title: Transcriptional Activation of Inflammatory Genes: Mechanistic Insight into Selectivity and Diversity.
abstract: Acute inflammation, an integral part of host defence and immunity, is a highly conserved cellular response to pathogens and other harmful stimuli. An inflammatory stimulation triggers transcriptional activation of selective pro-inflammatory genes that carry out specific functions such as anti-microbial activity or tissue healing. Based on the nature of inflammatory stimuli, an extensive exploitation of selective transcriptional activations of pro-inflammatory genes is performed by the host to ensure a defined inflammatory response. Inflammatory signal transductions are initiated by the recognition of inflammatory stimuli by transmembrane receptors, followed by the transmission of the signals to the nucleus for differential gene activations. The differential transcriptional activation of pro-inflammatory genes is precisely controlled by the selective binding of transcription factors to the promoters of these genes. Among a number of transcription factors identified to date, NF-κB still remains the most prominent and studied factor for its diverse range of selective transcriptional activities. Differential transcriptional activities of NF-κB are dictated by post-translational modifications, specificities in dimer formation, and variability in activation kinetics. Apart from the differential functions of transcription factors, the transcriptional activation of selective pro-inflammatory genes is also governed by chromatin structures, epigenetic markers, and other regulators as the field is continuously expanding.
authors.affiliation: The Centre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton VIC 3168, Australia. afsar.ahmed@hudson.org.au.
authors.forename: Afsar U
authors.initials: AU
authors.lastname: Ahmed
authors.affiliation: The Centre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton VIC 3168, Australia. bryan.williams@hudson.org.au.
authors.forename: Bryan R G
authors.initials: BR
authors.lastname: Williams
authors.affiliation: The Centre for Cancer Research, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton VIC 3168, Australia. greg.hannigan@hudson.org.au.
authors.forename: Gregory E
authors.initials: GE
authors.lastname: Hannigan
mesh_terms: D000818:Animals; D018925:Chemokines / Q000235:genetics* / Q000378:metabolism; D042002:Chromatin Assembly and Disassembly; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism; D020935:MAP Kinase Signaling System; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism*; D015533:Transcriptional Activation; D054875:Ubiquitination
chemical_list: D018925:Chemokines; D016328:NF-kappa B
keywords: MAPK; NF-κB; chromatin structures; epigenetic markers; inflammation; nucleosome remodeling; pro-inflammatory genes; transcriptional activation; ubiquitination