Zobrazeno 1 - 9
of 9
pro vyhledávání: '"H Kenny Kuo"'
Publikováno v:
PLoS Genetics, Vol 7, Iss 10, p e1002315 (2011)
DNA repair mechanisms in mitotically proliferating cells avoid generating crossovers, which can contribute to genome instability. Most models for the production of crossovers involve an intermediate with one or more four-stranded Holliday junctions (
Externí odkaz:
https://doaj.org/article/49c1c69e401e4f4fa86188b7c2c0eac2
5-Azacytidine (aza-C) and its derivatives are cytidine analogues used for leukemia chemotherapy. The primary effect of aza-C is the prohibition of cytosine methylation, which results in covalent methyltransferase-DNA (MTase-DNA) adducts at cytosine m
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1fff534f6e3e726afbcef56e81d0fb36
https://doi.org/10.1158/0008-5472.c.6496527
https://doi.org/10.1158/0008-5472.c.6496527
Supplementary Figures 1-5 from 5-Azacytidine–Induced Methyltransferase-DNA Adducts Block DNA Replication In vivo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::57cc24d8ec9beaedd71342f49c98f0cb
https://doi.org/10.1158/0008-5472.22370760.v1
https://doi.org/10.1158/0008-5472.22370760.v1
Publikováno v:
Chemistry Education Research and Practice. 19:1199-1215
Noncovalent interactions determine the three-dimensional structure of macromolecules and the binding interactions between molecules. Students struggle to understand noncovalent interactions and how they relate to structure–function relationships. A
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::de90bc790456078ae3534c237b5fd9c7
https://doi.org/10.1039/c8rp00075a
https://doi.org/10.1039/c8rp00075a
Publikováno v:
DNA Repair. 28:48-59
Pathways for tolerating and repairing DNA-protein crosslinks (DPCs) are poorly defined. We used transposon mutagenesis and candidate gene approaches to identify DPC-hypersensitive Escherichia coli mutants. DPCs were induced by azacytidine (aza-C) tre
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d08b7936272bc261b8f1312d09c385ea
https://doi.org/10.1016/j.dnarep.2015.01.016
https://doi.org/10.1016/j.dnarep.2015.01.016
Publikováno v:
Molecular Microbiology. 78:686-700
Summary Anticancer drug 5-azacytidine (aza-C) induces DNA–protein cross-links (DPCs) between cytosine methyltransferase and DNA as the drug inhibits methylation. We found that mutants defective in the tmRNA translational quality control system are
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::aefeaf1d4963ed6141e7b21bc959b051
https://doi.org/10.1111/j.1365-2958.2010.07355.x
https://doi.org/10.1111/j.1365-2958.2010.07355.x
Several helicases function during repair of double-strand breaks and handling of blocked or stalled replication forks to promote pathways that prevent formation of crossovers. Among these are the Bloom syndrome helicase BLM and the Fanconi anemia gro
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a3c090dae9507693496ef1e1e2859368
https://europepmc.org/articles/PMC4224181/
https://europepmc.org/articles/PMC4224181/
Publikováno v:
PLoS Genetics, Vol 7, Iss 10, p e1002315 (2011)
PLoS Genetics
PLoS Genetics
DNA repair mechanisms in mitotically proliferating cells avoid generating crossovers, which can contribute to genome instability. Most models for the production of crossovers involve an intermediate with one or more four-stranded Holliday junctions (
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::02d9196b1d2f663c79fcab1c4507141a
Publikováno v:
Cancer research. 67(17)
5-Azacytidine (aza-C) and its derivatives are cytidine analogues used for leukemia chemotherapy. The primary effect of aza-C is the prohibition of cytosine methylation, which results in covalent methyltransferase-DNA (MTase-DNA) adducts at cytosine m
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f2b0bad8d0326073722d0641e6a8943d
https://pubmed.ncbi.nlm.nih.gov/17804739
https://pubmed.ncbi.nlm.nih.gov/17804739