Nucleotide excision repair is more complex, in eukaryotes to prokaryotes, the basic principle is similar. There are nine main protein involved in NER in mammalian cells. Disadvantages of proteins particular result is associated with a disease diseases Protein Name. XPG XPA, XPB, XPC, XPD, XPE, XPF and is rooted is a protein CSB xeroderma pigmentosum and CSA and is associated with Cockayne syndrome. In addition, protein ERCC1, RPA, RAD23A, also RAD23B,, and in others that are involved in nucleotide excision repair. Here are the complete list of proteins involved in NER. Nucleotide excision repair of eukaryotic organisms can be divided into 2 subpathways: link global genome transcription and NER NER (GG-NER) and (TC-NER). Two groups of proteins are involved in recognizing DNA damage per subpathway. Damage recognition after collection for both subpathways, the stage of ligation and repair of dual incision.
Global genome NER repair damage to the non-transcribed DNA strand and transcription of the gene of active and inactive of the entire genome. – This process is not dependent on transcription. And allow the spiral failure and scan XPC-Rad23B complex genome continuously DNA damage binding of XPC-Rad23B complex with (DDB), using some “damage observation” protein, DDB1 this time The (XPE is responsible violates confirmed) DDB2, it is possible to recognize a particular type of damage by UV light and. In addition, XPA acts as a damage recognition is insufficient defined yet. To identify the site of damaged mobilize damaged DNA to confirm the presence of DNA damage then, DNA was subjected to excise duty damage lesions surrounding the repair patch then repair proteins following fill.
At any time, the majority of the genome in vivo, but not in the course of the transfer, but the performance difference between the transcriptional activation region and transcriptionally channel of the genome. For many types of disabilities, and repair of NER of transcribed strand of transcriptionally active genes more rapidly than DNA repair transcription silent and non-transcribed strand. GGR and TC-NER is different only in the initial stage of detection of DNA damage. The TC-NER, main differences GG-NER and TC-NER is that it requires the DDB strain or recognition XPC protein in mammalian cells. Stalls of RNA polymerase in lesions of the DNA when you start the TC-NER instead: RNA polymerase blocked, which acts as a fault signal recognition, to replace the need for recognition properties of the distortion of the DDB complex with XPC-RAD23B. Not damage DNA, CSB and CSA CS protein associates the type of XPC-Rad23B specific. Repair other mechanisms are possible, efficient and very accurate.
Is an important enzyme (TFIIH) is involved in the double resection transcription factor II H. The XPG and TFIIH, (XPG to stabilize the TFIIH) is recruited to sites of DNA damage first. They help to generate the junction between single-stranded DNA and double-stranded around the transcription bubble and relaxing the DNA – the XPD each TFIIH subunit XPB, to function as ATP ATPase and helicase You. In addition to the stabilization of TFIIH, while it decreases the damage to the DNA of the side “of the three having endonuclease activity, XPG is hetero XPF-ERCC1 protein 5 ‘end at 25 to 30 nucleotides difference circuit Double incision results in the removal of. single-stranded DNA cut dimer. Replication protein is a protein of the last two related to the repair of NER complex and XPA main (RPA). Before you bind TFIIH as engaged in the verification of DNA damage, these two proteins are present they. They also, it is possible to protect the single-stranded DNA. Verification, after the side of 5 ‘side incision is made in three before, DNA repair is’ a. It helps to reduce the single-stranded DNA that is exposed during the repair process.
(Also called Neil Dingwall syndrome or Weber-Cockayne syndrome,) fault growth, development of the failure of the nervous system, Cockayne syndrome, rare always an abnormal sensitivity, and is characterized by premature aging sunlight (photosensitive) It is a congenital disorder of chromosome recessive. I heard an abnormal loss and other common and (pigmentary retinopathy) eye, but the problem of some or all of the internal organs can be considered. In addition, I related to the group of diseases called white matter atrophy. Basic conditions, a defect in DNA repair mechanisms. It is named after the English doctor Frederick Parkes Weber and physician Edward Alfred Cockayne of English. Neil Dingwall syndrome cause of Cockayne syndrome Neill.Mutations of Catherine A. and Dingwall of ERCC8 gene ERCC6 named Mary M. is attached. The transcription-coupled repair mechanism of DNA specific, proteins made by these genes are involved in the repair of damaged DNA in the active gene. If it is changed or ERCC6 ERCC8 gene, DNA damage is not adjusted. This damage because the accumulation, may lead to cell death or cell malfunction. Mutation of a gene mutation will make 70% of the cases ERCC6.