TITLE: The pseudokinase tribbles homolog 3 interacts with ATF4 to negatively regulate insulin exocytosis in human and mouse beta cells
Rohit N. Kulkarni
Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts, USA.
Phone: 617.713.3460; Fax: 617.713.3476; E-mail: Rohit.Kulkarni@joslin.harvard.edu.
View this article at: http://www.jci.org/articles/view/36849?key=53f83115ab8916a3b1e0
ONCOLOGY: Silencing genes that protect from cancer: a role for the protein hNaa10p
Tumor suppressor genes are genes that generate proteins that protect cells from becoming cancerous. Loss or reduction in their expression contributes to the onset of cancer. One mechanism by which tumor suppressor genes are silenced in cancer cells is excessive modification of their promoter (the region of the gene that drives expression) with molecules known as methyl groups. Understanding the mechanism underlying hypermethylation of tumor suppressor gene promoters might provide new approaches to cancer treatment.
In this regard, a team of researchers, led by Cheng-Wen Wu and Li-Jung Juan, at Academia Sinica, Taiwan, has now identified a role for the protein hNaa10p in mediating tumor suppressor gene silencing by promoting the function of the protein DNMT1, which transfers methyl groups to DNA. Importantly, depletion of hNaa10p impaired human lung cancer cell proliferation in vitro and upon transplantation into mice. Consistent with hNaa10p having a role in promoting lung tumor development, it was found to be overexpressed in
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Journal of Clinical Investigation