Robert P Fuchs
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Explore the profile of Robert P Fuchs including associated specialties, affiliations and a list of published articles.
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48
Citations
1359
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Recent Articles
1.
Fujii S, Fuchs R
Int J Mol Sci
. 2024 Aug;
25(15).
PMID: 39125763
In clinics, chemotherapy is often combined with surgery and radiation to increase the chances of curing cancers. In the case of glioblastoma (GBM), patients are treated with a combination of...
2.
Fujii S, Sobol R, Fuchs R
DNA Repair (Amst)
. 2022 Feb;
112:103303.
PMID: 35219626
The cellular response to alkylation damage is complex, involving multiple DNA repair pathways and checkpoint proteins, depending on the DNA lesion, the cell type, and the cellular proliferation state. The...
3.
Fuchs R, Isogawa A, Paulo J, Onizuka K, Takahashi T, Amunugama R, et al.
Elife
. 2021 Jul;
10.
PMID: 34236314
Temozolomide (TMZ), a DNA methylating agent, is the primary chemotherapeutic drug used in glioblastoma treatment. TMZ induces mostly N-alkylation adducts (N7-methylguanine and N3-methyladenine) and some O-methylguanine (OmG) adducts. Current models...
4.
Isogawa A, Fuchs R, Fujii S
STAR Protoc
. 2021 Mar;
2(2):100399.
PMID: 33786464
Translesion synthesis (TLS) is an event to cope with DNA damages. During TLS, the responsible TLS polymerase frequently elicits untargeted mutagenesis as potentially a source of genetic diversity. Identifying such...
5.
Fujii S, Fuchs R
Microbiol Mol Biol Rev
. 2020 Jun;
84(3).
PMID: 32554755
The lesion bypass pathway, translesion synthesis (TLS), exists in essentially all organisms and is considered a pathway for postreplicative gap repair and, at the same time, for lesion tolerance. As...
6.
Isogawa A, Fuchs R, Fujii S
Methods Mol Biol
. 2020 Jan;
2119:183-199.
PMID: 31989525
Identification of the protein complexes associated with defined DNA sequence elements is essential to understand the numerous transactions in which DNA is involved, such as replication, repair, transcription, and chromatin...
7.
Chang S, Naiman K, Thrall E, Kath J, Jergic S, Dixon N, et al.
Proc Natl Acad Sci U S A
. 2019 Dec;
116(51):25591-25601.
PMID: 31796591
DNA lesions stall the replisome and proper resolution of these obstructions is critical for genome stability. Replisomes can directly replicate past a lesion by error-prone translesion synthesis. Alternatively, replisomes can...
8.
Tsuda M, Ogawa S, Ooka M, Kobayashi K, Hirota K, Wakasugi M, et al.
PLoS One
. 2019 Mar;
14(3):e0213383.
PMID: 30840704
Replicative DNA polymerases are frequently stalled at damaged template strands. Stalled replication forks are restored by the DNA damage tolerance (DDT) pathways, error-prone translesion DNA synthesis (TLS) to cope with...
9.
Fujii S, Isogawa A, Fuchs R
Toxicol Res
. 2018 Oct;
34(4):297-302.
PMID: 30370004
Cells are constantly exposed to endogenous and exogenous chemical and physical agents that damage their genome by forming DNA lesions. These lesions interfere with the normal functions of DNA such...
10.
Isogawa A, Ong J, Potapov V, Fuchs R, Fujii S
Cell Rep
. 2018 Aug;
24(5):1290-1300.
PMID: 30067983
In vivo, replication forks proceed beyond replication-blocking lesions by way of downstream repriming, generating daughter strand gaps that are subsequently processed by post-replicative repair pathways such as homologous recombination and...