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Microhomology-mediated End Joining
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, 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 break. MMEJ is frequently associated with chromosome abnormalities such as deletions, translocations, inversions and other complex rearrangements. There are multiple pathways for repairing double strand breaks, mainly non-homologous end joining (NHEJ), homologous recombination (HR), and MMEJ. NHEJ directly joins both ends of the double strand break and is relatively accurate, although small (usually less than a few nucleotides) insertions or deletions sometimes occur. HR is highly accurate and uses the sister chromatid as a template for accurate repair of the DSB. MMEJ is distinguished from thes ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Double-strand Break
DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. A weakened capacity for DNA repair is a risk factor for the development of cancer. DNA is constantly modified in cells, by internal metabolic by-products, and by external ionizing radiation, ultraviolet light, and medicines, resulting in spontaneous DNA damage involving tens of thousands of individual molecular lesions per cell per day. DNA modifications can also be programmed. Molecular lesions can cause structural damage to the DNA molecule, and can alter or eliminate the cell's ability for transcription and gene expression. Other lesions may induce potentially harmful mutations in the cell's genome, which affect the survival of its daughter cells following mitosis. Consequently, DNA repair as part of the DNA damage response (DDR) is constantly active. When normal repair processes fail, including apoptosis, irreparable DNA damage may occur, ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
LIG3
DNA ligase 3 also DNA ligase III, is an enzyme that, in humans, is encoded by the ''LIG3'' gene. ''LIG3'' encodes ATP-dependent DNA ligases that seal interruptions in the phosphodiester backbone of duplex DNA. There are three families of ATP-dependent DNA ligases in eukaryotes. These enzymes utilize the same three step reaction mechanism; (i) formation of a covalent enzyme-adenylate intermediate; (ii) transfer of the adenylate group to the 5' phosphate terminus of a DNA nick; (iii) phosphodiester bond formation. Unlike '' LIG1'' and '' LIG4'' family members that are found in almost all eukaryotes, ''LIG3'' family members are less widely distributed. ''LIG3'' encodes several distinct DNA ligase species by alternative translation initiation and alternative splicing mechanisms that are described below. Structure, DNA binding and catalytic activities Eukaryotic ATP-dependent DNA ligases have related catalytic region that contains three domains, a DNA binding domain, an aden ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Crustacean
Crustaceans (from Latin meaning: "those with shells" or "crusted ones") are invertebrate animals that constitute one group of arthropods that are traditionally a part of the subphylum Crustacea (), a large, diverse group of mainly aquatic arthropods including decapods (shrimps, prawns, crabs, lobsters and crayfish), seed shrimp, branchiopods, fish lice, krill, remipedes, isopods, barnacles, copepods, opossum shrimps, amphipods and mantis shrimp. The crustacean group can be treated as a subphylum under the clade Mandibulata. It is now well accepted that the hexapods (insects and entognathans) emerged deep in the Crustacean group, with the completed pan-group referred to as Pancrustacea. The three classes Cephalocarida, Branchiopoda and Remipedia are more closely related to the hexapods than they are to any of the other crustaceans ( oligostracans and multicrustaceans). The 67,000 described species range in size from '' Stygotantulus stocki'' at , to the Japanese ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Penaeus Monodon
''Penaeus monodon'', commonly known as the giant tiger prawn, Asian tiger shrimp, black tiger shrimp, and other names, is a marine crustacean that is widely reared for food. Taxonomy ''Penaeus monodon'' was species description, first described by Johan Christian Fabricius in 1798. That name was overlooked until 1949, when Lipke Holthuis clarified to which species it referred. Holthuis also showed that ''P. monodon'' had to be the type species of the genus ''Penaeus''. Description Females can reach about long, but are typically long and weigh ; males are slightly smaller at long and weighing . The carapace and abdomen are transversely banded with alternative red and white. The antennae are grayish brown. Brown pereiopods and pleopods are present with fringing setae in red. Distribution Its natural distribution is the Indo-Pacific, ranging from the eastern coast of Africa and the Arabian Peninsula, as far as Southeast Asia, the Pacific Ocean, and northern Australia. It ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
XRCC1
DNA repair protein XRCC1, also known as X-ray repair cross-complementing protein 1, is a protein that in humans is encoded by the ''XRCC1'' gene. XRCC1 is involved in DNA repair, where it complexes with DNA ligase III. Function XRCC1 is involved in the efficient repair of DNA single-strand breaks formed by exposure to ionizing radiation and alkylating agents. This protein interacts with DNA ligase III, polymerase beta and poly (ADP-ribose) polymerase to participate in the base excision repair pathway. It may play a role in DNA processing during meiogenesis, i.e. during the induction of meiosis and recombination in germ cells. A rare microsatellite polymorphism in this gene is associated with cancer in patients of varying radiosensitivity. The XRCC1 protein does not have enzymatic activity, but acts as a scaffolding protein that interacts with multiple repair enzymes. The scaffolding allows these repair enzymes to then carry out their enzymatic steps in repairing DNA. XRC ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
PARP1
Poly DP-ribosepolymerase 1 (PARP-1) also known as NAD+ ADP-ribosyltransferase 1 or poly DP-ribosesynthase 1 is an enzyme that in humans is encoded by the ''PARP1'' gene. It is the most abundant of the PARP family of enzymes, accounting for 90% of the NAD+ used by the family. PARP1 is mostly present in cell nucleus, but cytosolic fraction of this protein was also reported. Function PARP1 works: * By using NAD+ to synthesize poly ADP ribose (PAR) and transferring PAR moieties to proteins ( ADP-ribosylation). * In conjunction with BRCA, which acts on double strands; members of the PARP family act on single strands; or, when BRCA fails, PARP takes over those jobs as well (in a DNA repair context). PARP1 is involved in: * Differentiation, proliferation, and tumor transformation * Normal or abnormal recovery from DNA damage * May be the site of mutation in Fanconi anemia * Induction of inflammation. * The pathophysiology of type I diabetes. PARP1 is activated by: * Helico ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Nibrin
Nibrin, also known as NBN or NBS1, is a protein which in humans is encoded by the ''NBN'' gene. Function Nibrin is a protein associated with the repair of double strand breaks (DSBs) which pose serious damage to a genome. It is a 754 amino acid protein identified as a member of the NBS1/hMre11/RAD50(N/M/R, more commonly referred to as MRN) double strand DNA break repair complex. This complex recognizes DNA damage and rapidly relocates to DSB sites and forms nuclear foci. It also has a role in regulation of N/M/R (MRN) protein complex activity which includes end-processing of both physiological and mutagenic DNA double strand breaks (DSBs). Cellular response to DSBs Cellular response is performed by damage sensors, effectors of lesion repair and signal transduction. The central role is carried out by ataxia telangiectasia mutated (ATM) by activating the DSB signaling cascade, phosphorylating downstream substrates such as histone H2AX and NBS1. NBS1 relocates to DSB sit ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
MRE11A
Double-strand break repair protein MRE11 (Meiotic recombination 11) is an enzyme that in humans is encoded by the ''MRE11'' gene. The gene has been designated ''MRE11A'' to distinguish it from the pseudogene ''MRE11B'' that is nowadays named ''MRE11P1''. Function This gene encodes a nuclear protein involved in homologous recombination, telomere length maintenance, and DNA double-strand break repair. By itself, the protein has 3' to 5' exonuclease activity and endonuclease activity. The protein forms a complex with the RAD50 homolog; this complex is required for nonhomologous joining of DNA ends and possesses increased single-stranded DNA endonuclease and 3' to 5' exonuclease activities. In conjunction with a DNA ligase, this protein promotes the joining of noncomplementary ends in vitro using short homologies near the ends of the DNA fragments. This gene has a pseudogene on chromosome 3. Alternative splicing of this gene results in two transcript variants encoding different is ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
FEN1
Flap endonuclease 1 is an enzyme that in humans is encoded by the ''FEN1'' gene. Function The protein encoded by this gene removes 5' overhanging "flaps" (or short sections of single stranded DNA that "hang off" because their nucleotide bases are prevented from binding to their complementary base pair—despite any base pairing downstream) in DNA repair and processes the 5' ends of Okazaki fragments in lagging strand DNA synthesis. Direct physical interaction between this protein and AP endonuclease 1 during long-patch base excision repair provides coordinated loading of the proteins onto the substrate, thus passing the substrate from one enzyme to another. The protein is a member of the XPG/RAD2 endonuclease family and is one of ten proteins essential for cell-free DNA replication. DNA secondary structure can inhibit flap processing at certain trinucleotide repeats in a length-dependent manner by concealing the 5' end of the flap that is necessary for both binding and cleavag ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Non-homologous End Joining
Non-homologous end joining (NHEJ) is a pathway that repairs double-strand breaks in DNA. It is called "non-homologous" because the break ends are directly ligated without the need for a homologous template, in contrast to homology directed repair (HDR), which requires a homologous sequence to guide repair. NHEJ is active in both non-dividing and proliferating cells, while HDR is not readily accessible in non-dividing cells. The term "non-homologous end joining" was coined in 1996 by Moore and Haber. NHEJ is typically guided by short homologous DNA sequences called microhomologies. These microhomologies are often present in single-stranded overhangs on the ends of double-strand breaks. When the overhangs are perfectly compatible, NHEJ usually repairs the break accurately. Imprecise repair leading to loss of nucleotides can also occur, but is much more common when the overhangs are not compatible. Inappropriate NHEJ can lead to translocations and telomere fusion, hallmarks of t ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
Mutagen
In genetics, a mutagen is a physical or chemical agent that permanently changes genetic material, usually DNA, in an organism and thus increases the frequency of mutations above the natural background level. As many mutations can cause cancer in animals, such mutagens can therefore be carcinogens, although not all necessarily are. All mutagens have characteristic mutational signatures with some chemicals becoming mutagenic through cellular processes. The process of DNA becoming modified is called mutagenesis. Not all mutations are caused by mutagens: so-called "spontaneous mutations" occur due to spontaneous hydrolysis, errors in DNA replication, repair and recombination. Discovery The first mutagens to be identified were carcinogens, substances that were shown to be linked to cancer. Tumors were described more than 2,000 years before the discovery of chromosomes and DNA; in 500 B.C., the Greek physician Hippocrates named tumors resembling a crab ''karkinos'' (from which the ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
S-phase
S phase (Synthesis phase) is the phase of the cell cycle in which DNA is DNA replication, replicated, occurring between G1 phase, G1 phase and G2 phase, G2 phase. Since accurate duplication of the genome is critical to successful cell division, the processes that occur during S-phase are tightly regulated and widely conserved. Regulation Entry into S-phase is controlled by the G1 restriction point (R), which commits cells to the remainder of the cell-cycle if there is adequate nutrients and growth signaling. This transition is essentially irreversible; after passing the restriction point, the cell will progress through S-phase even if environmental conditions become unfavorable. Accordingly, entry into S-phase is controlled by molecular pathways that facilitate a rapid, unidirectional shift in cell state. In yeast, for instance, cell growth induces accumulation of Cln3 cyclin, which complexes with the Cyclin-dependent kinase, cyclin dependent kinase CDK2. The Cln3-CDK2 complex ... [...More Info...] [...Related Items...] OR: [Wikipedia] [Google] [Baidu] |
