Novel Protein RGPR-p117: New Aspects in Cell RegulationMasayoshi Yamaguchi*
Department of Hematology and Medical Oncology, Emory University School of Medicine, Atlanta, USA
- *Corresponding Author:
- Masayoshi Yamaguchi
Department of Hematology and Medical Oncology
Emory University School of Medicine
1365 C Clifton Road, NE, Atlanta, GA 30322, USA
E-mail: [email protected]
Received date: July 11, 2013; Accepted date: July 12, 2013; Published date: July 15, 2013
Citation:Yamaguchi M (2013) Novel Protein RGPR-p117: New Aspects in Cell Regulation. J Mol Genet Med 7:072. doi: 10.4172/1747-0862.1000072
Copyright: © 2013 Yamaguchi M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
RGPR-p117 was initially discovered as novel protein which binds to the nuclear factor I (NF1)-like motif TTGGC(N)6CC in the regucalcin gene promoter region (RGPR). RGPR-p117 is localized to the nucleus with stimulation of protein kinase C-related signaling process. Overexpression of RGPR-p117 has been shown to enhance regucalcin mRNA expression in the cloned normal rat kidney proximal tubularepithelial NRK52E cells in vitro. This process is mediated through phosphorylated RGPR-p117. Overexpression of RGPR-p117 was found to suppress apoptotic cell death induced after stimulation with various signaling factors in NRK52E cells, while it did not have an effect on cell proliferation. Moreover, RGPR-p117 was found to localize in the plasma membranes, mitochondria and microsomes, suggesting an involvement in the regulation of function of these organelles. After that, RGPR-p117 was renamed as Sec16B that is involved in the endoplasmic reticulum export. However, this is not suitable name with many findings of the role of RGPR-p117 in cell regulation. RGPR-p117 may play an essential role as transcription factor, and the elucidation of other roles in cell regulation will be expected.