Zobrazeno 1 - 10
of 31
pro vyhledávání: '"Hirohiko Yajima"'
Autor:
Hirohiko Yajima, David J. Chen, Yanyong Yang, Aroumougame Asaithamby, Steven M. Yannone, Subroto Ghose, Souparno Bhattacharya, Salim Abdisalaam, Ritu Mishra, Fengtao Su, Kalayarasan Srinivasan, Shibani Mukherjee
Publikováno v:
Oncotarget
Faithful and complete genome replication in human cells is essential for preventing the accumulation of cancer-promoting mutations. WRN, the protein defective in Werner syndrome, plays critical roles in preventing replication stress, chromosome insta
Autor:
Hirohiko Yajima, Moito Iijima, Tiara Bunga Mayang Permata, Shigeru Yamada, Nakako Izumi Nakajima, Sumitaka Hasegawa, Atsushi Shibata, Liu Cuihua, Motohiro Yamauchi, Reona Kato, Takaaki Yasuhara, Sangeeta Kakoti
Publikováno v:
DNA Repair. :102872
The cell-killing effect of radiotherapy largely depends on unrepaired DNA double-stranded breaks (DSBs) or lethal chromosome aberrations induced by DSBs. Thus, the capability of DSB repair is critically important for the cancer-cell-killing effect of
Autor:
Ryuichi Okayasu, Lian Xue, Hirohiko Yajima, Yoshitaka Matsumoto, Masahiko Miura, Xing Cui, Cuihua Liu, Yoshiya Furusawa, Ryoichi Hirayama, Dong Yu
Publikováno v:
DNA Repair. 25:72-83
DNA double strand break (DSB) repair pathway choice following ionizing radiation (IR) is currently an appealing research topic, which is still largely unclear. Our recent paper indicated that the complexity of DSBs is a critical factor that enhances
Autor:
Momoko Takahashi, Akira Fujimori, Hirohiko Yajima, Nakako Izumi-Nakajima, Ryuichi Okayasu, Hirokazu Hirakawa
Publikováno v:
International journal of radiation biology. 90(12):1125-1132
Purpose: To obtain human glioblastoma cells A172 expressing stem cell-related protein and comparison of radiosensitivity in these cells with X-rays and carbon beam. Methods: Human monolayer-type A172 glioblastoma cells were maintained in normal mediu
Autor:
Akira Fujimori, Yuki Hirota, Koji Ono, Hirohiko Yajima, Natsuko Kondo, Toshihiko Kuroiwa, Shin-ichiro Masunaga, Shinji Kawabata, Shin-Ichi Miyatake, Hirokazu Hirakawa
Publikováno v:
Journal of Radiation Research
Ionizing radiation is applied as the standard treatment for glioblastoma multiforme (GBM). However, radiotherapy remains merely palliative, not curative, because of the existence of glioma stem cells (GSCs), which are regarded as highly radioresistan
Autor:
Lian Xue, Hirohiko Yajima
The DNA double-strand break (DSB) is the most deleterious of the ionizing radiation- induced DNA damages. Two major repair pathways for DSBs have been well studied, nonhomologous end-joining and homologous recombination. It is known that high linear
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::deaaa2a1c7b8e3b2befdb90c14006e93
https://europepmc.org/articles/PMC6874202/
https://europepmc.org/articles/PMC6874202/
Autor:
Samuel F. Bunting, Nancy Wong, Michael D. Story, André Nussenzweig, Eric J. Gapud, Elsa Callen, Junke Zheng, Hirohiko Yajima, Barry P. Sleckman, Shichuan Zhang, Yu Fen Lin, David J. Chen, Hua Tang Chen, Mengxia Li, Hoang Dinh Huynh, Benjamin P C Chen, Cheng Cheng Zhang, Kyung Jone Lee
Publikováno v:
The Journal of Cell Biology
Phosphorylation of DNA-PKcs is essential for activation of DNA damage repair and for the maintenance of tissue stem cell populations.
The nonhomologous end-joining (NHEJ) pathway is essential for radioresistance and lymphocyte-specific V(D)J (va
The nonhomologous end-joining (NHEJ) pathway is essential for radioresistance and lymphocyte-specific V(D)J (va
Publikováno v:
Molecular and Cellular Biology. 26:7520-7528
Phosphorylation of the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) upon ionizing radiation (IR) is essential for cellular radioresistance and nonhomologous-end-joining-mediated DNA double-strand break repair. In addition to IR induction
Publikováno v:
International Congress Series. 1258:233-237
We have examined the cell-type-dependent sensitivity to UV-induced apoptosis using mouse lymphoma 3SB and human leukemic Jurkat cells and three human carcinoma cell lines (HeLa S3, HeLa SC and MCF-7). Exposure of 3SB and Jurkat cells resulted in larg
Autor:
Hirohiko Yajima, Fumio Suzuki
Publikováno v:
Biochemical and Biophysical Research Communications. 309:520-527
CED-4, a pro-apoptotic factor in Caenorhabditis elegans, activates the cell death protease CED-3. CED-9 directly binds to CED-4 and represses this. However, it has remained unclear whether a mammalian CED-9 homologue, Bcl-XL, inhibits the function of