DNA synthesis, also known as DNA replication, is a fundamental process in vertebrates that ensures the faithful duplication of genetic material during cell division. This process is highly regulated and involves a complex interplay of proteins and enzymes. DNA replication begins at specific sites on the DNA called origins of replication. In vertebrates, the origin recognition complex (ORC) binds to these origins and recruits other initiation proteins. In humans, the ORC complex consists of ORC1 to ORC6 subunits. Mutations in ORC genes can lead to Meier-Gorlin syndrome, a disorder characterized by growth problems due to impaired DNA replication initiation. DNA replication requires the separation of the two DNA strands to provide a template for the synthesis of new strands. DNA helicases, such as the CMG complex (composed of CDC45, MCM2-7, and GINS), unwind the DNA at the replication fork. MCM proteins are other essential components of the pre-replication complex (pre-RC), which assembles at the origin of replication during G1. This complex marks the site where DNA replication will begin. MCM proteins load onto the DNA and facilitate its unwinding. Mutation of MCM genes can lead to various developmental disorders, including primordial dwarfism, a group of severe forms of dwarfism characterized by profound growth delay due to mutations in MCM5. DNA synthesis initiates with the synthesis of short RNA primers by the enzyme primase. These primers provide a starting point for DNA polymerases. Primase is an essential component of the DNA replication machinery, and defects in primase function can lead to impaired DNA replication and genetic instability. DNA polymerase δ (Pol δ) and DNA polymerase ε (Pol ε) are the primary DNA polymerases involved in synthesizing the leading and lagging strands, respectively. Mutations in the POLD1 gene, which encodes the catalytic subunit of Pol δ, are associated with a rare condition called Polymerase Proofreading-Associated Polyposis (PPAP), characterized by an increased risk of colorectal cancer due to replication errors. DNA polymerases have exonuclease activity that allows them to remove mismatched nucleotides. This proofreading function ensures high fidelity in DNA replication. Mutations in the exonuclease domain of DNA polymerases can lead to a higher mutation rate and an increased risk of cancer. The lagging strand in DNA replication is synthesized in short, discontinuous fragments called Okazaki fragments. DNA ligase then joins these fragments together. Mutations in genes encoding proteins involved in Okazaki fragment maturation can lead to disorders like Fanconi anaemia, characterized by bone marrow failure and cancer susceptibility. Telomeres, the protective ends of chromosomes, require special mechanisms for replication. Telomerase, an enzyme that includes a reverse transcriptase subunit, extends telomeres by adding repetitive DNA sequences using an RNA template. Dysfunctional telomerase can lead to telomere shortening, premature aging, and an increased risk of cancer. DNA replication is tightly regulated through cell cycle checkpoints to ensure accurate duplication of the genome. Checkpoint proteins, such as cyclins and cyclin-dependent kinases (CDKs), monitor the progress of DNA replication, with dysregulation of checkpoint control leading to uncontrolled cell proliferation and cancer. We offer a comprehensive product catalogue of research tools for investigating DNA synthesis, including PCNA antibodies, Topoisomerase II alpha antibodies, Nucleolin antibodies, MCM7 antibodies, and Telomerase reverse transcriptase ELISA Kits. Explore our full DNA synthesis product range below and discover more, for less. Alternatively, you can explore our Topoisomerases, DNA Polymerases, and Translesion Synthesis product ranges.