Nuclear Function

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Life, Death, and Everything in Between
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Chromosomal Change

DNA is organized into chromosomes, in part so that an entire genome can physically fit inside the nucleus, but also so that the cell can differentiate, divide, and endure environmental stresses while protecting its valuable genetic information. DNA structure and organization enables the cell to divide DNA evenly between mother and daughter cells, avoiding aneuploidy, unnecessary gene duplication or deletion. Chromosomal instability is a hallmark of many cancers, and is seen as either a cause or a symptom of the unchecked proliferation exhibited by tumor cells.

DNA Damage

The cell protects the genome from damage by tightly regulating chromosome duplication, movement and separation during the cell cycle. However, a certain amount of damage, either due to DNA replication errors, age-shortened telomeres, or environmental causes, is unavoidable. To repair DNA damage, or to minimize its tumor-causing potential, cells rely on a multicomponent damage detection and repair system. Studying the mechanisms by which cells control changes in DNA structure and respond to DNA damage help elucidate the factors that cause aging, cellular degeneration, cancer, and death.

Telomerase Maintenance

Located at the ends of eukaryotic chromosomes, telomeres consist of thousands of DNA repeats. Telomeres protect chromosome ends, limiting fusion, rearrangement and translocation. In somatic cells, telomere length is progressively shortened with each cell division, because DNA polymerase cannot synthesize the 5’ end of the lagging strand. Telomerase is a ribonucleoprotein that synthesizes telomeric repeats using its RNA component as a template. The expression of telomerase and the stabilization of telomere length have been linked to tumor suppression and extension of cell life.

Cell Cycle

Cell cycle, or the process of cell growth and duplication, is the regulatory point for proliferation and development of multicellular organisms. Nuclear signaling controls most checkpoints of the cell cycle, and is in turn regulated by chromatin structure. Merck offers cell cycle assay kits and antibodies for the entire cell cycle research workflow.

DNA Repair

High content screening kit for multiparametric analysis of drug induced human cytotoxicity.
Merck’s hepatotoxicity assay for human HepG2 cells is a high content screening kit for multiparametric analysis of druginduced human cytotoxicity. In addition to visualizing the response to DNA damage by monitoring activated p53, the kit allows measurement of ten additional parameters: cell loss, cell cycle arrest, DNA degradation/apoptosis, nuclear size, oxidative stress, stress pathway activation, mitochondrial membrane potential, mitochondrial mass, mitotic arrest, cytoskeletal
Response to DNA damage is initiated by recognition of double-strand breaks by ATM kinase and the Nbs1/Mre11/ Rad50 complex. Phospho-H2A.X binds MDC1 to help recruit other damage response proteins. ATM phosphorylates BRCA1, a key effector of checkpoint/repair signaling. Other proteins localize the signaling to the damage site, such as 53BP1, which recruits p53. p53 causes the cell cycle to pause, providing repair machinery the opportunity to fix the damage. If the damage is too severe, p53 signals the cell to undergo apoptosis.