التفاصيل البيبلوغرافية
| العنوان: |
DNA-dependent protein kinase: Epigenetic alterations and the role in genomic stability of cancer. |
| المؤلفون: |
George, Vazhappilly Cijo1,2 (AUTHOR), Ansari, Shabbir Ahmed3 (AUTHOR), Chelakkot, Vipin Shankar4 (AUTHOR), Chelakkot, Ayshwarya Lakshmi5 (AUTHOR), Chelakkot, Chaithanya6 (AUTHOR), Menon, Varsha2 (AUTHOR), Ramadan, Wafaa2,7 (AUTHOR), Ethiraj, Kannatt Radhakrishnan8 (AUTHOR), El-Awady, Raafat2,9,10 (AUTHOR), Mantso, Theodora1,11 (AUTHOR), Mitsiogianni, Melina1,11 (AUTHOR), Panagiotidis, Mihalis I.11 (AUTHOR), Dellaire, Graham12 (AUTHOR), Vasantha Rupasinghe, H.P.1,12 (AUTHOR) vrupasinghe@dal.ca |
| المصدر: |
Mutation Research/Reviews in Mutation Research. Apr2019, Vol. 780, p92-105. 14p. |
| مصطلحات موضوعية: |
*PROTEIN kinases, *BIOMOLECULES, *DNA repair, *DOUBLE-strand DNA breaks, *SMALL molecules, *CYCLIN-dependent kinases |
| مستخلص: |
DNA-dependent protein kinase (DNA-PK), a member of phosphatidylinositol-kinase family, is a key protein in mammalian DNA double-strand break (DSB) repair that helps to maintain genomic integrity. DNA-PK also plays a central role in immune cell development and protects telomerase during cellular aging. Epigenetic deregulation due to endogenous and exogenous factors may affect the normal function of DNA-PK, which in turn could impair DNA repair and contribute to genomic instability. Recent studies implicate a role for epigenetics in the regulation of DNA-PK expression in normal and cancer cells, which may impact cancer progression and metastasis as well as provide opportunities for treatment and use of DNA-PK as a novel cancer biomarker. In addition, several small molecules and biological agents have been recently identified that can inhibit DNA-PK function or expression, and thus hold promise for cancer treatments. This review discusses the impact of epigenetic alterations and the expression of DNA-PK in relation to the DNA repair mechanisms with a focus on its differential levels in normal and cancer cells. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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