Results 51 to 60 of about 48,126 (189)

DNA Repair Gene Polymorphisms May Be Associated with Prognosis of Upper Urinary Tract Transitional Cell Carcinoma

open access: yesNeoplasia: An International Journal for Oncology Research, 2008
Upper urinary tract transitional cell carcinoma (UUT-TCC) is quite an uncommon disease, and its prognosis differs among individuals irrespective of tumor stage. DNA repair gene polymorphisms are reported to result in the modulation of the repair capacity
Miwa Sasaki   +8 more
doaj   +1 more source

Relationships among the nucleotide content of human genome sequence, gene structure, and gene expression features (PhD synopsis) [PDF]

open access: yesarXiv, 2010
The Dissertation is focused on the studies of associations between functional elements in human genome and their nucleotide structure. The asymmetry in nucleotide content (skew, bias) was chosen as the main feature for nucleotide structure. A significant difference in nucleotide content asymmetry was found for human exons vs. introns.
arxiv  

Phosphorylated HBO1 at UV irradiated sites is essential for nucleotide excision repair

open access: yesNature Communications, 2017
Repair of cyclobutane pyrimidine dimers requires access to DNA by the nucleotide excision repair machinery. Here the authors show that HBO1 facilitates accumulation of SNF2H and ACF1 to make chromatin more accessible after ultraviolet damage.
Hiroyuki Niida   +14 more
doaj   +1 more source

DNA ADP-Ribosylation Stalls Replication and Is Reversed by RecF-Mediated Homologous Recombination and Nucleotide Excision Repair

open access: yesCell Reports, 2020
Summary: ADP-ribosylation of proteins is crucial for fundamental cellular processes. Despite increasing examples of DNA ADP-ribosylation, the impact of this modification on DNA metabolism and cell physiology is unknown. Here, we show that the DarTG toxin-
Emeline Lawarée   +5 more
doaj  

C. elegans survival assays to discern global and transcription-coupled nucleotide excision repair

open access: yesSTAR Protocols, 2021
Summary: Global genome nucleotide excision repair (GG-NER) and transcription-coupled nucleotide excision repair (TC-NER) protect cells against a variety of helix-distorting DNA lesions. In C. elegans, GG-NER primarily acts in proliferative germ cells and
Melanie van der Woude, Hannes Lans
doaj  

ERCC1 and XRCC1 as biomarkers for lung and head and neck cancer

open access: yesPharmacogenomics and Personalized Medicine, 2011
Alec Vaezi1,2, Chelsea H Feldman2, Laura J Niedernhofer2,31Department of Otolaryngology and Head and Neck Surgery, University of Pittsburgh School of Medicine, 2University of Pittsburgh Cancer Institute, 3Department of Microbiology and Molecular Genetics,
Vaezi A, Feldman CH, Niedernhofer LJ
doaj  

Interplay of replication timing, DNA repair, and translesion synthesis in UV mutagenesis in yeast

open access: yesNucleus
Replication timing during S-phase impacts mutation rates in yeast and human cancers; however, the exact mechanism involved remains unclear. Here, we analyze the impact of replication timing on UV mutagenesis in Saccharomyces cerevisiae.
Allysa Sewell, John J. Wyrick
doaj   +1 more source

Chromatin structure and DNA damage repair

open access: yesEpigenetics & Chromatin, 2008
The integrity of the genome is continuously challenged by both endogenous and exogenous DNA damaging agents. These damaging agents can induce a wide variety of lesions in the DNA, such as double strand breaks, single strand breaks, oxidative lesions and ...
Dinant Christoffel   +2 more
doaj   +1 more source

Structural basis of TFIIH activation for nucleotide excision repair

open access: yesNature Communications, 2019
The NER machinery contains the multisubunit transcription factor IIH (TFIIH) that opens the DNA repair bubble, scans for the lesion, and coordinates excision of the damaged site.
Goran Kokic   +5 more
doaj   +1 more source

Interpreting the dependence of mutation rates on age and time [PDF]

open access: yesarXiv, 2015
Mutations can arise from the chance misincorporation of nucleotides during DNA replication or from DNA lesions that are not repaired correctly. We introduce a model that relates the source of mutations to their accumulation with cell divisions, providing a framework for understanding how mutation rates depend on sex, age and absolute time. We show that
arxiv  

Home - About - Disclaimer - Privacy