Bleomycin-induced over-replication involves sustained inhibition of mitotic entry through the ATM/ATR pathway

Nakayama, Yuji; Igarashi, Asae; Kikuchi, Ikue; Obata, Yuichi; Fukumoto, Yasunori; Yamaguchi, Naoto

doi:10.1016/j.yexcr.2009.06.007

Cited by 45 publications

(33 citation statements)

References 58 publications

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“…HeLa S3-TR cells were subsequently transfected with pcDNA4-TO-neo/v-Src and selected with G418. The neomycin-resistant pcDNA4-TO-neo vector was described previously (56). The expression of v-Src was induced with 1 g/ml doxycycline.…”

Section: Methodsmentioning

confidence: 99%

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Src Family Kinases Promote Silencing of ATR-Chk1 Signaling in Termination of DNA Damage Checkpoint

Fukumoto

Morii

Miura

et al. 2014

Journal of Biological Chemistry

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Background: Once DNA repair is completed, the DNA damage checkpoint is terminated, and the cell cycle is resumed. Results: Src inhibition induced a delay in G 2 checkpoint recovery and persistent ATR-Chk1 activation. Conclusion: Src inhibits ATR signaling to promote recovery from G 2 checkpoint arrest. Significance: Src sends a termination signal between the completion of DNA repair and the initiation of checkpoint termination.

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Section: Methodsmentioning

confidence: 99%

“…Flow Cytometry-Flow cytometric analyses were performed as described previously (56,61). For analysis of Chk1-Ser 317 phosphorylation, HeLa S3 cells were transfected 24 h after seeding.…”

Section: Methodsmentioning

confidence: 99%

Src Family Kinases Promote Silencing of ATR-Chk1 Signaling in Termination of DNA Damage Checkpoint

Fukumoto

Morii

Miura

et al. 2014

Journal of Biological Chemistry

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“…[27][28][29] We decided to use the I-PpoI endonuclease system [30][31][32] that generates double-stranded breaks in rRNA genes, which is very useful for studying nucleolar reorganization and DDR in the nucleolus. Using this system, we sought to examine the complex nucleolar reorganization in response to directed DSB introduction.…”

Section: Introductionmentioning

confidence: 99%

Nucleolar Reorganization Upon Site-Specific Double-Strand Break Induction

Franek

Kovaříková

Bártová

et al. 2016

J Histochem Cytochem.

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SummaryDNA damage response (DDR) in ribosomal genes and mechanisms of DNA repair in embryonic stem cells (ESCs) are less explored nuclear events. DDR in ESCs should be unique due to their high proliferation rate, expression of pluripotency factors, and specific chromatin signature. Given short population doubling time and fast progress through G1 phase, ESCs require a sustained production of rRNA, which leads to the formation of large and prominent nucleoli. Although transcription of rRNA in the nucleolus is relatively well understood, little is known about DDR in this nuclear compartment. Here, we directed formation of double-strand breaks in rRNA genes with I-PpoI endonuclease, and we studied nucleolar morphology, DDR, and chromatin modifications. We observed a pronounced formation of I-PpoI-induced nucleolar caps, positive on BRCA1, NBS1, MDC1, γH2AX, and UBF1 proteins. We showed interaction of nucleolar protein TCOF1 with HDAC1 and TCOF1 with CARM1 after DNA injury. Moreover, H3R17me2a modification mediated by CARM1 was found in I-PpoI-induced nucleolar caps. Finally, we report that heterochromatin protein 1 is not involved in DNA repair of nucleolar caps. (J Histochem Cytochem 64:669-686, 2016)

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“…Flow Cytometry-For cell cycle analysis, cells detached by trypsinization were fixed in 1.5% paraformaldehyde for 1 h and permeabilized with 70% ethanol for at least 1 h at Ϫ30°C (11)(12)(13). For DNA staining, cells were treated with 200 g/ml RNase A and 50 g/ml propidium iodide at 37°C for 30 min.…”

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confidence: 99%

“…RNA Interference-Knockdown of ATM was performed by shRNA for silencing ATM (GCACCAGTCCAGTATTG-GCTT and GGATTTGCGTATTACTCAG) (11). The nucleotides for shRNA were annealed and subcloned into the SpeI site of the pEBmulti-Neo vector (Wako Pure Chemical Industries).…”

mentioning

confidence: 99%

Activation of the Prereplication Complex Is Blocked by Mimosine through Reactive Oxygen Species-activated Ataxia Telangiectasia Mutated (ATM) Protein without DNA Damage

Kubota

Fukumoto

Ishibashi

et al. 2014

Journal of Biological Chemistry

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Background: Mimosine is a cell synchronization reagent used for arresting cells in late G 1 and S phases. Results: Replication fork assembly is reversibly blocked by ATM activation through mimosine-generated reactive oxygen species. Conclusion: Mimosine induces cell cycle arrest strictly at the G 1 -S phase boundary, which prevents replication fork stallinginduced DNA damage. Significance: These findings provide a novel mechanism of the mimosine-induced G 1 checkpoint.

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Bleomycin-induced over-replication involves sustained inhibition of mitotic entry through the ATM/ATR pathway

Cited by 45 publications

References 58 publications

Src Family Kinases Promote Silencing of ATR-Chk1 Signaling in Termination of DNA Damage Checkpoint

Src Family Kinases Promote Silencing of ATR-Chk1 Signaling in Termination of DNA Damage Checkpoint

Nucleolar Reorganization Upon Site-Specific Double-Strand Break Induction

Activation of the Prereplication Complex Is Blocked by Mimosine through Reactive Oxygen Species-activated Ataxia Telangiectasia Mutated (ATM) Protein without DNA Damage

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