Cell cycle inhibitors play crucial regulatory roles in the regulation of cell division and proliferation. These inhibitors act at various cell cycle checkpoints to regulate and control cell division and are of two main types: cyclin-dependent kinase (CDK) inhibitors (CDKIs) and checkpoint inhibitors. CDKs are a family of protein kinase enzymes that act to regulate the progression of the cell cycle by phosphorylating specific target proteins. CDK inhibitors directly bind to CDKs and prevent their activity, leading to cell cycle arrest. CDKIs can be further divided into two classes: 1) INK4 family, this family includes p16INK4a, p15INK4b, p18INK4c, and p19INK4d. These inhibitors specifically inhibit CDK4 and CDK6 kinases, which are responsible for promoting the G1-to-S phase cell cycle transition. By binding to CDK4/6, INK4 family members prevent the phosphorylation of the retinoblastoma tumour suppressor protein (Rb) and keep it in an active, growth-suppressive state; 2) Cip/Kip family: this family consists of p21Cip1, p27Kip1, and p57Kip2. They can inhibit multiple CDKs, including those involved in the G1/S and G2/M transitions. These inhibitors act by binding to CDK/cyclin complexes, preventing their activation and subsequent cell cycle progression. In addition to inhibitors of CDKs a variety of cell cycle checkpoint inhibitors have been identified. Cell cycle checkpoints are critical control stages that ensure the integrity of the genome during cell division. Checkpoint inhibitors target proteins involved in the checkpoint pathways thereby regulating cell cycle progression. They include: 1) Checkpoint kinase 1 (Chk1) and checkpoint kinase 2 (Chk2) which are involved in the DNA damage checkpoint response. They phosphorylate and activate downstream effectors to arrest the cell cycle, allowing time for DNA repair; 2) Wee1 kinase, an inhibitor of CDK1, which is crucial for the G2/M transition. Wee1 kinase phosphorylates CDK1, keeping it inactive. Inhibiting Wee1 can therefore override the G2 checkpoint, leading to premature mitosis and cell death; 3) Aurora kinases. These are protein kinases involved in various stages of mitosis and are therefore potential targets for cancer therapy in the same manner as microtubule-binding drugs such as vinblastine, vincristine and paclitaxel. Inhibiting these kinases disrupts mitotic progression and can therefore induce cell cycle arrest. Cell cycle inhibitors are actively investigated in cancer research and drug development. By interfering with cell division and proliferation, these inhibitors aim to limit the growth of cancer cells and potentially induce their death. They are often used in combination with other therapies, such as chemotherapy or targeted therapies, to enhance treatment efficacy and overcome resistance mechanisms. We offer a wide product range of research reagents for studying cell cycle inhibitors, including p53 antibodies, p27 KIP 1 antibodies, MDM2 antibodies, p53 ELISA Kits, and mTOR ELISA Kits. Explore our full cell cycle inhibitors product range below and discover more, for less. Alternatively, you can explore our p53 Pathway, Cip & Kip, and INK4 product ranges.