Telomeres are essential structures located at the ends of linear eukaryotic chromosomes, where they play a key role in maintaining genome stability, protecting against DNA degradation, and regulating cellular aging. Telomeres consist of repetitive DNA sequences composed of the nucleotide sequence TTAGGG in vertebrates, which are repeated thousands of times. These sequences form a cap structure at the end of the chromosome. Within the telomeric repeats, the G-rich sequence can fold into secondary structures called G-quadruplexes. These structures stabilize the telomeres and play a role in regulating telomere length. Telomeres are coated with a specialized protein complex called shelterin. Shelterin consists of several proteins, including TRF1 (Telomeric Repeat-binding Factor 1), TRF2 (Telomeric Repeat-binding Factor 2), POT1 (Protection of Telomeres 1), TIN2 (TRF1-Interacting Nuclear Factor 2), TPP1 (POT1-Interacting Protein 1), and Rap1 (Repressor/Activator Protein 1). Shelterin proteins help protect telomeres and regulate their length. Telomerase is the enzyme responsible for adding telomeric repeats to the ends of chromosomes. It consists of an RNA template and a reverse transcriptase enzyme. Telomerase is essential for maintaining telomere length and is highly active in stem cells, germ cells, and certain cancer cells. One of the primary functions of telomeres is to act as protective caps for chromosomes. They prevent the natural ends of linear DNA from being recognized as damaged DNA, which could lead to the activation of DNA repair mechanisms or fusion of chromosome ends.Telomeres also protect against exonucleolytic degradation of the chromosome ends. Without telomeres, the DNA replication machinery would remove nucleotides from the ends of linear chromosomes, gradually eroding genetic information. Telomeres serve as a buffer zone for the loss of genetic material during DNA replication. In each cell division, a small portion of telomeric DNA is typically lost due to the end-replication problem in which a small segment of the lagging strand near the end of the chromosome cannot be replicated. Telomerase counteracts this loss by adding new telomeric repeats, thereby maintaining telomere length. As cells divide, telomeres gradually shorten. When telomeres become critically short, cells can enter a state termed replicative senescence, in which they cease dividing but maintain metabolic activity. This limits the number of divisions a cell can undergo, serving as a cellular clock that contributes to aging and tissue homeostasis. Telomere shortening also acts as a tumour suppression mechanism, limiting the number of cell divisions and preventing cells with damaged DNA from continuously dividing. Inactivation of telomere maintenance mechanisms is a hallmark of many cancer cells, allowing them to evade senescence and continue dividing indefinitely. Stem cells, which can self-renew and differentiate into various cell types, often have active telomerase and longer telomeres. This enables them to continuously replenish tissues throughout an organism's life. Telomere shortening is associated with aging and age-related diseases. As telomeres shorten over time, cells in various tissues lose their proliferative capacity, contributing to reduced tissue function and the impaired regeneration seen with aging. We offer a wide product catalogue of research tools for studying telomeres, including Telomerase reverse transcriptase antibodies, TRF2 antibodies, Mre11 antibodies, TRF1 antibodies, and Telomerase reverse transcriptase ELISA Kits. Explore our full telomeres product range below and discover more, for less.