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|Title:||Mechanistic insights into the substrate-mediated regulation of p300 autoacetylation: implications in tumor suppressor/oncogene functions|
|Authors:||Kundu, Tapas Kumar|
|Publisher:||Jawaharlal Nehru Centre for Advanced Scientific Research|
|Citation:||Kaypee, Stephanie. 2017, Mechanistic insights into the substrate-mediated regulation of p300 autoacetylation: implications in tumor suppressor/oncogene functions, Ph.D thesis, Jawaharlal Nehru Centre for Advanced Scientific Research, Bengaluru|
|Abstract:||The vast eukaryotic genome is present within the confines of the nuclei as a compact nucleoprotein complex known as chromatin. Chromatin is fundamentally made up of repeating nucleosomal units which consists of 147 base pairs of DNA double helix wrapped around an octameric core of histone proteins (H3-H4 tetramer and two H2A-H2B dimers) (Luger et al., 1997). In the presence of linker histone H1, the string of nucleosomes can further fold to form higher ordered structures. In 1942, the term „epigenetics‟ was coined by Conrad Waddington which described how the interaction between gene expression and the external environment could modulate cellular phenotype, a phenomenon which was not dictated by genetics alone (Waddington, 1942). Even though the term was coined in the development perspective, the understanding of epigenetics has evolved over the years to encompass several biological events. Epigenetics is defined as a heritable alteration in the gene expression or phenotype without any change in the underlying DNA sequences. In a broad sense, epigenetics is the link between the genotype and the exhibited phenotype (Goldberg et al., 2007). The molecular machinery of epigenetics incorporates several factors which modulate chromatin structural dynamicity and gene expression.|
|Appears in Collections:||Student Theses (MBGU)|
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