A General Sight about Linking PARP-1 and NFKB1 Variations to the Inflammatory EventsSultuybek GK, Yenmis G* and Koc A
Department of Medical Biology, Cerrahpasa Medical Faculty, Istanbul University, PO Box 34098, Istanbul, Turkey
- *Corresponding Author:
- Yenmis G
Department of Medical Biology
Cerrahpasa Medical Faculty, Istanbul University
PO Box 34098, Istanbul, Turkey
E-mail: [email protected]
Received date: October 15, 2014; Accepted date: November 17, 2014; Published date: November 19, 2014
Citation: Sultuybek GK, Yenmis G, Koc A (2014) A General Sight about Linking PARP-1 and NFKB1 Variations to the Inflammatory Events. Interdiscip J Microinflammation 1:117. doi: 10.4172/2381-8727.1000117
Copyright: © 2014, Sultuybek GK, et al. 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.
Poly (ADP-ribose) polymerase-1 (PARP-1) has various roles in cellular processes such as DNA repair, genomic stability, transcription, stress response, and cell death via regulating death and inflammation signalling pathways. On the other hand, PARP-1 inhibition has been shown to provide benefits in experimental models of animals with inflammatory diseases such as asthma, atherosclerosis and diabetes. PARP-1 also acts a transcriptional coactivator of nuclear factor kappa B (NFKB). The NFKB is a ubiquitous transcription factor that controls the expression of genes encoding cell adhesion molecules, growth factors, cytokines, and some acute phase proteins. Inappropriate activation of NFKB has been mostly searched with inflammatory events. In complete and persistent inhibition studies of NFKB, apoptosis, inappropriate immune cell development and delayed cell growth were investigated. These findings might provide new perceptions in the pathogenesis of inflammatory disorders regarding the roles of PARP-1 and NFKB1 proteins. In this review, we focus on some variations (rs28362491, rs696, rs1136410, rs2793378, rs7527192) of PARP-1 and NFKB1 genes in relation to susceptibility to common inflammatory diseases including rheumatoid arthritis, systemic lupus erythematosus, allergic rhinitis, Graves’ disease, Hashimoto’s thyroiditis, asthma and Behcet’s disease.