User profiles for Junya Tomida
Junya TomidaAssistant Professor Verified email at uncc.edu Cited by 1749 |
[HTML][HTML] Mechanism of suppression of chromosomal instability by DNA polymerase POLQ
Although a defect in the DNA polymerase POLQ leads to ionizing radiation sensitivity in
mammalian cells, the relevant enzymatic pathway has not been identified. Here we define the …
mammalian cells, the relevant enzymatic pathway has not been identified. Here we define the …
FANCI phosphorylation functions as a molecular switch to turn on the Fanconi anemia pathway
In response to DNA damage or replication fork stress, the Fanconi anemia pathway is
activated, leading to monoubiquitination of FANCD2 and FANCI and their colocalization in foci. …
activated, leading to monoubiquitination of FANCD2 and FANCI and their colocalization in foci. …
[HTML][HTML] Human DNA helicase HELQ participates in DNA interstrand crosslink tolerance with ATR and RAD51 paralogs
Mammalian HELQ is a 3′–5′ DNA helicase with strand displacement activity. Here we
show that HELQ participates in a pathway of resistance to DNA interstrand crosslinks (ICLs). …
show that HELQ participates in a pathway of resistance to DNA interstrand crosslinks (ICLs). …
FAM 35A associates with REV 7 and modulates DNA damage responses of normal and BRCA 1‐defective cells
To exploit vulnerabilities of tumors, it is urgent to identify associated defects in genome
maintenance. One unsolved problem is the mechanism of regulation of DNA double‐strand break …
maintenance. One unsolved problem is the mechanism of regulation of DNA double‐strand break …
[PDF][PDF] FANCD2 binds CtIP and regulates DNA-end resection during DNA interstrand crosslink repair
The Fanconi anemia (FA) pathway is critically involved in the maintenance of hematopoietic
stem cells and the suppression of carcinogenesis. A key FA protein, FANCD2, is …
stem cells and the suppression of carcinogenesis. A key FA protein, FANCD2, is …
Identification of a novel REV1‐interacting motif necessary for DNA polymerase κ function
…, T Hanafusa, K Kamei, I Song, J Tomida… - Genes to …, 2009 - Wiley Online Library
When a replicative DNA polymerase (Pol) is stalled by damaged DNA, a “polymerase switch”
recruits specialized translesion synthesis (TLS) DNA polymerase(s) to sites of damage. …
recruits specialized translesion synthesis (TLS) DNA polymerase(s) to sites of damage. …
ATR–ATRIP kinase complex triggers activation of the Fanconi anemia DNA repair pathway
ATR kinase activates the S-phase checkpoint when replication forks stall at sites of DNA
damage. This event also causes phosphorylation of the Fanconi anemia (FA) protein FANCI, …
damage. This event also causes phosphorylation of the Fanconi anemia (FA) protein FANCI, …
FANCD 2 protects genome stability by recruiting RNA processing enzymes to resolve R‐loops during mild replication stress
R‐loops, which consist of DNA : RNA hybrids and displaced single‐strand DNA , are a major
threat to genome stability. We have previously reported that a key Fanconi anemia protein, …
threat to genome stability. We have previously reported that a key Fanconi anemia protein, …
REV7 is essential for DNA damage tolerance via two REV3L binding sites in mammalian DNA polymerase ζ
DNA polymerase zeta (pol ζ) is exceptionally important for controlling mutagenesis and genetic
instability. REV3L comprises the catalytic subunit, while REV7 (MAD2L2) is considered …
instability. REV3L comprises the catalytic subunit, while REV7 (MAD2L2) is considered …
A novel interplay between the Fanconi anemia core complex and ATR-ATRIP kinase during DNA cross-link repair
When DNA replication is stalled at sites of DNA damage, a cascade of responses is activated
in the cell to halt cell cycle progression and promote DNA repair. A pathway initiated by the …
in the cell to halt cell cycle progression and promote DNA repair. A pathway initiated by the …