ner of bulky and non-bulky dna lesions in nucleosome

Nucleotide excision repair of abasic DNA lesions

Accordingly NER of a number of structurally defined DNA lesions was efficiently measured by a host cell reactivation (HCR) principle using reporter constructs harbouring a stretch of synthetic DNA with a lesion in the transcribed strand of a reporter gene (40 44 45) To adjust the HCR approach towards specific measurement of NER of abasic

Molecular mechanisms of DNA damage recognition for

Aug 01 2016Nucleotide excision repair (NER) is a highly versatile system that can deal with an extremely broad spectrum of DNA base lesions including dipyrimidinic photolesions induced by ultraviolet (UV) irradiation and bulky base adducts induced by various chemical carcinogens Depending on where the lesions are generated this crucial repair pathway

Effects of Endogenous DNA Base Lesions on Transcription

Effects of Endogenous DNA Base Lesions on Transcription Elongation by Mammalian RNA Polymerase II II (pol II) is thought to be a trigger for transcription-coupled repair in the pathway of nucleotide excision repair Purified pol II and oligo(dC)-tailed templates containing a single non-bulky DNA lesion on the transcribed strand such as an

Emerging roles for histone modifications in DNA excision

DNA excision repair pathways are responsible for repairing a majority of DNA lesions arising in the genome Excision repair pathways include nucleotide excision repair (NER) and base excision repair (BER) which repair bulky and non-bulky DNA lesions respectively

Organization of DNA damage excision repair and

Sep 01 20191 Introduction DNA damage is a major threat to genomic integrity in living cells [] Different types of DNA damage including small base modifications bulky DNA lesions and strand breaks can interfere with DNA replication and gene transcription causing cytotoxicity or mutagenesis

Mechanism and regulation of DNA damage recognition in

Jan 25 2019Nucleotide excision repair (NER) is a versatile DNA repair pathway which can remove an extremely broad range of base lesions from the genome In mammalian global genomic NER the XPC protein complex initiates the repair reaction by recognizing sites of DNA damage and this depends on detection of disrupted/destabilized base pairs within the DNA duplex

Entrapment of a Histone Tail by a DNA Lesion in a

Nucleotide excision repair (NER) is a conserved multistep reaction that removes a wide range of generally bulky and/or helix-distorting DNA lesions Although the core biochem mechanism of NER is relatively well known how cells detect and repair lesions in diverse chromatin environments is still under intensive research

A Bulky DNA Lesion Derived from a Highly Potent Polycyclic

The impact of a bulky DNA lesion on the structure and dynamics of a nucleosome core particle (NCP) containing a lesion derived from the unusually potent tumorigen dibenzo[a l]pyrene that resists nucleotide excision repair (NER) in free DNA was investigated using 65 ns molecular dynamics simulations Our results reveal that relative to unmodified NCP the lesion stabilizes the nucleosome

Nucleotide excision repair of abasic DNA lesions

Accordingly NER of a number of structurally defined DNA lesions was efficiently measured by a host cell reactivation (HCR) principle using reporter constructs harbouring a stretch of synthetic DNA with a lesion in the transcribed strand of a reporter gene (40 44 45) To adjust the HCR approach towards specific measurement of NER of abasic

DNA: Mao Peng

Excision repair pathways include nucleotide excision repair (NER) and base excision repair (BER) which repair bulky and non-bulky DNA lesions respectively Numerous studies have suggested that chromatin inhibits both NER and BER in vitro and in vivo Growing evidence demonstrates that histone modifications have important roles in regulating

Nucleotide excision repair and chromatin remodeling

Introduction In vivo eukaryotic DNA is packaged with histones and other accessory proteins into chromatin The assembly of nucleosomes the basic unit of chromatin changes the structure of DNA and restricts access of DNA binding factors to their recognition sites [[]] In particular DNA within the nucleosome is highly bent with ≈ 150 bp of DNA wrapped in ≈ loops around a central

DNA Oxidation and Excision Repair Pathways

2 3 Nucleotide Excision Repair NER is famous for the unique repair pathway in humans to remove photolesions produced by UV radiation (sun exposure) that mainly forms cyclobutane pyrimidine dimer (CPD) a non-bulky lesion and pyrimidine-(6 4)-pyrimidone product (6-4PP) a bulky lesion

NER of Bulky and Non

NER of Bulky and Non-Bulky DNA Lesions in Nucleosome Environments Polycyclic aromatic hydrocarbons (PAH) are byproducts of fossil fuel combustion and are present in our air food and water the presence of these genotoxic environmental carcinogens in our environment continues to be a hazard to human health The PAH are

Emerging roles for histone modifications in DNA excision

DNA excision repair pathways are responsible for repairing a majority of DNA lesions arising in the genome Excision repair pathways include nucleotide excision repair (NER) and base excision repair (BER) which repair bulky and non-bulky DNA lesions respectively

Molecular Mechanism of DNA Damage Recognition for Global

Dec 31 2018Nucleotide excision repair (NER) is a versatile DNA repair pathway responsible for removal of ultraviolet light (UV)-induced DNA photolesions from the genome but not by a non-bulky abasic lesion UV-induced formation of pyrimidine dimers in nucleosome core DNA is strongly modulated with a period of 10 3 bases Proc Natl Acad Sci U S A

True Lies: The Double Life of the Nucleotide Excision

Nucleotide excision repair (NER) is a major DNA repair pathway in eukaryotic cells NER removes structurally diverse lesions such as pyrimidine dimers arising upon UV irradiation or bulky chemical adducts arising upon exposure to carcinogens and some chemotherapeutic drugs NER defects lead to three genetic disorders that result in predisposition to cancers accelerated aging neurological

Dna Excision Repairs And Implication On Human Health

DNA lesions arising from the ROS attack can generate both non-bulky (non-helix distorting) and bulky (helix distorting) lesions In human cells BER and NER are the two DNA excision repair pathways responsible for the removal of non-bulky and bulky DNA lesions respectively Both repair pathways share three common

Xeroderma pigmentosum group C sensor: unprecedented

Oct 31 2015Initiation of GG-NER activity by the heterotrimeric XPC complex The XPC subunit is a thermodynamic sensor that recognizes base pair destabilizations of the DNA double helix caused by bulky lesions such as UV light-induced 6-4PPs or carcinogen-DNA adducts (symbolized by the red rectangle in the upper damaged strand) Briefly the GG-NER reaction proceeds by a stepwise

Dna Excision Repairs And Implication On Human Health

In human cells BER and NER are the two DNA excision repair pathways responsible for the removal of non-bulky and bulky DNA lesions respectively Both repair pathways share three common steps which include 1) lesion recognition 2) excision of damaged nucleotide and 3) resynthesis using error-free DNA polymerases (Figure 1)

Dna Excision Repairs And Implication On Human Health

In human cells BER and NER are the two DNA excision repair pathways responsible for the removal of non-bulky and bulky DNA lesions respectively Both repair pathways share three common steps which include 1) lesion recognition 2) excision of damaged nucleotide and 3) resynthesis using error-free DNA polymerases (Figure 1)

Molecular Mechanism of DNA Damage Recognition for Global

Dec 31 2018Nucleotide excision repair (NER) is a versatile DNA repair pathway responsible for removal of ultraviolet light (UV)-induced DNA photolesions from the genome but not by a non-bulky abasic lesion UV-induced formation of pyrimidine dimers in nucleosome core DNA is strongly modulated with a period of 10 3 bases Proc Natl Acad Sci U S A

DNA Oxidation and Excision Repair Pathways

DNA lesions arising from the ROS attack can generate both non-bulky (non-helix distorting) and bulky (helix distorting) lesions In human cells BER and NER are the two DNA excision repair pathways responsible for the removal of non-bulky and bulky DNA lesions respectively Both repair

Differences in the Access of Lesions to the Nucleotide

In nucleosomes the access of DNA lesions to nucleotide excision repair is hindered by histone proteins However evidence that the nature of the DNA lesions may play a role in facilitating access is emerging but these phenomena are not well-understood We have used molecular dynamics simulations to elucidate the structural dynamic and energetic properties of the R and S 5′-8-cyclo-2

Nucleotide Excision Repair and Impact of Site

The nonbulky 5′ 8-cyclopurine DNA lesions (cP) and the bulky benzo[a]pyrene diol epoxide-derived stereoisomeric cis- and trans-N 2-guanine adducts (BPDE-dG) are good substrates of the human nucleotide excision repair (NER) mechanism These DNA lesions were embedded at the In or Out rotational settings near the dyad axis in nucleosome core particles reconstituted either with native

Detection of bulky DNA lesions: DDB2 at the interface of

Bulky DNA damage is corrected by the nucleotide excision repair (NER) pathway Although the core biochemical mechanism of NER is understood details including lesion recognition and repair in the context of chromatin remain to be elucidated As more data become available the complexity of lesion recognition in chromatin is becoming clear