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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 ...
Microhomology-mediated end joining (MMEJ), also known as alternative nonhomologous end-joining (Alt-NHEJ) is one of the pathways for repairing double-strand breaks in DNA. As reviewed by McVey and Lee, [1] the foremost distinguishing property of MMEJ is the use of microhomologous sequences during the alignment of broken ends before joining, thereby resulting in deletions flanking the original ...
Susumu Tonegawa (利根川 進, Tonegawa Susumu, born September 5, 1939) is a Japanese scientist who was the sole recipient of the Nobel Prize for Physiology or Medicine in 1987 for his discovery of V(D)J recombination, the genetic mechanism which produces antibody diversity. [1]
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 ...
The Fanconi anemia complementation group (FANC) currently includes FANCA, FANCB, FANCC, FANCD1 (also called BRCA2), FANCD2, FANCE, FANCF, FANCG, and FANCL. Fanconi anemia is a genetically heterogeneous recessive disorder characterized by cytogenetic instability, hypersensitivity to DNA crosslinking agents, increased chromosomal breakage, and defective DNA repair.
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]
Getting HVR1 and HVR2 DNA tests can help determine one's haplogroup. In the revised Cambridge Reference Sequence of the human mitogenome, the most variable sites of HVR1 are numbered 16024-16383 (this subsequence is called HVR-I), and the most variable sites of HVR2 are numbered 57-372 ( i.e., HVR-II) and 438-574 ( i.e., HVR-III).