Base excision repair

In genetics and biochemistry, (BER) repair, during the cell cycle, base excision repair is the cellular mechanisms that damage the DNA. This small genome, is responsible mainly for the removal of non-stop violation basic lesion. helix-distorting lesions bulky related to the repair of nucleotide excision repair pathway. The BER, eliminating the base damaged can result in loss of DNA replication in, or cause mutations by mating erroneous is particularly important. BER is initiated by DNA glycosylase, which recognizes the base inappropriate or damage specific to form the AP sites, delete. Is then cleaved by the AP endonuclease it. it is possible that one strand breaks short handle (nucleotides new 2-10 are synthesized here) by the length patch BER (one nucleotide is substituted) or patches.

Base excision repair

Base excision repair (BER) is the main pathway of DNA repair to correct the lesion and the underlying result from depurinatiation / depyrimidination oxidative damage, alkylation, and deamination. Patch short and long – manner two common 2, BER, and promotes the repair of DNA that is damaged. In shortpatch BER pathway results in the repair of single nucleotide tube. In addition, the long patch BER pathway, I will generate a repair tube of at least two nucleotides. And is initiated by either DNA glycosylase numerous recognized the BER, which catalyzes the removal of bases damaged. Complete path BER can be achieved by coordinated action of enzymes additional at least three. These enzymes perform ligation and downstream cross-section gap filling. I have led to advances in our understanding of the BER of the mammalian high conservation degree between mammalian and E. coli BER. This review provides an overview of the one-way mammalian BER.

Base excision repair pathway, have evolved to protect cells from the damaging effects of DNA damage endogenous induced by intracellular metabolites other changing the primary structure of DNA hydrolysis and reactive oxygen species. However, the base excision repair, it is opposed, an alkylating agent and a powerful ionizing radiation lesions are similar to those induced by endogenous factors are also important.

DNA repair, is a multi-step process aggregate multi several enzymes, maintaining the cellular genome intact for genetic insult. Single-strand breaks, such as oxidative base damage, alkylation, and losses under deamination site: one of these processes, acting on the base excision repair is the base excision repair, dealing with disease most common in the DNA enzymes individual has been identified. In recent years, we have seen great progress in the understanding of the interaction of many to make a flexible system and base excision repair function and its structure. This review describes the current knowledge of the biochemistry and structural biology of the various stages of the interaction of the recovery process and other cellular processes base excision repair, and base excision repair pathway, a few subpathways common.

Base excision repair (BER) is a path that is evolutionarily conserved it can be regarded as a repair mechanism “Horse” of the cells. More specifically, as well as most forms of spontaneous hydrolysis decay product of DNA, BER, fixes modification of sugar phosphate backbone or base and alkylating agent daily. Repair response follow the steps of key enzymes and five aims to remove the recovery and initial DNA damage of genetic material back to its original state. Sealing the participants of the DNA of the last remaining and filling to replace the nucleotide cut, cut difference phosphodiester backbone, connecting participants and reduce repair synthesis and / or cleaning base site conditions result in the removal of the base damaged or incorrect I to allow. Repair These steps are performed by a set of enzymes including DNA glycosylase, apyrimidinic / apurinic endonuclease, phosphatase, phosphodiesterase, kinase, polymerase and ligase. Mutation rate of decrease of cell survival, increased, and defects in components of the BER results in DNA-damaging agent hypersensitivity. Further, plays an important role alkylating agents such as clinical anti-cancer agent which time the relevant nucleoside analogues, and to determine the cellular response to ionizing radiation. Molecular data for the contribution of treatment-resistant time is described here and BER.

This is an important machine that mutation to prevent a recurrence of base excision repair and fix the DNA damage. Base excision repair process can be achieved by sequential enzymatic activity specific. It is identified by DNA glycosylase / AP lyase, which bases the damaged violate the β-N-glycoside bond in order to create a (AP) site DNA abasic first and repaired. Removal of the base, according to the early events of revenue or repair through a (2-10 nucleotides) repair pathway short patch or long patch (1 nucleotide). This has been recognized by the AP endonuclease have adopted for the DNA polymerase and DNA damage nickname fill the gap of the DNA site. The new DNA strand, ultimately, base excision repair is complete when it is closed by DNA ligase. R & D Systems, Inc. provides a qualitative base excision repair products, including endonuclease DNA glycosidase, and polymerase.