نتایج جستجو برای: aprataxin aptx

تعداد نتایج: 112  

Journal: :Molecular and cellular biology 2007
Natasha Iles Stuart Rulten Sherif F El-Khamisy Keith W Caldecott

Aprataxin and polynucleotide kinase (PNK) are DNA end processing factors that are recruited into the DNA single- and double-strand break repair machinery through phosphorylation-specific interactions with XRCC1 and XRCC4, respectively. These interactions are mediated through a divergent class of forkhead-associated (FHA) domain that binds to peptide sequences in XRCC1 and XRCC4 that are phospho...

Journal: :Journal of Biological Chemistry 2021

DNA ligase I (LIG1) completes the base excision repair (BER) pathway at last nick-sealing step after polymerase (pol) ? gap-filling synthesis. However, mechanism by which LIG1 fidelity mediates faithful substrate–product channeling and ligation of intermediates final steps BER remains unclear. We previously reported that pol 8-oxo-2'-deoxyribonucleoside 5'-triphosphate insertion confounds LIG1,...

Journal: :The FEBS journal 2013
Kimberly M Maize Carston R Wagner Barry C Finzel

The histidine triad proteins (HITs) constitute a large and ubiquitous superfamily of nucleotide hydrolases. The human histidine triad nucleotide-binding proteins (hHints) are a distinct class of HITs noted for their acyl-AMP hydrolase and phosphoramidase activity. The first high-resolution crystal structures of hHint2 with and without bound AMP are described. The differences between hHint2 and ...

2016
Xia Wang Qing Li Hua Jin Hua Zou Wei Xia Nan Dai Xiao-Yan Dai Dong Wang Cheng-Xiong Xu Yi Qing

Previous studies have shown that some dysregulated miRNAs are involved in radioresistance of tumor cells. Here, we identified significantly decreased miR-424 expression in radioresistant cervical cancer cells and specimens from cervical cancer patients with radioresistance compared to their radiosensitive parental cells and specimens from radiosensitive patients, respectively. Ectopic expressio...

2015
Ramona Jühlen Jan Idkowiak Angela E. Taylor Barbara Kind Wiebke Arlt Angela Huebner Katrin Koehler

Triple A syndrome is caused by mutations in AAAS encoding the protein ALADIN. We investigated the role of ALADIN in the human adrenocortical cell line NCI-H295R1 by either over-expression or down-regulation of ALADIN. Our findings indicate that AAAS knock-down induces a down-regulation of genes coding for type II microsomal cytochrome P450 hydroxylases CYP17A1 and CYP21A2 and their electron don...

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