Role of Epigenetics in Inflammation-Associated Diseases

作者: Muthu K. Shanmugam , Gautam Sethi

DOI: 10.1007/978-94-007-4525-4_27

关键词:

摘要: There is considerable evidence suggesting that epigenetic mechanisms may mediate development of chronic inflammation by modulating the expression pro-inflammatory cytokine TNF-α, interleukins, tumor suppressor genes, oncogenes and autocrine paracrine activation transcription factor NF-κB. These molecules are constitutively produced a variety cells under inflammatory conditions, which in turn leads to major diseases such as autoimmune disorders, obstructive pulmonary diseases, neurodegenerative cancer. Distinct or global changes landscape hallmarks driven diseases. Epigenetics include distinct markers on genome associated cellular transcriptional machinery copied during cell division (mitosis meiosis). appear for short span time they necessarily do not make permanent primary DNA sequence itself. However, most frequently observed aberrant methylation, histone acetylation deacetylation. In this chapter, we focus regulated enzymes involved modifications arginine lysine methyl transferases, methyltransferase, acetyltransferases deacetylases their role Agents modulate inhibit these modifications, HAT HDAC inhibitors have shown great potential inhibiting progression Given plasticity readiness respond intervention small molecule inhibitors, there tremendous novel therapeutics will serve direct adjuvant therapeutic compounds treatment

参考文章(263)
August Heidland, Przemyslaw Rutkowski, Udo Bahner, André Klassen, The contribution of Rudolf Virchow to the concept of inflammation: what is still of importance? Journal of Nephrology. ,vol. 10, pp. 102- 109 ,(2006)
Bharat B. Aggarwal, Nuclear factor-κB: The enemy within Cancer Cell. ,vol. 6, pp. 203- 208 ,(2004) , 10.1016/J.CCR.2004.09.003
S. N. Khleif, F. J. Kaye, Weidong Chen, A. B. Coxon, G. A. Otterson, CDKN2 gene silencing in lung cancer by DNA hypermethylation and kinetics of p16INK4 protein induction by 5-aza 2'deoxycytidine. Oncogene. ,vol. 11, pp. 1211- 1216 ,(1995)
A. Aoike, N. Ohtani-Fujita, T. Sakai, Paul D Robbins, T. Fujita, N. E. Osifchin, CpG methylation inactivates the promoter activity of the human retinoblastoma tumor-suppressor gene Oncogene. ,vol. 8, pp. 1063- 1067 ,(1993)
Nobuhisa Iwata, Satoshi Tsubuki, Emi Hama, Yoshie Takaki, Keiro Shirotani, Takaomi C. Saido, Reply to: 'Clearance of amyloid β-peptide from brain: transport or metabolism?' Nature Medicine. ,vol. 6, pp. 718- 719 ,(2000) , 10.1038/77399
David Baltimore, Ranjan Sen, Multiple nuclear factors interact with the immunoglobulin enhancer sequences. Cell 1986. 46: 705-716. Journal of Immunology. ,vol. 177, pp. 7485- 7496 ,(2006)
Adrian L. Harris, Hypoxia — a key regulatory factor in tumour growth Nature Reviews Cancer. ,vol. 2, pp. 38- 47 ,(2002) , 10.1038/NRC704
Hui-Juan Yang, Vincent WS Liu, Yue Wang, Percy CK Tsang, Hextan YS Ngan, Differential DNA methylation profiles in gynecological cancers and correlation with clinico-pathological data. BMC Cancer. ,vol. 6, pp. 212- 212 ,(2006) , 10.1186/1471-2407-6-212
Peter A. Jones, Stephen B. Baylin, The fundamental role of epigenetic events in cancer Nature Reviews Genetics. ,vol. 3, pp. 415- 428 ,(2002) , 10.1038/NRG816