CHEK2CHEK2 (Checkpoint kinase 2) is a tumor suppressor gene that encodes the protein CHK2, a serine-threonine kinase. CHK2 is involved in DNA repair, cell cycle arrest or apoptosis in response to DNA damage. Mutations to the CHEK2 gene have been linked to a wide range of cancers. The CHEK2 gene is located on the long (q) arm of chromosome 22 at position 12.1. Its location on chromosome 22 stretches from base pair 28,687,742 to base pair 28,741,904. The CHEK2 protein encoded by the CHEK2 gene is a serine threonine kinase.
Ozone depletionOzone depletion consists of two related events observed since the late 1970s: a steady lowering of about four percent in the total amount of ozone in Earth's atmosphere, and a much larger springtime decrease in stratospheric ozone (the ozone layer) around Earth's polar regions. The latter phenomenon is referred to as the ozone hole. There are also springtime polar tropospheric ozone depletion events in addition to these stratospheric events.
Structural integrity and failureStructural integrity and failure is an aspect of engineering that deals with the ability of a structure to support a designed structural load (weight, force, etc.) without breaking and includes the study of past structural failures in order to prevent failures in future designs. Structural integrity is the ability of an item—either a structural component or a structure consisting of many components—to hold together under a load, including its own weight, without breaking or deforming excessively.
Fusion geneA fusion gene is a hybrid gene formed from two previously independent genes. It can occur as a result of translocation, interstitial deletion, or chromosomal inversion. Fusion genes have been found to be prevalent in all main types of human neoplasia. The identification of these fusion genes play a prominent role in being a diagnostic and prognostic marker. The first fusion gene was described in cancer cells in the early 1980s.
Cellular senescenceCellular senescence is a phenomenon characterized by the cessation of cell division. In their experiments during the early 1960s, Leonard Hayflick and Paul Moorhead found that normal human fetal fibroblasts in culture reach a maximum of approximately 50 cell population doublings before becoming senescent. This process is known as "replicative senescence", or the Hayflick limit. Hayflick's discovery of mortal cells paved the path for the discovery and understanding of cellular aging molecular pathways.
