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This results in an abasic site, from which both ends are trimmed by poly polymerase and polynucleotide kinase to facilitate repair synthesis.In mammals, the socalled shortpatch repair is the dominant mode for the remainder of the reaction.The second mode of activation occurs when RNA polymerase II is blocked by a damage during transcription.This stalled polymerase must be displaced to make the damage accessible for repair, which requires at least two transcriptioncoupled repair proteins: CSA and CSB. After the recognition step, both pathways are identical.NUCLEOTIDE EXCISION REPAIR AA GLOBAL GENOME NER TRANSCRIPTION COUPLED REPAIR DNA DAMAGE DAMAGE RECOGNITION PROCESSING OF DAMAGED DNA REPAIR ADHESION of ENDS XPC TFIIH XPA XPG ERCC IXPF <a href="http://www.targetmol.com/compound/Palbociclib"></a> replication FACTORS A.These agents cause singlestrand breaks or small alteration of bases.The mechanism of repair through BER is shown in the figure and explained in the text.This type of damage can be caused by UV light, cisplatin, and other chemotherapeutic drugs.Disruption of the DNA helix interferes with base pairing and obstructs transcription and normal replication.The mechanism of repair through NER is shown in the figure and explained in the text.This figure shows a simplification of both models for DSB repair.During HR, the damaged DNA as a template to repair the DNA accurately.NHEJ repairs the DNA by simply joining the DNA ends in a way that is not necessarily error free, since no template is used for the newly synthesized DNA at the damaged sites. A number of proteins involved in each pathway are indicated and discussed in the text.Finally, XPG cleaves the damaged strand V of the damage, and the XPFERCC complex cleaves the same strand V of the lesion, generating a or base oligonucleotide fragment containing the injury.Phosphorylation already occurs within min after induction of DNA damage.The exact reason of this phenomenon is not yet clarified, although a role in DNA damage repair and chromosomal stability is evident.The two main differences between these pathways are the requirement for extensive DNA homology on the sister chromatid in HR and the accuracy of repair.After this, the missing information on the broken strand is copied in, and the damage is repaired without loss of genetic information.In NHEJ, on the contrary, there is no need for homology.NHEJ is less accurate and might give rise to deletions.Although both DSB repair pathways are operational in mammals, their relative contribution might differ depending on the stage of the cell cycle or the cell type.For HR to occur, there is a need for a sister chromatid, which is not   produced until the S phase.For this reason, HR can only take place in dividing cells that are in the S or G phase.Cells in G and G or terminally differentiated cells will have to rely on NHEJ.A number of the previously mentioned DNA DSB repair proteins and gHAX relocate into bright nuclear foci after induction of DNA damage. It should be emphasized that many issues remain unsolved yet.View publication stats View publication stats The user has requested enhancement of the downloaded file.These receptors have been intensely studied, not only to understand the mechanisms underlying their oncogenic potential, but also to exploit them as therapeutic targets.

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