Cyclins are a family of key regulatory proteins that play critical roles in controlling the various processes that constitute the eukaryotic cell cycle, ensuring that each phase proceeds in a coordinated manner. Epigenetic mechanisms, involving modifications to DNA and histones, can influence the expression and activity of cyclins, thereby impacting cell cycle progression and cellular proliferation. Cyclin D1 is a critical regulator of the G1 phase of the cell cycle, binding to cyclin-dependent kinases (CDKs) to promote the transition from G1 to S phase. Epigenetic mechanisms, particularly histone modifications, can influence the expression of cyclin D1. For example, histone acetylation at the cyclin D1 promoter region can enhance its transcription. In some cancers, aberrant histone acetylation patterns at the cyclin D1 locus can lead to its overexpression, contributing to uncontrolled cell proliferation. Cyclin E also plays a crucial role in the G1 phase of the cell cycle, facilitating the transition to S phase by activating CDK2. Epigenetic mechanisms can also modulate cyclin E expression. For example, DNA methylation of the cyclin E promoter region can silence the gene, leading to reduced cyclin E levels. Dysregulation of DNA methylation at the cyclin E locus is also observed in various cancers, promoting aberrant cell cycle progression. Cyclin A is essential for both S phase and G2 phase progression by binding to CDK2 and CDK1. Histone acetylation and methylation can also influence cyclin A expression, with the promoter region of the cyclin A gene undergoing epigenetic modifications that affect its transcription. Acetylation of histones at the cyclin A promoter region promotes the binding of transcription factors, such as E2F, which then activate cyclin A gene transcription. This can occur in cancer cells through the overactivation of HATs or the inhibition of histone deacetylases (HDACs), which normally remove acetyl groups from histones. Cyclin B1 is a key regulator of the G2 to M phase transition, where it complexes with CDK1 to promote mitosis. Epigenetic mechanisms can also regulate cyclin B1 expression. For example, histone deacetylase inhibitors (HDACIs) can alter histone acetylation patterns at the cyclin B1 promoter, leading to increased transcription and premature entry into mitosis, with this epigenetic modulation having implications in HDACI cancer therapy. The miR-17-92 cluster targets multiple cyclins, including cyclin D1 and cyclin E. Epigenetic mechanisms can control the expression of such miRNAs that target cyclins. Dysregulation of miRNA expression through epigenetic changes can therefore lead to aberrant cyclin expression in cancer and other diseases. Epigenetic drugs, such as DNA demethylating agents and HDACIs, have been explored to modulate cyclin expression in cancer therapy. These drugs can alter histone modifications and DNA methylation patterns at cyclin gene promoters, thereby influencing their expression and cell cycle regulation. Thus, cyclins are critical regulators of the cell cycle, and their expression and activity are impacted by epigenetic mechanisms. Epigenetic modifications, including DNA methylation and histone modifications, can modulate cyclin expression, leading to aberrant cell cycle progression in diseases like cancer. We provide a comprehensive product range of research reagents for studying cyclins, including Cyclin D1 antibodies, Cyclin B1 antibodies, Cyclin E1 antibodies, Cyclin D2 antibodies, and Cyclin D1 ELISA Kits. Explore our full cyclin product range below and discover more, for less. Alternatively, you can explore our Cyclin D Family, Cyclin B Family, and Other Cyclins product ranges.