Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
Yoshimichi Nakatsu Last modified date:2020.06.30

Associate Professor / Bioregulation / Department of Basic Medicine / Faculty of Medical Sciences


Papers
1. Yusuke Matsuno, Yuko Atsumi, Md Alauddin, Md Masud Rana, Haruka Fujimori, Mai Hyodo, Atsuhiro Shimizu, Tomoki Ikuta, Hiroko Tani, Hidetaka Torigoe, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Michio Komai, Hitoshi Shirakawa, Ken ichi Yoshioka, Resveratrol and its Related Polyphenols Contribute to the Maintenance of Genome Stability, Scientific reports, 10.1038/s41598-020-62292-5, 10, 1, 2020.12, Genomic destabilisation is associated with the induction of mutations, including those in cancer-driver genes, and subsequent clonal evolution of cells with abrogated defence systems. Such mutations are not induced when genome stability is maintained; however, the mechanisms involved in genome stability maintenance remain elusive. Here, resveratrol (and related polyphenols) is shown to enhance genome stability in mouse embryonic fibroblasts, ultimately protecting the cells against the induction of mutations in the ARF/p53 pathway. Replication stress-associated DNA double-strand breaks (DSBs) that accumulated with genomic destabilisation were effectively reduced by resveratrol treatment. In addition, resveratrol transiently stabilised the expression of histone H2AX, which is involved in DSB repair. Similar effects on the maintenance of genome stability were observed for related polyphenols. Accordingly, we propose that polyphenol consumption can contribute to the suppression of cancers that develop with genomic instability, as well as lifespan extension..
2. Haruka Fujimori, Mai Hyodo, Yusuke Matsuno, Atsuhiro Shimizu, Yusuke Minakawa, Yuko Atsumi, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Yasufumi Murakami, Ken ichi Yoshioka, Mismatch repair dependence of replication stress-associated DSB recognition and repair, Heliyon, 10.1016/j.heliyon.2019.e03057, 5, 12, 2019.12, Most cancers develop with one of two types of genomic instability, namely, chromosomal instability (CIN) or microsatellite instability (MSI). Both are induced by replication stress-associated DNA double-strand breaks (DSBs). The type of genomic instability that arises is dependent on the choice of DNA repair pathway. Specifically, MSI is induced via a PolQ-dependent repair pathway called microhomology-mediated end joining (MMEJ) in a mismatch repair (MMR)-deficient background. However, it is unclear how the MMR status determines the choice of DSB repair pathway. Here, we show that replication stress-associated DSBs initially targeted by the homologous recombination (HR) system were subsequently hijacked by PolQ-dependent MMEJ in MMR-deficient cells, but persisted as HR intermediates in MMR-proficient cells. PolQ interacting with MMR factors was effectively loaded onto damaged chromatin in an MMR-deficient background, in which merged MRE11/γH2AX foci also effectively formed. Thus, the choice of DNA repair pathway according to the MMR status determines whether CIN or MSI is induced. Biological sciences; Cell biology; Genetics; DNA repair; Molecular biology; Genomic instability; DNA repair; Mismatch repair; Microhomology-mediated end joining; DNA polymerase theta.
3. Yusuke Matsuno, Yuko Atsumi, Atsuhiro Shimizu, Kotoe Katayama, Haruka Fujimori, Mai Hyodo, Yusuke Minakawa, Yoshimichi Nakatsu, Syuzo Kaneko, Ryuji Hamamoto, Teppei Shimamura, Satoru Miyano, Teruhisa Tsuzuki, Fumio Hanaoka, Ken ichi Yoshioka, Replication stress triggers microsatellite destabilization and hypermutation leading to clonal expansion in vitro, Nature communications, 10.1038/s41467-019-11760-2, 10, 1, 2019.12, Mismatch repair (MMR)-deficient cancers are characterized by microsatellite instability (MSI) and hypermutation. However, it remains unclear how MSI and hypermutation arise and contribute to cancer development. Here, we show that MSI and hypermutation are triggered by replication stress in an MMR-deficient background, enabling clonal expansion of cells harboring ARF/p53-module mutations and cells that are resistant to the anti-cancer drug camptothecin. While replication stress-associated DNA double-strand breaks (DSBs) caused chromosomal instability (CIN) in an MMR-proficient background, they induced MSI with concomitant suppression of CIN via a PARP-mediated repair pathway in an MMR-deficient background. This was associated with the induction of mutations, including cancer-driver mutations in the ARF/p53 module, via chromosomal deletions and base substitutions. Immortalization of MMR-deficient mouse embryonic fibroblasts (MEFs) in association with ARF/p53-module mutations was ~60-fold more efficient than that of wild-type MEFs. Thus, replication stress-triggered MSI and hypermutation efficiently lead to clonal expansion of cells with abrogated defense systems..
4. Genki Hayashida, Seijiro Shioi, Kyoko Hidaka, Ryosuke Fujikane, Masumi Hidaka, Toshiki Tsurimoto, Teruhisa Tsuzuki, Shinya Oda, Yoshimichi Nakatsu, Differential genomic destabilisation in human cells with pathogenic MSH2 mutations introduced by genome editing, Experimental Cell Research, 10.1016/j.yexcr.2019.02.020, 377, 1-2, 24-35, 2019.04, Repeat destabilisation is variously associated with human disease. In neoplastic diseases, microsatellite instability (MSI) has been regarded as simply reflecting DNA mismatch repair (MMR) deficiency. However, several discrepancies have been pointed out. Firstly, the MSI + phenotype is not uniform in human neoplasms. Established classification utilises the frequency of microsatellite changes, i.e. MSI-H (high) and -L (low), the former regarded as an authentic MMR-defective phenotype. In addition, we have observed the qualitatively distinct modes of MSI, i.e. Type A and Type B. One discrepancy we previously pointed out is that tumours occurring in MMR gene knockout mice exhibited not drastic microsatellite changes typical in MSI-H tumours (i.e. Type B mode) but minor and more subtle alterations (i.e. Type A mode). In the present study, MSH2 mutations reported in Lynch syndrome (LS) kindred have been introduced into HeLa cells using the CRISPR/Cas9 system. The established mutant clones clearly exhibited MMR-defective phenotypes with alkylating agent-tolerance and elevated mutation frequencies. Nevertheless, microsatellites were not markedly destabilised as in MSI-H tumours occurring in LS patients, and all the observed alterations were uniformly Type A, which confirms the results in mice. Our findings suggest added complexities to the molecular mechanisms underlying repeat destabilisation in human genome..
5. Matsubara Y, Matsumoto T, Yoshiya K,Yoshida A,Ikeda S, Furuyama T, Nakatsu Y, Tsuzuki T,Nomura M, Maehara Y., Budding Uninhibited by Benzimidazole-1 Insufficiency Prevents Acute Renal Failure in Severe Sepsis by Maintaining Anticoagulant Functions of Vascular Endothelial Cells., SHOCK, 10.1097/SHK.0000000000001147, 51, 3, 364-371, 2019.03.
6. Tetsuya Suzuki, Yuri Yanai, Natsuki Nishigaki, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Hiroyuki Kamiya, Effects of mismatches distant from the target position on gene correction with a 5′-tailed duplex, Journal of Bioscience and Bioengineering, 10.1016/j.jbiosc.2017.12.017, 125, 5, 619-623, 2018.05, The introduction of a 5′-tailed duplex (5′-TD) fragment into cells corrects a base-substitution mutation in a target DNA. We previously reported that the gene correction efficiency was improved when a frameshift type of second mismatch was present ∼330 bases distant from the target position, between the target DNA and the 5′-TD fragment. In this study, the effects of the second mismatches on the gene correction were further examined. Base–base mismatches 332 bases distant from the target position slightly enhanced gene correction, but less efficiently than the previously studied frameshift mismatches. The gene correction efficiency was also increased when the distance between the target position and the second frameshift mismatch was changed to ∼270 bases. These results suggested that the introduction of an appropriate second frameshift mismatch into the 5′-TD fragment improves the gene correction efficiency..
7. Issei Egashira, Fumi Takahashi-Yanaga, Risa Nishida, masaki arioka, Kazunobu Igawa, Katsuhiko Tomooka, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Yusaku Nakabeppu, Takanari Kitazono, Toshiyuki Sasaguri, Celecoxib and 2,5-dimethylcelecoxib inhibit intestinal cancer growth by suppressing the Wnt/β-catenin signaling pathway, Cancer Science, 10.1111/cas.13106, 108, 1, 108-115, 2017.01, We previously reported that celecoxib, a selective COX-2 inhibitor, strongly inhibited human colon cancer cell proliferation by suppressing the Wnt/β-catenin signaling pathway. 2,5-Dimethylcelecoxib (DM-celecoxib), a celecoxib analog that does not inhibit COX-2, has also been reported to have an antitumor effect. In the present study, we elucidated whether DM-celecoxib inhibits intestinal cancer growth, and its underlying mechanism of action. First, we compared the effect of DM-celecoxib with that of celecoxib on the human colon cancer cell lines HCT-116 and DLD-1. 2,5-Dimethylcelecoxib suppressed cell proliferation and inhibited T-cell factor 7-like 2 expression with almost the same strength as celecoxib. 2,5-Dimethylcelecoxib also inhibited the T-cell factor-dependent transcription activity and suppressed the expression of Wnt/β-catenin target gene products cyclin D1 and survivin. Subsequently, we compared the in vivo effects of celecoxib and DM-celecoxib using the Mutyh−/− mouse model, in which oxidative stress induces multiple intestinal carcinomas. Serum concentrations of orally administered celecoxib and DM-celecoxib elevated to the levels enough to suppress cancer cell proliferation. Repeated treatment with celecoxib and DM-celecoxib markedly reduced the number and size of the carcinomas without showing toxicity. These results suggest that the central mechanism for the anticancer effect of celecoxib derivatives is the suppression of the Wnt/β-catenin signaling pathway but not the inhibition of COX-2, and that DM-celecoxib might be a better lead compound candidate than celecoxib for the development of novel anticancer drugs..
8. Daisuke Matsuda, Takuya Matsumoto, Kenichi Honma, Ayae Ikawa-Yoshida, Mitsuho Onimaru, Tadashi Furuyama, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Yoshihiko Maehara, BUBR1 insufficiency in mice increases their sensitivity to oxidative stress, In Vivo, 10.21873/invivo.10993, 30, 6, 769-776, 2016.11, Background/Aim: Budding uninhibited by benzimidazole-related 1 (BUBR1) plays an important role in the spindle assembly checkpoint to prevent chromosome missegregation and aneuploidy during mitosis. We previously generated mutant mice that express BUBR1 at only 20% of the normal level (BubR1L/L mice). Here, we examined the effect of low BUBR1 expression on oxidative stress-induced carcinogenesis in mice. Materials and Methods: We orally administered either a potassium bromate (KBrO3) solution (2 g/l) or tap water to BubR1L/L and wild-type (BubR1+/+) mice for 16 weeks and examined the subsequent incidence of tumours. Results: KBrO3-treated BubR1L/L mice showed significantly higher mortality than the KBrO3-treated BubR1+/+ and control tap water-treated mice (p=0.0082). Histopathological and immunohistochemical analyses revealed that the spleens of surviving BubR1L/L mice were occupied by non-B-, non-T-cells with high proliferative potential. Conclusion: Our results indicate that low BUBR1 expression increases oxidative stress-induced mortality in mice, possibly caused by splenic neoplasms..
9. Ayae Ikawa-Yoshida, Takuya Matsumoto, Shinji Okano, Yukihiko Aoyagi, Yutaka Matsubara, Tadashi Furuyama, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Mitsuho Onimaru, Tomoko Ohkusa, Masatoshi Nomura, Yoshihiko Maehara, BubR1 Insufficiency Impairs Liver Regeneration in Aged Mice after Hepatectomy through Intercalated Disc Abnormality, Scientific Reports, 10.1038/srep32399, 6, 2016.08, A delay in liver regeneration after partial hepatectomy (PHx) leads to acute liver injury, and such delays are frequently observed in aged patients. BubR1 (budding uninhibited by benzimidazole-related 1) controls chromosome mitotic segregation through the spindle assembly checkpoint, and BubR1 down-regulation promotes aging-associated phenotypes. In this study we investigated the effects of BubR1 insufficiency on liver regeneration in mice. Low-BubR1-expressing mutant (BubR1L/L) mice had a delayed recovery of the liver weight-to-body weight ratio and increased liver deviation enzyme levels after PHx. Microscopic observation of BubR1L/L mouse liver showed an increased number of necrotic hepatocytes and intercalated disc anomalies, resulting in widened inter-hepatocyte and perisinusoidal spaces, smaller hepatocytes and early-stage microvilli atrophy. Up-regulation of desmocollin-1 (DSC1) was observed in wild-type, but not BubR1L/L, mice after PHx. In addition, knockdown of BubR1 expression caused down-regulation of DSC1 in a human keratinocyte cell line. BubR1 insufficiency results in the impaired liver regeneration through weakened microstructural adaptation against PHx, enhanced transient liver failure and delayed hepatocyte proliferation. Thus, our data suggest that a reduction in BubR1 levels causes failure of liver regeneration through the DSC1 abnormality..
10. Hiroyuki Kamiya, Natsuki Nishigaki, Akihiro Ikeda, Seiya Yukawa, Yukiko Morita, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Hideyoshi Harashima, Insertion and deletion mismatches distant from the target position improve gene correction with a tailed duplex, Nucleosides, Nucleotides and Nucleic Acids, 10.1080/15257770.2016.1163384, 35, 7, 379-388, 2016.07, A 5′-tailed duplex (TD) DNA corrects a base-substitution mutation. In this study, the effects of insertion and deletion (indel) mismatches distant from the target position on the gene correction were examined. Three target plasmid DNAs with and without indel mismatches ∼330 bases distant from the correction target position were prepared, and introduced into HeLa cells together with the TD. The indel mismatches improved the gene correction efficiency and specificity without sequence conversions at the indel mismatch site. These results suggested that the gene correction efficiency and specificity are increased when an appropriate second mismatch is introduced into the TD fragment..
11. Hiroyuki Yamamoto, Masataka Ishimura, Masayuki Ochiai, Hidetoshi Takada, K. Kusuhara, Yoshimichi Nakatsu, Teruhisa Tsuzuki, K. Mitani, Toshiro Hara, BTK gene targeting by homologous recombination using a helper-dependent adenovirus/adeno-associated virus hybrid vector, 10.1038/gt.2015.91, 23, 2, 205-213, 2015.08.
12. Rie Kanao, Masayuki Yokoi, Tsuyoshi Ohkumo, Yasutaka Sakurai, Kantaro Dotsu, Shinobu Kura, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Chikahide Masutani, Fumio Hanaoka, UV-induced mutations in epidermal cells of mice defective in DNA polymerase η and/or ι, DNA Repair, 10.1016/j.dnarep.2015.02.006, 29, 139-146, 2015.05, Xeroderma pigmentosum variant (XP-V) is a human rare inherited recessive disease, predisposed to sunlight-induced skin cancer, which is caused by deficiency in DNA polymerase η (Polη). Polη catalyzes accurate translesion synthesis (TLS) past pyrimidine dimers, the most prominent UV-induced lesions. DNA polymerase ι (Polι) is a paralog of Polη that has been suggested to participate in TLS past UV-induced lesions, but its function in vivo remains uncertain. We have previously reported that Polη-deficient and Polη/Polι double-deficient mice showed increased susceptibility to UV-induced carcinogenesis. Here, we investigated UV-induced mutation frequencies and spectra in the epidermal cells of Polη- and/or Polι-deficient mice. While Polη-deficient mice showed significantly higher UV-induced mutation frequencies than wild-type mice, Polι deficiency did not influence the frequencies in the presence of Polη. Interestingly, the frequencies in Polη/Polι double-deficient mice were statistically lower than those in Polη-deficient mice, although they were still higher than those of wild-type mice. Sequence analysis revealed that most of the UV-induced mutations in Polη-deficient and Polη/Polι double-deficient mice were base substitutions at dipyrimidine sites. An increase in UV-induced mutations at both G:C and A:T pairs associated with Polη deficiency suggests that Polη contributes to accurate TLS past both thymine- and cytosine-containing dimers in vivo. A significant decrease in G:C to A:T transition in Polη/Polι double-deficient mice when compared with Polη-deficient mice suggests that Polι is involved in error-prone TLS past cytosine-containing dimers when Polη is inactivated..
13. Naoya Kubokura, Fumi Takahashi, Masaki Ariuoka, Yoshihara Tatsuya, Kazunobu Igawa, Katsuhiko Tomooka, Sachio Morimoto, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Yusaku Nakabeppu, Takayuki Matsumoto, Kitazono T, Toshiyuki Sasaguri, Differentiation-inducing factor-3 inhibits intestinal tumor growth in vitro and in vivo., 10.1016/j.jphs.2015.03.005, 127, 4, 446-455, 2015.04.
14. Ryoichi Kyuragi, Takuya Matsumoto, Yui Harada, Satoru Saito, Mitsuho Onimaru, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Masatoshi Nomura, Yoshikazu Yonemitsu, Yoshihiko Maehara, BubR1 insufficiency inhibits neointimal hyperplasia through impaired vascular smooth muscle cell proliferation in mice, Arterioscler. Thromb. Vasc. Biol., 10.1161/ATVBAHA.114.304737, 35, 341-347, 2015.02, Objective—BubR1, a cell cycle–related protein, is an essential component of the spindle checkpoint that regulates cell division. Mice with BubR1 expression reduced to 10% of the normal level display a phenotype characterized by progeria; however, the involvement of BubR1 in vascular diseases is still unknown. We generated mice in which BubR1 expression was reduced to 20% (BubR1L/L mice) of that in wild-type mice (BubR1+/+) to investigate the effects of BubR1 on arterial intimal hyperplasia.
Approach and Results—Ten-week-old male BubR1L/L and age-matched wild-type littermates (BubR1+/+) were used in this study. The left common carotid artery was ligated, and histopathologic examinations were conducted 4 weeks later. Bone marrow transplantation was also performed. Vascular smooth muscle cells (VSMCs) were isolated from the thoracic aorta to examine cell proliferation, migration, and cell cycle progression. Severe neointimal hyperplasia was observed after artery ligation in BubR1+/+ mice, whereas BubR1L/L mice displayed nearly complete inhibition of neointimal hyperplasia. Bone marrow transplantation from all donors did not affect the reconstitution of 3 hematopoietic lineages, and neointimal hyperplasia was still suppressed after bone marrow transplantation from BubR1+/+ mice to BubR1L/L mice. VSMC proliferation was impaired in BubR1L/L mice because of delayed entry into the S phase. VSMC migration was unaffected in these BubR1L/L mice. p38 mitogen–activated protein kinase–inhibited VSMCs showed low expression of BubR1, and BubR1-inhibited VSMCs showed low expression of p38.
Conclusions—BubR1 may represent a new target molecule for treating pathological states of vascular remodeling, such as restenosis after angioplasty. .
15. Takuro Isoda, Yoshimichi Nakatsu, Kazumi Yamauchi, Takashi Yao, Jingshu Piao, Hiroshi Honda, Yusaku Nakabeppu, Teruhisa Tsuzuki, Abnormality in Wnt Signaling is Causatively Associated with Oxidative Stress-Induced Intestinal Tumorigenesis in MUTYH-Null Mice, Int. J. Biol. Sci., 10.7150/ijbs.9241, 10, 8, 940-947, 2014.08.
16. Fumi Takahashi, Yoshihara Tatsuya, Kentaro Jingushi, Kazunobu Igawa, KATSUHIKO TOMOOKA, Yutaka Watanabe, Sachio Morimoto, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Yusaku Nakabeppu, Toshiyuki Sasaguri, DIF-1 inhibits tumor growth in vivo reducing phosphorylation of GSK-3β and expressions of cyclin D1 and TCF7L2 in cancer model mice, Biochemical pharmacology, 10.1016/j.bcp.2014.03.006, 89, 340-348, 2014.06.
17. Jingshu Piao, Yoshimichi Nakatsu, Mizuki Ohno, Ken-ichi Taguchi, Teruhisa Tsuzuki, Mismatch repair deficient mice show susceptibility to oxidative stress-induced intestinal carcinogenesis, International Journal of Biological Sciences, 10.7150/ijbs.5750, 10, 1, 73-79, 2013.12.
18. Teik How Lim, Ryosuke Fujikane, Shiori Sano, Ryuji Sakagami, Yoshimichi Nakatsu, Teruhisa Tsuzuki, Mutsuo Sekiguchi, Masumi Hidaka, Activation of AMP-activated protein kinase by MAPO1 and FLCN induces apoptosis triggered by alkylated base mismatch in DNA, DNA Repair, 10.1016/j.dnarep.2011.11.006, 11, 3, 259-266, 2012.03, O 6-Methylguanine produced in DNA by the action of simple alkylating agents, such as N-methyl-N-nitrosourea (MNU), causes base-mispairing during DNA replication, thus leading to mutations and cancer. To prevent such outcomes, the cells carrying O 6-methylguanine undergo apoptosis in a mismatch repair protein-dependent manner. We previously identified MAPO1 as one of the components required for the induction of apoptosis triggered by O 6-methylguanine. MAPO1, also known as FNIP2 and FNIPL, forms a complex with AMP-activated protein kinase (AMPK) and folliculin (FLCN), which is encoded by the BHD tumor suppressor gene. We describe here the involvement of the AMPK-MAPO1-FLCN complex in the signaling pathway of apoptosis induced by O 6-methylguanine. By the introduction of siRNAs specific for these genes, the transition of cells to a population with sub-G 1 DNA content following MNU treatment was significantly suppressed. After MNU exposure, phosphorylation of AMPKα occurred in an MLH1-dependent manner, and this activation of AMPK was not observed in cells in which the expression of either the Mapo1 or the Flcn gene was downregulated. When cells were treated with AICA-ribose (AICAR), a specific activator of AMPK, activation of AMPK was also observed in a MAPO1- and FLCN-dependent manner, thus leading to cell death which was accompanied by the depolarization of the mitochondrial membrane, a hallmark of the apoptosis induction. It is therefore likely that MAPO1, in its association with FLCN, may regulate the activation of AMPK to control the induction of apoptosis triggered by O 6-methylguanine..
19. Ito R, Sekiguchi M, Setoyama D, Nakatsu Y, Yamagata Y, Hayakawa H., Cleavage of Oxidized Guanine Nucleotide and ADP-sugar by Human NUDT5 Protein, The Journal of Biochemistry, 149, 6, 731-738, 2011.06.
20. Teruhisa Tsuzuki, Jingshu Piao, Takuro Isoda, Kunihiko Sakumi, Yusaku Nakabeppu, Yoshimichi Nakatsu, Oxidative stress-induced tumorigenesis in the small intestine of various types of DNA repair-deficient mice, Health Physics, 100, 293-294, 2011.05.
21. H. Kamiya M. Uchiyam, J.-S. Piao, Y. Nakatsu, T. Tsuzuki and H. Harashima, Targeted sequence alteration of a chromosomal locus in mouse liver, Inter. J. Pharmaceutics, 387, 1-2, 180-183, 2010.03.
22. Komori K, Takagi Y, Sanada M, Lim TH, Nakatsu Y, Tsuzuki T, Sekiguchi M, Hidaka M, A novel protein, MAPO1, that functions in apoptosis triggered by O6-methylguanine mispair in DNA, Oncogene, 28(8):1142-1150, 2009.02.
23. Nakane H, Hirota S, Brooks PJ, Nakabeppu Y, Nakatsu Y, Nishimune Y, Iino A, Tanaka K, Impaired spermatogenesis and elevated spontaneous tumorigenesis in xeroderma
pigmentosum group A gene (Xpa)-deficient mice, DNA Repair, 7(12):1938-1950, 2008.12.
24. Kamiya H, Uchiyama M, Nakatsu Y, Tsuzuki T, Harashima H, Effects of Target Sequence and Sense versus Anti-sense Strands on Gene Correction with Single-stranded DNA Fragments, J. Biochem., 144:431-436, 2008.10.
25. Tsuchiya H, Uchiyama M, Hara K, Nakatsu Y, Tsuzuki T, Inoue H, Harashima H, Kamiya H, Improved gene correction efficiency with a tailed duplex DNA fragment, Biochemistry, 47(33):8754-8459, 2008.08.
26. Kuraoka I, Ito S, Wada T, Hayashida M, Lee L, Saijo M, Nakatsu Y, Matsumoto M, Matsunaga T, Handa H, Qin J, Nakatani Y, Tanaka K, Isolation of XAB2 complex involved in pre-mRNA splicing, transcription, and transcription-coupled repair, J Biol Chem, 283(2):940-950, 2008.01.
27. Sanada M, Hidaka M, Takagi Y, Takano TY, Nakatsu Y, Tsuzuki T, Sekiguchi M, Modes of Actions of Two Types of Antineoplastic Drugs, Dacarbazine and ACNU, to Induce Apoptosis, Carcinogenesis, 28(12):2657-2663 , 2007.12.
28. Sakamoto K, Tominaga Y, Yamauchi K, Nakatsu Y, Sakumi K, Yoshiyama K, Egashira A, Kura S, Yao T, Tsuneyoshi M, Maki H, Nakabeppu Y, Tsuzuki T, MUTYH-null mice are susceptible to spontaneous and oxidative stress induced intestinal tumorigenesis, Cancer Research, 67(14):6599-6604, 2007.07.
29. Yonemasu R, Minami M, Nakatsu Y, Takeuchi M, Kuraoka I, Matsuda Y, Higashi Y, Kondoh H, Tanaka K., Disruption of mouse XAB2 gene involved in pre-mRNA splicing, transcription and transcription-coupled DNA repair results in preimplantation lethality., DNA Repair, 4;4:479-491, 2005.01.
30. Ren Y, Saijo M, Nakatsu Y, Nakai H, Yamaizumi M, Tanaka K., Three novel mutations responsible for Cockayne syndrome group A., Genes abd Genetic Systems, 78: 93-102, 2003.01.
31. Yoshino M, Nakatsu Y, te Riele H, Hirota S, Kitamura Y, Tanaka K., Additive roles of XPA and MSH2 genes in UVB-induced skin tumorigenesis in mice., DNA Repair, 1: 935-940., 2002.01.
32. Tanaka K, Kamiuchi S, Ren Y, Yonemasu R, Ichikawa M, Murai H, Yoshino M, Takeuchi S, Saijo M, Nakatsu Y, Miyauchi-Hashimoto H, Horio T., UV-induced skin carcinogenesis in xeroderma pigmentosum group A (XPA) gene-knockout mice with nucleotide excision repair-deficiency., Mutation Research, 477: 31-40, 2001.01.
33. Murai M, Enokido Y, Inamura N, Yoshino M, Nakatsu Y, van der Horst GT, Hoeijmakers JH, Tanaka K, Hatanaka H., Early postnatal ataxia and abnormal cerebellar development in mice lacking Xeroderma pigmentosum Group A and Cockayne syndrome Group B DNA repair genes., Proc Natl Acad Sci U S A., 98: 13379-13384, 2001.01.