DNA Modifications: Function and Applications in Normal and Disease States

Liyanage, Vichithra R. B.; Jarmasz, Jessica S.; Murugeshan, Nanditha; Bigio, Marc R. Del; Rastegar, Mojgan; Davie, James R.

doi:10.3390/biology3040670

Cited by 120 publications

(101 citation statements)

References 281 publications

(394 reference statements)

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“…27 De novo metiltransferazlar adı verilen DNMT3a, DNMT3b ve DNMT3L embriyonik kök hücrelerinde yüksek derecede ifade edilir, imprinting işleminde DNA metilasyonundan sorumludur. [28,29] DNA metilasyonu gelişim ve farklılaşma, genomik imprinting, X kromozomunun inaktivasyonu, genomu transpozonlardan koruma gibi farklı biyolojik fonksiyonlara aracılık etmektedir. 19,28,30 DNA metilasyon düzeyinin yaşlanmaya bağlı olarak değişimi çeşitli çalışmalarda gösterilmiştir.…”

Section: Dna Meti̇lasyon Deği̇şi̇mleri̇ Ve Yaşlanmaunclassified

“…[28,29] DNA metilasyonu gelişim ve farklılaşma, genomik imprinting, X kromozomunun inaktivasyonu, genomu transpozonlardan koruma gibi farklı biyolojik fonksiyonlara aracılık etmektedir. 19,28,30 DNA metilasyon düzeyinin yaşlanmaya bağlı olarak değişimi çeşitli çalışmalarda gösterilmiştir. Yaşlanma ve DNA metilasyonu arasındaki ilişki ilk kez somon balığında yapılan çalışmalarda öne sü-rülmüştür.…”

Section: Dna Meti̇lasyon Deği̇şi̇mleri̇ Ve Yaşlanmaunclassified

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Epigenetic Alterations in Aging and Aging-Associated Diseases: Review

Güneş¹,

Bayramov²

2016

Turkiye Klinikleri J Med Sci

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Section: Dna Meti̇lasyon Deği̇şi̇mleri̇ Ve Yaşlanmaunclassified

Epigenetic Alterations in Aging and Aging-Associated Diseases: Review

Güneş¹,

Bayramov²

2016

Turkiye Klinikleri J Med Sci

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“…Correct methylation occurrence is necessary for the suitable binding of MBPs. Different roles of MBPs can be seen in different types of cancers 17 . Alternative splicing and their role in cancer is also getting more interest, as both changes in splicing factor expression and cis-mutations can cause disease.…”

Section: Some Other Diseasementioning

confidence: 99%

“…It was determined that DNA methylation effect several genes by misregulating, which could lead to cardiovascular diseases. Also; loss of function of DNA methyltransferases cause to increased resistance to brain damaged by ischemia and together, it was shown that; there is a possible link between DNA methylation and cerebral ischemia 17 .…”

Section: Cardiovascular Diseases and Cerebral Ischemiamentioning

confidence: 99%

Intron and Its Splicing Mechanism and Their Connection with Human Disease

Dosay-Akbulut

2016

Bangladesh J Med Sci

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Abstract:In the maturation mechanism of a messenger RNA, splicing play an important role with removing the noncoding introns and ligating the coding exons. Alternative splicing (AS) gives an extra difficulty to this mechanism and to the regulation of gene expression. The possible disturbing in the alternative RNA splicing mechanism can be a reason to several diseases like cancers and neurodegenerative disorders. Intronless genes (IGs) are seen in almost 3% of the human genome. Functionality of IGs has an important role in signal transduction genes and related regulatory proteins. This diversity can be reason to IG-associated diseases, especially neuropathies, developmental disorders, and cancer. The retroelements can be seen in almost half of the human genome. The known informations indicate that insertion of retroelement into exons and introns of genes promote different types of genetic disease, including cancer. The retroelement connected mutagenesis cause to fifty different types of human disease. The molecular informations and bioinformatic analyses can be used to explain the connection with splicing mutations and genetic mechanisms of several different human disease and understanding of this mechanism play an important role in the formation of treatment programme against to these diseases.

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“…Genome-wide association studies have identified that some CDKN2A or CDKN2B genetic variants are susceptible to CHD (8)(9)(10). As recently reported, many human diseases, including cardiovascular disease, could be influenced by aberrant DNA methylation modification (11). Aberrant methylation of cytosine-phosphate-guanine (CpG) islands in gene promoters is associated with transcription silencing and activity (3).…”

Section: Introductionmentioning

confidence: 99%

CDKN2A and CDKN2B methylation in coronary heart disease cases and controls

Zhong

Chen

et al. 2017

Exp Ther Med

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Abstract. The aim of the present study was to investigate the association between cyclin-dependent kinase inhibitor 2A (CDKN2A) and cyclin-dependent kinase inhibitor 2B (CDKN2B) methylation, and coronary heart disease (CHD), and to explore the interaction between methylation status and CHD clinical characteristics in Han Chinese patients. A total of 189 CHD (96 males, 93 females) and 190 well-matched non-CHD controls (96 males, 94 females) were recruited for the study. Methylation-specific polymerase chain reaction technology was used to examine gene promoter methylation status. Comparisons of methylation frequencies between CHD and non-CHD patients were carried out using the Chi-square test. Methylation levels of CDKN2A and CDKN2B genes were not found to be associated with the risk of CHD. However, the mean age of CDKN2A-hypermethylated participants was significantly lower than CDKN2A-unmethylated participants (58.73±5.88 vs. 62.62±5.36 years, adjusted P<0.001). Conversely, the mean age of CDKN2B-hypermethylated participants was significantly higher compared with CDKN2B-unmethylated participants (62.26±5.48 vs. 58.33±7.47 years, adjusted P=0.048). In addition, CDKN2B methylation frequencies were significantly increased in female participants compared with males (99.47 vs. 11.98%, P=0.032). In conclusion, the results indicated that CDKN2A and CDKN2B promoter methylation frequencies were significantly associated with age, and there was a gender dimorphism in CDKN2B methylation. IntroductionCoronary heart disease (CHD) is a complex chronic disease that is caused by an imbalance between blood supply and demand in myocardium. Various environmental and genetic factors are known to contribute to onset and development of CHD (1). As of 2010, CHD was the leading cause of mortality globally, resulting in over 7 million cases of mortality (2). Therefore, association studies for CHD biomarkers have been performed worldwide (3-5) for future forefront diagnostics for the early assessment of cardiac risks.The genetic locus at chromosome 9p21 has been demonstrated to be strongly associated with the risk of CHD (6,7). Cyclin-dependent kinase inhibitor 2A (CDKN2A) and cyclin-dependent kinase inhibitor 2B (CDKN2B) genes both encode putative regulators of cyclin-dependent kinases on chromosome 9p21. Genome-wide association studies have identified that some CDKN2A or CDKN2B genetic variants are susceptible to CHD (8-10). As recently reported, many human diseases, including cardiovascular disease, could be influenced by aberrant DNA methylation modification (11). Aberrant methylation of cytosine-phosphate-guanine (CpG) islands in gene promoters is associated with transcription silencing and activity (3). However, the exact role of CDKN2A and CDKN2B methylation in cardiovascular system has not yet been fully elucidated.CDKN2A gene is involved in the regulation of cell proliferation, cell aging and apoptosis (12). However, a bidirectional role of CDKN2A gene expression has been reported in previous studies. Knösel et al (13) reported...

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DNA Modifications: Function and Applications in Normal and Disease States

Cited by 120 publications

References 281 publications

Epigenetic Alterations in Aging and Aging-Associated Diseases: Review

Epigenetic Alterations in Aging and Aging-Associated Diseases: Review

Intron and Its Splicing Mechanism and Their Connection with Human Disease

CDKN2A and CDKN2B methylation in coronary heart disease cases and controls

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