Epigenetic changes play a pivotal role in regulating gene expression and maintaining cellular identity through cell division cycles. These changes involve epigenetic modifications to DNA and histones that are stably inherited from one generation to the next. Maintenance of patterns of DNA methylation during cell division is critical for silencing of inappropriate gene expression and maintaining cellular identity. DNA methyltransferase 1 (DNMT1) maintains such DNA methylation patterns, recognizing hemi-methylated DNA and methylating the newly synthesized strand during DNA replication in S phase, thereby maintaining epigenetic marks. Acetylation of histone proteins loosens chromatin structure, making genes more accessible for the transcriptional apparatus. Acetylation is maintained through cell division by histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDACs remove acetyl groups from histones, restoring a condensed chromatin state. Dysregulation of HDACs, and therefore in appropriate gene activation, has been linked to various diseases, including cancer. Histone marks are also maintained through the cell cycle. For example, H3K27me3 and H3K9me3 are associated with gene repression and are propagated through cell division by specific enzymes. For H3K9me3, methylation is carried out by SUV39H1 (Suppressor of Variegation 3-9 Homolog 1), whilst H3K9me3 methylation is catalysed by Enhancer of Zeste Homolog 2 (EZH2). Mutations in EZH2 have been observed in a subset of patients with myelodysplastic syndromes, a group of blood disorders. Various protein complexes recognize, write, and erase epigenetic marks. They play roles in both reading existing marks and establishing new ones during the process of DNA replication. For example, the Polycomb Repressive Complex 2 (PRC2) can catalyse the addition of H3K27me3 marks, whilst the Lysine-Specific Demethylase 1 (LSD1) erases methyl marks from histones. Certain genes are imprinted, meaning that only one allele is active, depending on whether it was inherited from the mother or father. Imprinting is maintained through repeated cell divisions and is essential for correct development. For example, the insulin-like growth factor 2 (IGF2) gene is imprinted, and its expression is determined by the parent of origin. Aberrant imprinting can lead to growth disorders and cancer. For example, in some cases of colorectal cancer there is hypermethylation of the promoter region of the MLH1 gene, a mismatch repair gene. This hypermethylation silences the MLH1 gene and impairs DNA repair mechanisms, leading to genomic instability and an increased risk of developing colorectal cancer. ATP-dependent chromatin remodelling complexes, such as SWI/SNF, actively move nucleosomes to control access to DNA. These complexes help maintain chromatin states during cell division. SWI/SNF complexes play critical roles in development and have been implicated in various cancers when their components are mutated. Finally, throughout the cell cycle, checkpoints ensure that DNA and epigenetic information are accurately duplicated and preserved. Failure to maintain epigenetic integrity can lead to genomic instability and disease. Checkpoints monitor DNA damage and repair processes, including the preservation of epigenetic marks. Epigenetic marks can also influence the expression of checkpoint genes, ensuring the proper functioning of the cell cycle. We provide a wide product catalogue of research tools for studying the cell cycle, including p53 antibodies, Cyclin D1 antibodies, AKT1 antibodies, AKT1 ELISA Kits, and Cdk4 ELISA Kits. Explore our full cell cycle product range below and discover more, for less. Alternatively, you can explore our Cell Cycle Inhibitors, Apoptosis, and Cell Differentiation product ranges.