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DNA-PK forms a complex that leads to its autophosphorylation, resulting in activation of Artemis. The coding end hairpins are opened by the activity of Artemis. [17] If they are opened at the center, a blunt DNA end will result; however in many cases, the opening is "off-center" and results in extra bases remaining on one strand (an overhang).
Exonucleases remove these unpaired nucleotides and the gaps are filled by DNA synthesis and repair machinery. [1] [3] Exonucleases may also cause shortening of this junction, however this process is still poorly understood. [4] Junctional diversity is liable to cause frame-shift mutations and thus production of non-functional proteins ...
Eukaryotic Ku is a heterodimer consisting of Ku70 and Ku80, and forms a complex with DNA-PKcs, which is present in mammals but absent in yeast. Ku is a basket-shaped molecule that slides onto the DNA end and translocates inward. Ku may function as a docking site for other NHEJ proteins, and is known to interact with the DNA ligase IV complex ...
Random rearrangements and recombinations of the gene segments at DNA level to form one kappa or lambda light chain occurs in an orderly fashion. As a result, "a functional variable region gene of a light chain contains two coding segments that are separated by a non-coding DNA sequence in unrearranged germ-line DNA" (Barbara et al., 2007).
Somatic recombination, as opposed to the genetic recombination that occurs in meiosis, is an alteration of the DNA of a somatic cell that is inherited by its daughter cells. The term is usually reserved for large-scale alterations of DNA such as chromosomal translocations and deletions and not applied to point mutations .
In biology, a gene cassette is a type of mobile genetic element that contains a gene and a recombination site. Each cassette usually contains a single gene and tends to be very small; on the order of 500–1,000 base pairs.
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Recombinational repair of DNA double-strand damage - some key steps. ATM (ATM) is a protein kinase that is recruited and activated by DNA double-strand breaks. DNA double-strand damages also activate the Fanconi anemia core complex (FANCA/B/C/E/F/G/L/M). [7] The FA core complex monoubiquitinates the downstream targets FANCD2 and FANCI. [8]