Mechanisms of NF-κB p65 and strategies for therapeutic manipulation
Sivagami Giridharan,1 Mythily Srinivasan2,3 1Department of Oral Medicine, Madha Dental College, Kundrathur, Chennai, TN, India; 2Department of Oral Pathology, Medicine and Radiology, Indiana University School of Dentistry, Indiana University Purdue University at Indianapolis, Indianapolis, IN, USA;...
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Dove Medical Press
2018
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oai:doaj.org-article:ca6cd55d3360416c89c10fa8ad6e24c82021-12-02T05:14:13ZMechanisms of NF-κB p65 and strategies for therapeutic manipulation1178-7031https://doaj.org/article/ca6cd55d3360416c89c10fa8ad6e24c82018-10-01T00:00:00Zhttps://www.dovepress.com/mechanisms-of-nf-kappab-p65-and-strategies-for-therapeutic-manipulatio-peer-reviewed-article-JIRhttps://doaj.org/toc/1178-7031Sivagami Giridharan,1 Mythily Srinivasan2,3 1Department of Oral Medicine, Madha Dental College, Kundrathur, Chennai, TN, India; 2Department of Oral Pathology, Medicine and Radiology, Indiana University School of Dentistry, Indiana University Purdue University at Indianapolis, Indianapolis, IN, USA; 3Provaidya LLC, Indianapolis, IN, USA Abstract: The transcription factor NF-κB is a critical regulator of immune and inflammatory responses. In mammals, the NF-κB/Rel family comprises five members: p50, p52, p65 (Rel-A), c-Rel, and Rel-B proteins, which form homo- or heterodimers and remain as an inactive complex with the inhibitory molecules called IκB proteins in resting cells. Two distinct NF-κB signaling pathways have been described: 1) the canonical pathway primarily activated by pathogens and inflammatory mediators, and 2) the noncanonical pathway mostly activated by developmental cues. The most abundant form of NF-κB activated by pathologic stimuli via the canonical pathway is the p65:p50 heterodimer. Disproportionate increase in activated p65 and subsequent transactivation of effector molecules is integral to the pathogenesis of many chronic diseases such as the rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, and even neurodegenerative pathologies. Hence, the NF-κB p65 signaling pathway has been a pivotal point for intense drug discovery and development. This review begins with an overview of p65-mediated signaling followed by discussion of strategies that directly target NF-κB p65 in the context of chronic inflammation. Keywords: NF-κB, inflammation, therapyGiridharan SSrinivasan MDove Medical PressarticleNF-κBinflammationtherapyPathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 11, Pp 407-419 (2018) |
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DOAJ |
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EN |
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NF-κB inflammation therapy Pathology RB1-214 Therapeutics. Pharmacology RM1-950 |
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NF-κB inflammation therapy Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Giridharan S Srinivasan M Mechanisms of NF-κB p65 and strategies for therapeutic manipulation |
| description |
Sivagami Giridharan,1 Mythily Srinivasan2,3 1Department of Oral Medicine, Madha Dental College, Kundrathur, Chennai, TN, India; 2Department of Oral Pathology, Medicine and Radiology, Indiana University School of Dentistry, Indiana University Purdue University at Indianapolis, Indianapolis, IN, USA; 3Provaidya LLC, Indianapolis, IN, USA Abstract: The transcription factor NF-κB is a critical regulator of immune and inflammatory responses. In mammals, the NF-κB/Rel family comprises five members: p50, p52, p65 (Rel-A), c-Rel, and Rel-B proteins, which form homo- or heterodimers and remain as an inactive complex with the inhibitory molecules called IκB proteins in resting cells. Two distinct NF-κB signaling pathways have been described: 1) the canonical pathway primarily activated by pathogens and inflammatory mediators, and 2) the noncanonical pathway mostly activated by developmental cues. The most abundant form of NF-κB activated by pathologic stimuli via the canonical pathway is the p65:p50 heterodimer. Disproportionate increase in activated p65 and subsequent transactivation of effector molecules is integral to the pathogenesis of many chronic diseases such as the rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, and even neurodegenerative pathologies. Hence, the NF-κB p65 signaling pathway has been a pivotal point for intense drug discovery and development. This review begins with an overview of p65-mediated signaling followed by discussion of strategies that directly target NF-κB p65 in the context of chronic inflammation. Keywords: NF-κB, inflammation, therapy |
| format |
article |
| author |
Giridharan S Srinivasan M |
| author_facet |
Giridharan S Srinivasan M |
| author_sort |
Giridharan S |
| title |
Mechanisms of NF-κB p65 and strategies for therapeutic manipulation |
| title_short |
Mechanisms of NF-κB p65 and strategies for therapeutic manipulation |
| title_full |
Mechanisms of NF-κB p65 and strategies for therapeutic manipulation |
| title_fullStr |
Mechanisms of NF-κB p65 and strategies for therapeutic manipulation |
| title_full_unstemmed |
Mechanisms of NF-κB p65 and strategies for therapeutic manipulation |
| title_sort |
mechanisms of nf-κb p65 and strategies for therapeutic manipulation |
| publisher |
Dove Medical Press |
| publishDate |
2018 |
| url |
https://doaj.org/article/ca6cd55d3360416c89c10fa8ad6e24c8 |
| work_keys_str_mv |
AT giridharans mechanismsofnfkappabp65andstrategiesfortherapeuticmanipulation AT srinivasanm mechanismsofnfkappabp65andstrategiesfortherapeuticmanipulation |
| _version_ |
1718400498402328576 |