transcription factor 2 Homo sapiens
5 Polyamine depletion increased ATF-2/JunD complex and inhibited CDK4 transcription as indicated by a decrease in the levels of CDK4-promoter activity and its mRNA. Polyamines activating transcription factor 2 Homo sapiens
6 ATF-2 silencing not only prevented inhibition of CDK4 transcription in polyamine-deficient cells but also abolished repression of CDK4 expression induced by ectopic JunD overexpression. Polyamines activating transcription factor 2 Homo sapiens
7 ATF-2 silencing also promoted IEC growth in polyamine-depleted cells. Polyamines activating transcription factor 2 Homo sapiens
8 These results indicate that induced ATF-2/JunD association following polyamine depletion represses CDK4 transcription, thus contributing to the inhibition of IEC growth. Polyamines activating transcription factor 2 Homo sapiens