NPAT links cyclin E-Cdk2 to the regulation of replication-dependent histone gene transcription.
By Jiyong Zhao, Brian K. Kennedy, B. D. Lawrence, D. Barbie, A. Matera, Jonathan A. Fletcher, E. Harlow. Genes & Development, 2000
655 citations recorded by the source corpus.
In eukaryotic cells, histone gene expression is one of the major events that mark entry into S phase. While this process is tightly linked to cell cycle position, how it is regulated by the cell cycle machinery is not known. Here we show that NPAT, a substrate of the cyclin E-Cdk2 complex, is associated with human replication-dependent histone gene clusters on both chromosomes 1 and 6 in S phase. We demonstrate that NPAT activates histone gene transcription and that this activation is dependent on the promoter elements (SSCSs) previously proposed to mediate cell cycle-dependent transcription. Cyclin E is also associated with the histone gene loci, and cyclin E-Cdk2 stimulates the NPAT-mediated activation of histone gene transcription. Thus, our results both show that NPAT is involved in a key S phase event and provide a link between the cell cycle machinery and activation of histone gene transcription.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/302d0229307e9a41f126576746054fd8483d3b33
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Citations in the corpus
- The cell cycle: a review of regulation, deregulation and therapeutic targets in cancer (2003, background): “The protein level of NPAT peaks at the G1/S boundary and is thought to play a role in S phase entry (Zhao et al. 2000).”
- Metabolism and regulation of canonical histone mRNAs: life without a poly(A) tail (2008, background): “At the beginning of S phase cyclin E–CDK2 (cyclin-dependent kinase 2) phosphorylates NPAT in these bodie”
- Gene expression patterns in human liver cancers. (2002, background): “Interestingly, one of these genes, MST, also called hepatocyte growth factor-like protein, has been reported to be induced by p53 expression (Zhao et al., 2000), raising the possibility of a role for this putative growth factor in p53-dependent regulation of hepatocyte differentiation.”