Cyclins are a group of proteins that play critical roles in cell cycle regulation, ensuring the orderly progression of cells through the various stages of the cell cycle. They function as complexes with cyclin-dependent kinases (CDKs) to control the timing and progression of key events during the cell cycle. The binding of cyclins to specific CDKs activates these protein kinases by inducing a conformational change, allowing the CDKs to phosphorylate target proteins involved in cell cycle progression. This regulation of the transition between different phases of the cell cycle by activating CDKs occurs at specific checkpoints that ensure that the cell has completed critical processes before proceeding to the next cell cycle phase. Different cyclin-CDK complexes have specific substrate preferences, enabling them to phosphorylate distinct target proteins involved in different aspects of cell cycle regulation. As implied by their name, the expression of different cyclins varies through different phases of the cell cycle and is tightly regulated in normal cells. Cyclins can be classified in the following manner by such cell-cycle-dependent expression: 1) G1 phase cyclins. These cyclins (e.g., cyclin D) are involved in the early phase of the cell cycle, known as the G1 phase. They promote the transition from G1 to S phase by activating CDKs (in the case of cyclin D, Cdk4 and Cdk6), which then initiate DNA replication; 2) S phase cyclins. Cyclin E is an example of an S-phase cyclin. It is responsible for activating Cdk2 that facilitates the progression of DNA replication during the S phase of the cell cycle; 3) G2 phase cyclins: Cyclin A is a G2-phase cyclin that activates Cdc2, which helps prepare the cell for mitosis by ensuring proper DNA replication and repair; 4) M phase cyclins. Cyclin B is an M-phase cyclin that drives the cell into mitosis by activating CDK1, leading to chromosome condensation, spindle formation, and cell division. Deregulation of cyclin function is frequently observed in cancer and can contribute to uncontrolled cell growth. Increased production of specific cyclins for example can lead to excessive activation of CDKs, resulting in uncontrolled cell cycle progression and proliferation. Thus, overexpression of cyclin D1 is frequently observed in breast, lung, and oesophageal cancers. Alterations in cyclin-CDK interactions can also disrupt the normal regulatory mechanisms. For example, cyclin E-CDK2 complexes are commonly found to be overactive in various cancers, promoting uncontrolled cell cycle entry and DNA replication. Loss of negative regulators of cyclin-CDK complexes such as CDKIs p16INK4a and p21CIP1 are frequently found in different cancers. These CDKIs therefore act as tumour suppressors by inhibiting cyclin-CDK activity and their loss or inactivation in cancer can lead to uncontrolled cell cycle progression. Alterations in cyclin-CDK complex formation can disrupt the normal cell cycle checkpoints, allowing cells with damaged DNA to proceed through the cycle resulting in the accumulation of genetic abnormalities. Genomic alterations such as mutations or chromosomal rearrangements can also directly affect the regulated expression or function of cyclins, CDKs, or their regulators. These alterations can disrupt the delicate balance of cell cycle control mechanisms and contribute to tumour development. We offer a comprehensive product range of research reagents for investigating cyclins, including Cyclin D1 antibodies, Cyclin B1 antibodies, Cyclin E1 antibodies, Cyclin D2 antibodies, and Cyclin D1 ELISA Kits. Explore our full cyclins product range below and discover more, for less. Alternatively, you can explore our Cyclin D Family, Cyclin B Family, and Cyclin E Family product ranges.