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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
Gene activation can occur in response to various internal or external stimuli through the action of receptor proteins and signalling pathways. The end point of these pathways is usually the expression or activation of one or more DNA-binding proteins that, in turn, stimulates gene expression. In addition to the regulation of transcription, factors such as mRNA stability, transcriptional regulation and differential splicing may influence protein expression.
Role of Histone Methyltransferase in Breast Cancer
Published in Meenu Gupta, Rachna Jain, Arun Solanki, Fadi Al-Turjman, Cancer Prediction for Industrial IoT 4.0: A Machine Learning Perspective, 2021
Surekha Manhas, Zaved Ahmed Khan
Moreover, the role of G9a in gene repression studies has been studied predominantly by its histone methyltransferase activity; it is more clearly illustrated that G9a might play a role in active gene activation on certain specific conditions [100–102], that is markedly methyltransferase independent. In addition, this function mentioned above was clearly mapped in the N-protein terminal as 280 amino acids that present first in the protein chain as highly sufficient to promote the expression of the gene through acting as a scaffold to promote transcriptional co-activator recruitment including CARM1 and p300 [101,103]. At last, G9a is a protein with complexity that is highly involved in activating and repressing genes through specific but distinct mechanisms.
The Precision Medicine Approach in Oncology
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
Another mechanism involves a physical change in the location of nucleosomes. These noncovalent mechanisms play a significant role in chromatin structure and gene regulation. Nucleosomes not only help to pack the DNA within the nucleus of cells but also enable transcription factors to access the regulatory regions of DNA sequences to facilitate gene expression. At the 5’- and 3’-ends of genes there are nucleosome-free-regions (NFRs) (Figure 11.16) which are thought to be responsible for transcription factor assembly and disassembly. Having an NFR region at gene-promoter sites allows for rapid gene activation when stimulated. Conversely, if an NFR within a transcription start site is occluded, then this can lead to gene repression.
Trends in iron oxide nanoparticles: a nano-platform for theranostic application in breast cancer
Published in Journal of Drug Targeting, 2022
Jitu Halder, Deepak Pradhan, Prativa Biswasroy, Vineet Kumar Rai, Biswakanth Kar, Goutam Ghosh, Goutam Rath
Recent evidence shows that, many genetic changes have been observed in both pre-invasive and invasive BC. Comparative genomic hybridisation investigations (CGH) and loss of heterozygosity (LOH) investigation have discovered heterogeneous patterns of DNA structural variation (nucleotide losses, duplications, and amplifications) in BC cellular progression [33,34]. Various transcription factors responsible for the receptors’ gene activation pathway have been identified. The ‘stress-activated protein kinase 1 (JUN N-terminal kinase, JNK)’, ‘stress-activated protein kinase 2 (p38 kinase)’, and ‘extracellular signal-regulated kinase (ERK)’ cascades are among the protein kinases whose activity alter fast following receptor triggering [35,36]. Amongst the most significant signalling pathways is the JNK pathway, which is a ‘mitogen-activated protein kinase (MAPK)’ signalling pathway that can promote apoptosis [37]. It controls a range of cellular activities, including mitosis, embryogenesis, and apoptosis, by enhancing the transcription of pro-apoptotic genes via c-Jun/AP1-dependent or p53/73-dependent pathways [38]. Also, a recent finding shows in BRCA1-mutated BC, ‘EF2K’ is an atypical kinase that belongs to a family of α kinases. It is a key prognostic factor and prospective molecular target [39]. IONs itself or functionalised IONs can potentially be used for targeting these gene activation pathways and signalling kinases. Studies revealed that IONs have direct apoptosis induction efficacy by activating the JNK pathway [40].
Zinc affects nuclear factor kappa b and DNA methyltransferase activity in C3H cancer fibroblast cells induced by a 2100 MHz electromagnetic field
Published in Electromagnetic Biology and Medicine, 2022
D. Duzgun Ergun, N. Pastaci Ozsobaci, T. Yilmaz, D. Ozcelik, M. T. Kalkan
Epigenetic changes play an important role in tumor development and progression by affecting the pathways related to tumor development in cancer cells. Methylation, defined as the addition of a methyl group to a chemical compound, is a reaction that ensures the normal regulation and development of the genome. Methylation regulates gene expression by playing a role in epigenetic events such as gene activation, repression and chromatin remodeling. In biological systems, methylation occurs in two ways: DNA methylation and protein methylation. DNA methylation occurs by the binding of a methyl group (CH3) to the fifth carbon (C) atom of cytosine at the CpG (cytosine, phosphate, guanine) site via DNA methyltransferases (DNMTs) (Brito et al. 2020; Jarosz et al. 2017). There are three DNMTs in mammals: DNMT1, DNMT3A and DNMT3B. The pattern of DNA methylation is associated with under- or over-expression of some proteins and may cause pathologies such as obesity, cardiovascular, neurogenetic, renal and psychiatric disorders, and cancer in particular. Epigenetic mechanisms can be modified to prevent cancer development and DNMT inhibitors have an important place in the development of new therapeutic agents. The DNMT inhibitors can reverse epigenetic changes through induction of apoptosis, and anti-proliferative activity in cancer cells and are considered targets in cancer treatment. The DNMT inhibitors combined with various dietary supplements can exert an anti-proliferative effect on cancer cells (Coley 2008; Gros et al. 2012).
A look into the use of Raman spectroscopy for brain and breast cancer diagnostics: linear and non-linear optics in cancer research as a gateway to tumor cell identity
Published in Expert Review of Molecular Diagnostics, 2020
Halina Abramczyk, Beata Brozek-Pluska, Arkadiusz Jarota, Jakub Surmacki, Anna Imiela, Monika Kopec
Briefly, DNA/histone epigenetic modifications can be explained as follows. Genomic DNA is tightly packaged in chromatin by both histone and nonhistone proteins in the nucleus of eukaryotic cells. The basic chromatin subunits, nucleosomes, are formed by wrapping 146 base pairs (bp) of DNA around an octamer of four core histones: H2A, H2B, H3, and H4. Whereas the nucleosomal core is compact, eight flexible lysine-rich histone tails protrude from the nucleosome that modulates internucleosomal contacts and provides binding sites for nonhistone proteins. From the perspective of gene transcription, chromatin structure can be divided into two distinct categories: euchromatin and heterochromatin. ‘Euchromatin’ is an open chromatin structure that affords accessibility of transcription factors to DNA, resulting in gene activation. In contrast, ‘heterochromatin’ is a closed chromatin structure with a low interaction between transcription factors and the genome, leading to gene repression [94,95].