KINDAI UNIVERSITY


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MATSUDA Toshiro

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FacultyAtomic Energy Research Institute
PositionProfessor
Degree
Commentator Guidehttps://www.kindai.ac.jp/meikan/262-matsuda-toshirou.html
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Last Updated :2020/09/30

Education and Career

Education

  •   1982 04  - 1988 03 , Osaka University, Medical school

Research Activities

Research Areas

  • Life sciences, Cardiology
  • Life sciences, Internal medicine - General
  • Life sciences, Virology
  • Life sciences, Medical biochemistry
  • Life sciences, Pathobiochemistry

Published Papers

  • Future directions of research in radiation biology, 松田外志朗, 近畿大学原子力研究所年報(Web), 近畿大学原子力研究所年報(Web), 54, 39‐46 (WEB ONLY), Mar. 22 2018
  • 福島県における甲状腺がんについて, 松田外志朗, 近畿大学原子力研究所年報(Web), 近畿大学原子力研究所年報(Web), 53, 13‐18 (WEB ONLY), Mar. 24 2017
  • 【糖尿病強化療法-低血糖を巡る諸問題】 実臨床における重症低血糖とそのリスク ERにおける重症低血糖症例の臨床像, 平出 敦, 松田 外志朗, 窪田 愛恵, 田口 博一, 久村 正樹, 木下 理恵, 西内 辰也, Diabetes Frontier, Diabetes Frontier, 25(4), 402 - 406, Aug. 2014
  • Effects of ethyl esterization, chain length, and hyperthermia on carcinostatic effects of omega-hydroxylatede fatty acids, Experimental Oncology, Experimental Oncology, 29(2), 106 - 110, Jun. 2007
  • Inhibition of nucleotide excision repair by anti-XPA monoclonal antibodies which interfere with binding to RPA, ERCC1, and TFIIH., Saijo M, Matsuda T, Kuraoka I, Tanaka K, Biochem Biophys Res Commun., Biochem Biophys Res Commun., 321(4), 851 - 822, Sep. 2004 , Refereed
    Summary:The xeroderma pigmentosum group A protein (XPA) binds to three nucleotide excision repair (NER) factors: RPA, ERCC1, and TFIIH. XPA also binds preferentially to UV- or chemical carcinogen-damaged DNA. In this study, we prepared anti-XPA monoclonal antibodies and examined their effects on NER. Two clones inhibited cell-free NER reactions. The mode of inhibition appeared to differ; one clone inhibited both 5' and 3' incisions equally while the other inhibited the 5' incision more. The two clones inhibited the binding of XPA to RPA, ERCC1, and TFIIH. They did not inhibit the binding to damaged DNA either. These results suggest that the interaction of XPA with these NER factors is essential to the NER pathway. The epitopes of these antibodies were located outside of the binding regions for these NER factors. Steric hindrance or conformational changes of XPA brought about by the binding of anti-XPA IgG possibly cause the inhibitory effects.
  • A novel cytoplasmic GTPase XAB1 interacts with DNA repair protein XPA., Nucleic Acids Research, Nucleic Acids Research, 28(21), 4212 - 4218, Nov. 2001
    Summary:The xeroderma pigmentosum group A protein (XPA) plays a central role in nucleotide excision repair (NER). To identify proteins that bind to XPA, we screened a HeLa cDNA library using the yeast two-hybrid system. Here we report a novel cytoplasmic GTP-binding protein, designated XPA binding protein 1 (XAB1). The deduced amino acid sequence of XAB1 consisted of 374 residues with a molecular weight of 41 kDa and an isoelectric point of 4.65. Sequence analysis revealed that XAB1 has four sequence motifs G1?G4 of the GTP-binding protein family in the N-terminal half. XAB1 also contains an acidic region in the C-terminal portion. Northern blot analysis showed that XAB1 mRNA is expressed ubiquitously, and immunofluorescence analysis revealed that XAB1 is localized mainly in the cytoplasm. Consistent with the GTP-binding motif, purified recombinant XAB1 protein has intrinsic GTPase activity.
  • Proofreading of DNA polymerase eta-dependent replication errors., J Biol Chem., J Biol Chem., 276(4), 2317 - 2320, Jan. 2001
    Summary:Human DNA polymerase eta, the product of the skin cancer susceptibility gene XPV, bypasses UV photoproducts in template DNA that block synthesis by other DNA polymerases. Pol eta lacks an intrinsic proofreading exonuclease and copies DNA with low fidelity, such that pol eta errors could contribute to mutagenesis unless they are corrected. Here we provide evidence that pol eta can compete with other human polymerases during replication of duplex DNA, and in so doing it lowers replication fidelity. However, we show that pol eta has low processivity and extends mismatched primer termini less efficiently than matched termini.
  • Fidelity and processivity of DNA synthesis by DNA polymerase kappa, the product of the human DINB1 gene., J Biol Chem., J Biol Chem., 275(50), 39678 - 39684, Dec. 2000
    Summary:Mammalian DNA polymerase kappa (pol kappa), a member of the UmuC/DinB nucleotidyl transferase superfamily, has been implicated in spontaneous mutagenesis. Here we show that human pol kappa copies undamaged DNA with average single-base substitution and deletion error rates of 7 x 10(-3) and 2 x 10(-3), respectively. These error rates are high when compared to those of most other DNA polymerases. pol kappa also has unusual error specificity, producing a high proportion of T.CMP mispairs and deleting and adding non-reiterated nucleotides at extraordinary rates. Unlike other members of the UmuC/DinB family, pol kappa can processively synthesize chains of 25 or more nucleotides. This moderate processivity may reflect a contribution of C-terminal residues, which include two zinc clusters. The very low fidelity and moderate processivity of pol kappa is novel in comparison to any previously studied DNA polymerase, and is consistent with a role in spontaneous mutagenesis.
  • Mitotic genes are transcriptionally upregulated in the fibroblast irradiated with very low doses of UV-C, Seiji Takeuchi, Toshiro Matsuda, Ryusuke Ono, Mariko Tsujimoto, Chikako Nishigori, SCIENTIFIC REPORTS, SCIENTIFIC REPORTS, 6, 29233, Jul. 2016 , Refereed
    Summary:Ultraviolet (UV) radiation induces a variety of biological effects, including DNA damage response and cell signaling pathways. We performed transcriptome analysis using microarray in human primary cultured fibroblasts irradiated with UV-C (0.5 or 5 J/m(2)) and harvested at 4 or 12 h following UV exposure. All transcript data were analyzed by comparison with the corresponding results in non-irradiated (control) cells. The number of genes with significantly altered expression (>= 2-fold difference relative to the control) is higher in the sample irradiated with high dose of UV, suggesting that gene expression was UV dose-dependent. Pathway analysis on the upregulated genes at 12 h indicates that the expression of some cell cycle-related genes was predominantly induced irrespective of UV-dose. Interestingly, almost all the genes with significant altered expression were cell cycle-related genes designated as 'Mitotic Genes', which function in the spindle assembly checkpoint. Therefore, even a low dose of UV could affect the transcriptional profile.
  • Upregulated pleiotropic drug resistance genes in Saccharomyces cerevisiae yrr1–52, Naohiko Kodo, Shoei Sakata, Toshiro Matsuda, Nucleus (India), Nucleus (India), 58(3), 231 - 234, Dec. 01 2015 , Refereed
    Summary:Gain-of-function mutations of Saccharomyces cerevisiae pleiotropic drug resistance (PDR) genes PDR1, PDR3, and YRR1 cause constitutive high expression of membrane-associated drug efflux pumps, resulting in the excretion of antifungal drugs. We previously identified a novel mutation of YRR1 that conferred salicylic acid (SA) resistance to S. cerevisiae BY4741 cells randomly mutagenized with ethyl methane sulfonate. Yeast cells carrying the yrr1–52 allele activated several drug efflux pumps and exhibited resistance to 4-nitroquinoline-N-oxide and cycloheximide. However, the activated genes and other factors that are directly involved in SA resistance remain unclear. Therefore, microarray analyses of total RNA extracted from yrr1–52 and wild-type cells during the logarithmic phase were performed. Twenty genes demonstrating > 2-fold higher expression than the wild-type were selected. Among the upregulated genes, YOR1, SNQ2, AZR1, and FLR1 encode transport proteins previously associated with drug efflux pumps. YOR1 and SNQ2, which encode an ATP-binding cassette (ABC) transporter, were investigated as candidate genes involved in SA resistance. Spot assay results showed no changes in SA susceptibility after disruption of YOR1 or SNQ2 on a background of YRR1 and yrr1–52, indicating that Yor1p and Snq2p are not involved in SA resistance.
  • Salicylic acid resistance is conferred by a novel YRR1 mutation in Saccharomyces cerevisiae, Naohiko Kodo, Toshiro Matsuda, Syuichi Doi, Hiroshi Munakata, Biochemical and Biophysical Research Communications, Biochemical and Biophysical Research Communications, 434(1), 42 - 47, Apr. 26 2013 , Refereed
    Summary:Yeast cells can extrude intracellular drugs through membrane-associated efflux pumps, such as ATP-binding cassette (ABC) transporters and members of the major facilitator superfamily. Gene expression of drug efflux pumps is regulated by several transcription factors involved in pleiotropic drug resistance (PDR). Salicylic acid (SA) possesses weak antifungal activity. Although the excretion mechanisms of some antifungal drugs have been revealed, the mechanism of SA extrusion remains unclear. To elucidate the mechanism of SA excretion, we screened SA-resistant mutants from random mutagenized Saccharomyces cerevisiae BY4741 cells. We successfully isolated 60 SA-resistant clones (KinSal001-060). KinSal052, one of the strongest SA-resistant clones, also exhibited resistance to 4-nitroquinoline-1-oxide and cycloheximide, indicating that it acquired the PDR phenotype. We identified a novel mutation in YRR1 conferring SA resistance to KinSal052. YRR1 encodes a Zn(II)2Cys6-type zinc-finger transcription factor that reportedly activates gene expression involved in PDR. Yeast cells carrying the yrr1 allele (yrr1-52) activated expression of several efflux pump-encoding genes, including YOR1, SNQ2, AZR1, and FLR1. These results suggested that SA resistance in KinSal052 is conferred by the overexpression of efflux pumps constitutively activated by the mutant form of Yrr1p. © 2013 Elsevier Inc.
  • Effects of ethyl-esterization, chain-lengths, unsaturation degrees, and hyperthermia on carcinostatic effect of omega-hydroxylated fatty acids, K. Kusumoto, K. Kageyama, T. Matsuda, T. T. Tomura, H. Munakata, H. Tanaka, F. Yazama, N. Miwa, Experimental Oncology, Experimental Oncology, 29(2), 106 - 110, Jun. 2007
    Summary:Aim: To evaluate promotive effect of hyperthermia on the carcinostatic activity of synthesized omega-hydroxy fatty acids (ωHFAs) and their ethylesters agaist Ehrlich ascites tumor (EAT) cells. Methods: EAT cells were cultured with either ωHFAs or their ethylester derivatives in a water bath at either 37°C or 42°C for 30 min, followed by incubation in a CO 2 incubator for 20 or 72 h. Mitochondrial dehydrogenase-based WST-1 assay and trypan blue dye exclusion assay were then conducted after incubation. Morphological changes were observed by scanning electron microscopy (SEM). Results: Omega-HFA having a saturated 16-carbon straight-chain (ωH16:0) was the most carcinostatic (at 37°C - viability level: 60.0% at 42°C - 49.6% (WST-1)) among saturated and unsaturated ωHFAs with 12, 15 or 16 carbon atoms, when administrated to EAT cells at 100 μM for 20 h. Carcinostatic activity was markedly enhanced by ethyl-esterization of saturated fatty acids, such as ωH16:0 (at 37°C - 42.3% at 42°C - 11.2% , ibid) and ωH15:0 (at 37°C - 74.6% at 42°C - 25.3% , ibid), and their unsaturated counterparts were extremely effective only in combination with hyperthermia. Prolongation of the incubation period to 72 h at the same concentration increased appreciably their carcinostatic effect (ωH16:0 ethylesther: 1.3% ωH15:0 ethylesther: 8.0%). These values were also supported by dye exclusion assay. The carcinostatic activity enhanced more markedly by hyperthermia (1.2% 2.1%, ibid). SEM shows that ωH16:0 ethylester-exposed EAT cells underwent extensive injury, such as deformation of cell structure or disappearance of microvilli. Conclusions: ωH16:0 ethylester possesses high carcinostatic activity in vitro in combination with hyperthermia and may be utilized as potent anticancer therapeutic agent. Copyright © Experimental Oncology, 2007.
  • The base substitution fidelity of DNA polymerase beta-dependent single nucleotide base excision repair, T Matsuda, BJV Berg, K Bebenek, WP Osheroff, SH Wilson, TA Kunkel, JOURNAL OF BIOLOGICAL CHEMISTRY, JOURNAL OF BIOLOGICAL CHEMISTRY, 278(28), 25947 - 25951, Jul. 2003 , Refereed
    Summary:Damaged DNA bases are removed from mammalian genomes by base excision repair (BER). Single nucleotide BER requires several enzymatic activities, including DNA polymerase and 5',2'-deoxyribose-5-phosphate lyase. Both activities are intrinsic to four human DNA polymerases whose base substitution error rate during gap-filling DNA synthesis varies by more than 10,000-fold. This suggests that BER fidelity could vary over a wide range in an enzyme dependent manner. To investigate this possibility, here we describe an assay to measure the fidelity of BER reactions reconstituted with purified enzymes. When human uracil DNA glycosylase, AP endonuclease, DNA polymerase beta, and DNA ligase 1 replace uracil opposite template A or G, base substitution error rates are less than or equal to0.3 to less than or equal to2.8 x 10(-4). BER error rates are higher when excess incorrect dNTPs are included in the reaction or when wild type DNA polymerase beta is replaced by DNA polymerase beta variants that fill single nucleotide gaps with lower fidelity. Under these conditions, the base substitution fidelity of polymerase beta-dependent BER is 3-8-fold higher than is single nucleotide gap filling by polymerase beta alone. Thus other proteins in the BER reaction may enhance the base substitution fidelity of DNA polymerase beta during single nucleotide BER.
  • Error rate and specificity of human and murine DNA polymerase eta, T Matsuda, K Bebenek, C Masutani, IB Rogozin, F Hanaoka, TA Kunkel, JOURNAL OF MOLECULAR BIOLOGY, JOURNAL OF MOLECULAR BIOLOGY, 312(2), 335 - 346, Sep. 2001
    Summary:We describe here the error specificity of mammalian DNA polymerase eta (pol eta), an enzyme that performs translesion DNA synthesis and may participate in somatic hypermutation of immunoglobulin genes. Both mouse and human pol eta lack intrinsic proofreading exonuclease activity and both copy undamaged DNA inaccurately. Analysis of more than 1500 single-base substitutions by human pol eta indicates that error rates for all 12 mismatches are high and variable depending on the composition and symmetry of the mismatch and its location. pol eta also generates tandem base substitutions at an unprecedented rate, and kinetic analysis indicates that it extends a tandem double mismatch about as efficiently as other replicative enzymes extend single-base mismatches. This ability to use an aberrant primer terminus and the high rate of single and double-base substitutions support the idea that pol eta may forego strict shape complementarity in order to facilitate highly efficient lesion bypass. Relaxed discrimination is further indicated by pol eta infidelity for a wide variety of nucleotide deletion and addition errors. The nature and location of these errors suggest that some may be initiated by strand slippage, while others result from additional mechanisms.
  • Somatic mutation hotspots correlate with DNA polymerase eta error spectrum, IB Rogozin, YI Pavlov, K Bebenek, T Matsuda, TA Kunkel, NATURE IMMUNOLOGY, NATURE IMMUNOLOGY, 2(6), 530 - 536, Jun. 2001
    Summary:Mutational spectra analysis of 15 immunoglobulin genes suggested that consensus motifs R (G) under bar YW and W (A) under bar were universal descriptors of somatic hypermutation. Highly mutable sites, "hotspots", that matched W (A) under bar were preferentially found in one DNA strand and R (G) under bar YW hotspots were found in both strands, Analysis of base-substitution hotspots in DNA polymerase error spectra showed that 33 of 36 hotspots in the human polymerase eta spectrum conformed to the W (A) under bar consensus. This and four other characteristics of polymerase eta substitution specificity suggest that errors introduced by this enzyme during synthesis of the nontranscribed DNA strand in variable regions may contribute to strand-specific somatic hypermutagenesis of immunoglobulin genes at A-T base pairs.
  • XAB2, a novel tetratricopeptide repeat protein involved in transcription-coupled DNA repair and transcription, Yoshimichi Nakatsu, Hiroshi Asahina, Elisabetta Citterio, Suzanne Rademakers, Wim Vermeulen, Shinya Kamiuchi, Jing-Ping Yeo, Min-Cheh Khaw, Masafumi Saijo, Naohiko Kodo, Toshiro Matsuda, Jan H. J. Hoeijmakers, Kiyoji Tanaka, Journal of Biological Chemistry, Journal of Biological Chemistry, 275(45), 34931 - 34937, Nov. 10 2000
    Summary:Nucleotide excision repair is a highly versatile DNA repair system responsible for elimination of a wide variety of lesions from the genome. It is comprised of two subpathways: transcription-coupled repair that accomplishes efficient removal of damage blocking transcription and global genome repair. Recently, the basic mechanism of global genome repair has emerged from biochemical studies. However, little is known about transcription-coupled repair in eukaryotes. Here we report the identification of a novel protein designated XAB2 (XPA-binding protein 2) that was identified by virtue of its ability to interact with XPA, a factor central to both nucleotide excision repair subpathways. The XAB2 protein of 855 amino acids consists mainly of 15 tetratricopeptide repeats. In addition to interacting with XPA, immunoprecipitation experiments demonstrafed that a fraction of XAB2 is able to interact with the transcription-coupled repair-specific proteins CSA and CSB as well as RNA polymerase II. Furthermore, antibodies against XAB2 inhibited both transcription-coupled repair and transcription in vivo but not global genome repair when microinjected into living fibroblasts. These results indicate that XAB2 is a novel component involved in transcription-coupled repair and transcription.
  • Low fidelity DNA synthesis by human DNA polymerase-eta, T Matsuda, K Bebenek, C Masutani, F Hanaoka, TA Kunkel, NATURE, NATURE, 404(6781), 1011 - 1013, Apr. 2000
    Summary:A superfamily of DNA polymerases that bypass lesions in DNA has been described(1-4). Some family members are described as error-prone because mutations that inactivate the polymerase reduce damage-induced mutagenesis. In contrast, mutations in the skin cancer susceptibility gene XPV5,6, which encodes DNA polymerase (pol)-eta, lead to increased ultraviolet-induced mutagenesis(7-11). This, and the fact that pol-eta primarily inserts adenines during efficient bypass of thymine-thymine dimers in vitro(8,12,13), has led to the description of pol-eta as error-free. However, here we show that human pol-eta copies undamaged DNA with much lower fidelity than any other template-dependent DNA polymerase studied. Pol-eta lacks an intrinsic proofreading exonuclease activity and, depending on the mismatch, makes one base substitution error for every 18 to 380 nucleotides synthesized. This very low fidelity indicates a relaxed requirement for correct base pairing geometry and indicates that the function of pol-eta may be tightly controlled to prevent potentially mutagenic DNA synthesis.
  • Identification of a damaged-DNA binding domain of the XPA protein, Kuraoka, I, EH Morita, M Saijo, T Matsuda, K Morikawa, M Shirakawa, K Tanaka, MUTATION RESEARCH-DNA REPAIR, MUTATION RESEARCH-DNA REPAIR, 362(1), 87 - 95, Jan. 1996 , Refereed
    Summary:The XPA (xeroderma pigmentosum group A) protein is a zinc metalloprotein consisting of 273 amino acids which binds preferentially to UV- or chemical carcinogen-damaged DNA, suggesting that it is involved in the recognition of several types of DNA damage during nucleotide excision repair processes. Here we identify a DNA binding domain of the XPA protein, The region of the XPA protein responsible for preferential binding to DNA damaged by UV or cis-diammine-dichloroplatinum(II) (cisplatin) is contained within a truncated derivative of the XPA protein, MF122, consisting of 122 amino acids and containing a C-4 type zinc finger motif, CD (circular dichroism) measurements of the MF122 protein showed that it has a helix-rich secondary structure, suggesting that it is a discretely folded, functional mini-domain. The MF122 protein should be useful for structural investigation of the XPA protein and of its interaction with damaged DNA.
  • ENHANCEMENT OF DAMAGE-SPECIFIC DNA-BINDING OF XPA BY INTERACTION WITH THE ERCC1 DNA-REPAIR PROTEIN, A NAGAI, M SAIJO, KURAOKA, I, T MATSUDA, N KODO, Y NAKATSU, T MIMAKI, M MINO, M BIGGERSTAFF, RD WOOD, A SIJBERS, JHJ HOEIJMAKERS, K TANAKA, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 211(3), 960 - 966, Jun. 1995 , Refereed
    Summary:The human XPA and ERCC1 proteins, which are involved in early steps of nucleotide excision repair of DNA, specifically interacted in an in vitro binding assay and a yeast two-hybrid assay. A stretch of consecutive glutamic acid residues in XPA was needed for binding to ERCC1. Binding of XPA to damaged DNA was markedly increased by the interaction of the XPA and ERCC1 proteins. ERCC1 did not enhance binding to DNA when a truncated XPA protein, MF122, was used in place of the XPA protein. MF122 retains damaged DNA binding activity but lacks the region for protein-protein interaction including the E-cluster region. These results suggest that the XPA/ERCC1 interaction may participate in damage-recognition as well as in incision at the 5' site of damage during nucleotide excision repair. (C) 1995 Academic Press. Inc.
  • DNA-REPAIR PROTEIN XPA BINDS REPLICATION PROTEIN-A (RPA), T MATSUDA, M SAIJO, KURAOKA, I, T KOBAYASHI, Y NAKATSU, A NAGAI, T ENJOJI, C MASUTANI, K SUGASAWA, F HANAOKA, A YASUI, K TANAKA, JOURNAL OF BIOLOGICAL CHEMISTRY, JOURNAL OF BIOLOGICAL CHEMISTRY, 270(8), 4152 - 4157, Feb. 1995 , Refereed
    Summary:XPA is a zinc finger DNA-binding protein, which is missing or altered in group A xeroderma pigmentosum cells and known to be involved in the damage-recognition step of the nucleotide excision repair (NER) processes. Using the yeast two-hybrid system to search for proteins that interact with XPA, we obtained the 34-kDa subunit of replication protein A (RPA, also known as HSSB and RFA). RPA is a stable complex of three polypeptides of 70, 34, 11 kDa and has been shown to be essential in the early steps of NER as well as in replication and recombination. We also demonstrate here that the RPA complex associates with XPA. These results suggest that RPA may cooperate with XPA in the early steps of the NER processes.
  • GENOMIC CHARACTERIZATION OF THE HUMAN DNA EXCISION REPAIR-CONTROLLING GENE XPAC, SATOKATA, I, K IWAI, T MATSUDA, Y OKADA, K TANAKA, GENE, GENE, 136(1-2), 345 - 348, Dec. 1993 , Refereed
    Summary:We have characterized the human DNA excision repair gene, XPAC (xeroderma pigmentosum group A complementing). This gene of approximately 25 kb consists of six exons. The 5'-flanking region of the gene has a CAAT box, but no TATA box. The region upstream from the coding sequence of exon 1 is G+C rich (73%), and has a GC box. Transcriptional mapping analysis suggested that there is one major transcription start point (tsp). The presence of two polyadenylation signals suggests that the two XPAC mRNAs with different 3' untranslated regions in normal human cells are due to alternative polyadenylations. The promoter activity, measured by transient expression of the cat gene with the 5' flanking regions, indicated the presence of a functional promoter.

Conference Activities & Talks

  • Survey and decontamination of radium-223 dichloride for alpha-particle radionuclide therapy in clinical facilities, Hosono M, Hohara S, Inagaki M, Yamanishi H, Wakabayashi G, Matsuda T, Sakaguchi K, Hanaoka K, Ito T, EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING,   2016 10
  • Measurement and parameters of alpha-emitting radium-223 for radionuclide therapy in accordance with radiation protection standards, Hosono M, Hohara S, Yamanishi H, Inagaki M, Wakabayashi G, Matsuda T, Sakaguchi K, Hanaoka K, Itoh T, EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING,   2014 10
  • Salicylic acid resistance is conferred by the overexpression of SNG1 in Saccharomyces cerevisiae,   2013 12
  • Effects of β-adrenoceptor blockade on the disorganization of intercellular adherence junction molecules in cardiomyopathy,   2005 12
  • Msh2 deficiency reverts sensitivity and promotes S-phase progresion of UVC-damaged Xpa-deficient cell, 9th International Conference on Environmental Mutagens.,   2005 09 , 9th International Conference on Environmental Mutagens.
    Summary:Previously, we established 5 kinds of UVB-induced skin cancer cell lines from Xeroderma Pigmentosum A (XPA) deficient mice that has resisitant property against UVC comparing with non-cancerous Xpa-deficient fibroblast. Expression of several mismatch repair (MMR) proteins (Msh2, Msh3, Msh6, Mlh1, Pms2) are reduced in every skin cancer cells. MMR activity is actually down-regulated in addition to dificiency of nucleotide excision repair (NER) activity in the cancer cells. The cancer cells also show abnormal cell cycle profile after UV irradiation different from noncancerous cell.
  • Angiotensin Converting Enzyme Inhibitor Reduces Cardiac Hypertrophy and Fibrosis in Cardiomyopathic Hamsters via NO-dependent Mechanisms,   2005 03
    Summary:Background To evaluate whether L-nitroarginine methyl ester (L-NAME), an NO synthase inhibitor, may inhibit beneficial effects of ACEI on cardiac remodeling and function in cardiomyopathic hamsters(Bio14.6) . Methods and Results Bio14.6, received cilazapril (CP )combined with L-NAME from the age of 16 weeks (w). Cardiac hypertrophy (CH) and cardiac fibrosis (CF) treated with CP for 12w or 24w were less than those of the untreated group (n=6, p<0.01). The inhibitory effects of L-NAME on the ACEI-induced recovery in both CH and CF decreased after CP treatment for 24w as compared with 12w . The recovery in fractional shortening by CP was less inhibited with L-NAME in 24w than in 12w. Plasma NOx were higher in 24w than in 12w. CP increased plasma NOx in both stages), and the addition of L-NAME canceled them . Conclusions NO-dependent mechanisms play a major role in ACEI-induced reduction of CH and CF at the early HF stage.
  • The base substitution fidelity of DNA polymerase beta-dependent single nucleotide base excision repair., The 4th International 3R Symposium.,   2003 11 , The 4th International 3R Symposium.
    Summary:Damaged DNA bases are removed from mammalian genomes by base excision repair (BER). Single nucleotide BER requires several enzymatic activities, including DNA polymerase and 5',2'-deoxyribose-5-phosphate lyase. Both activities are intrinsic to four human DNA polymerases whose base substitution error rate during gap-filling DNA synthesis varies by more than 10,000-fold. This suggests that BER fidelity could vary over a wide range in an enzyme dependent manner. To investigate this possibility, here we describe an assay to measure the fidelity of BER reactions reconstituted with purified enzymes. When human uracil DNA glycosylase, AP endonuclease, DNA polymerase beta, and DNA ligase 1 replace uracil opposite template A or G, base substitution error rates are
  • Fidelity of DNA synthesis by DNA polymeraseⅣ, the product of the E.coli dinB gene., 8th International Conference on Environmental Mutagens.,   2001 10 , 8th International Conference on Environmental Mutagens.
  • Error specificity of DNA polymerase-η., 65th Cold Spring Harbor Symposium on Quantitative Biology.,   2000 06 , 65th Cold Spring Harbor Symposium on Quantitative Biology.
    Summary:We describe here the error specificity of mammalian DNA polymerase eta (pol eta), an enzyme that performs translesion DNA synthesis and may participate in somatic hypermutation of immunoglobulin genes. Both mouse and human pol eta lack intrinsic proofreading exonuclease activity and both copy undamaged DNA inaccurately. Analysis of more than 1500 single-base substitutions by human pol eta indicates that error rates for all 12 mismatches are high and variable depending on the composition and symmetry of the mismatch and its location. pol eta also generates tandem base substitutions at an unprecedented rate, and kinetic analysis indicates that it extends a tandem double mismatch about as efficiently as other replicative enzymes extend single-base mismatches.

Misc

  • 中性子線及び国立がん研究センターBNCTシステムによる生物学的影響の評価, 今道 祥二, 益谷 美都子, 伊丹 純, 中村 哲志, 伊藤 昌司, 岡本 裕之, 井垣 浩, 山西 弘城, 松田 外志朗, 日本放射線影響学会大会講演要旨集, 60回, 126, 126,   2017 10
  • 近畿大学原子炉に対する新規制基準適合確認の現状, 芳原新也, 杉山亘, 橋本憲吾, 山西弘城, 若林源一郎, 松田外志朗, 堀口哲男, 伊藤眞, 伊藤哲夫, 日本原子力学会秋の大会予稿集(CD-ROM), 2015, ROMBUNNO.M22,   2015 08 21 , http://jglobal.jst.go.jp/public/201502211656209837
  • 角化細胞と色素細胞における、UVB照射時のマイクロアレイを用いた遺伝子変動解析(Microarray analysis for the expression profiles in the keratinocyte and melanocyte with UVB irradiation), 竹内 聖二, 松田 外志朗, 正木 太朗, 錦織 千佳子, 日本癌学会総会記事, 73回, P, 3007,   2014 09
  • ナローバンド、ブロードバンドUVB照射後のケラチノサイトとメラノサイトにおけるマイクロアレイ解析(Pathway analysis through the microarray technology in the keratinocyte and melanocyte exposed by NB-UVB and BBUVB), 正木 太朗, 竹内 聖二, 錦織 千佳子, 松田 外志朗, 日本癌学会総会記事, 73回, P, 3025,   2014 09
  • 低線量紫外線照射が遺伝子発現プロファイルに与える影響, 松田 外志朗, 竹内 聖二, 小野 竜輔, 錦織 千佳子, 日本放射線影響学会大会講演要旨集, 57回, 143, 143,   2014 09
  • A群色素性乾皮症患者細胞における低線量紫外線照射時の網羅的遺伝子発現解析, 竹内 聖二, 松田 外志朗, 小野 竜輔, 錦織 千佳子, 日本放射線影響学会大会講演要旨集, 57回, 144, 144,   2014 09
  • 近畿大学における原子力人材育成事業の現状, 若林源一郎, 橋本憲吾, 伊藤哲夫, 山西弘城, 芳原新也, 堀口哲男, 杉山亘, 伊藤眞, 松田外志朗, 稲垣昌代, 山本友完, 日本原子力学会秋の大会予稿集(CD-ROM), 2014, ROMBUNNO.P02,   2014 08 22 , http://jglobal.jst.go.jp/public/201402225818268169
  • 糖尿病診療と低血糖 実臨床とその対策 ERにおける低血糖症例の検討, 平出 敦, 松田 外志朗, 田口 博一, 西内 辰也, 植嶋 利文, 村尾 佳則, 北澤 康秀, 糖尿病, 57, Suppl.1, S, 20,   2014 04
  • 市立病院救急外来における低血糖症例 入院を要する症例の検討, 栗原 敏修, 小川 義高, 松本 伸治, 辻 真由美, 木戸 里佳, 大江 洋介, 福島 幸男, 星田 四朗, 松田 外志朗, 日本内科学会雑誌, 103, Suppl., 198, 198,   2014 02
  • 大学病院救急外来における低血糖症例 注意を要する症例の検討, 栗原 敏修, 松田 外志朗, 浅沼 博司, 平出 敦, 日本内科学会雑誌, 102, Suppl., 259, 259,   2013 02
  • 大学病院救急外来における低血糖症例の初期診療時の症候と既往歴の分析, 栗原 敏修, 松田 外志朗, 冨吉 浩雅, 中江 晴彦, 平出 敦, 日本内科学会雑誌, 101, Suppl., 234, 234,   2012 02
  • 大学病院救急外来における低血糖症例の初期診療時の身体所見および検査結果の解析, 松田 外志朗, 栗原 敏修, 森田 正則, 浅沼 博司, 平出 敦, 日本内科学会雑誌, 101, Suppl., 239, 239,   2012 02
  • 過去3年間のER実習における症候診断能力の評価, 栗原 敏修, 松田 外志朗, 富吉 浩雅, 中江 晴彦, 森田 正則, 窪田 愛恵, 平出 敦, 医学教育, 42, Suppl., 136, 136,   2011 07
  • 救急診療部門(ER)は院内感染の検知および制御システムとして活用できる, 松田 外志朗, 冨吉 浩雅, 中江 晴彦, 浅沼 博司, 栗原 敏修, 橋本 直樹, 嶋津 岳士, 日本救急医学会雑誌, 19, 8, 636, 636,   2008 08
  • non-surgical treatment for abdomominal emergency disease, 32, 5, 512, 516,   2008 05
  • リンパ節転移陽性乳癌におけるThymidylate Synthase(TS)遺伝子多型の検討(Thymidylate Synthase (TS) genotype in node positive breast cancer), 藤島 成, 乾 浩己, 松田 外志朗, 綿谷 正弘, 橋本 幸彦, 塩崎 均, 日本癌学会総会記事, 66回, 540, 540,   2007 08
  • 心筋症における細胞間接着関連分子異常に対するβ受容体遮断薬の効果 分子発現と構造に対する評価, 栗原 敏修, 松田 外志朗, 富吉 浩雅, 橋本 直樹, 宗像 浩, 東野 英明, 鍵谷 俊文, 米田 悦啓, 北風 政史, 臨床薬理, 37, Suppl., S178, S178,   2006 11
  • コケイン症候群B群細胞における紫外線照射後の遺伝子発現変化の解析, 永田 有希, 松田 外志朗, 竹内 聖二, 田中 亀代次, 日本放射線影響学会大会講演要旨集, 47回, 98, 98,   2004 11
  • Inhibitory effect of cardiac hypertrophiy and myocardial tissue fibrillation by selective inhibitors of atrial natriuresis peptide degrading enzyme in spontaneous cardiomyopathy hamsters., 栗原 敏修, 鍵谷 俊文, 苅田 真子, 船矢 寛治, 松田 外志朗, 北風 政史, 是恒 之宏, 楠岡 英雄, 武田 裕, 堀 正二, Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics, 28, 1, 149, 150,   1997 03 31 , 10.3999/jscpt.28.149, http://ci.nii.ac.jp/naid/10011505756
  • Molecular Biology of Xeroderma Pigmentosum., 倉岡功, 松田外志朗, 田中亀代次, DNAトランスアクションと遺伝情報の安定性資料集 平成6年度 No.06354023, 134, 142,   1995 , http://jglobal.jst.go.jp/public/200902174431682230
  • DNA修復 変異と発がんの抑制機構 ヒト色素性乾皮症の分子生物学, 倉岡 功, 松田 外志朗, 田中 亀代次, 細胞工学, 13, 8, 701, 709,   1994 08
  • 急性心筋梗塞に合併する徐脈性不整脈に対する心房心室順次ペーシングの臨床的意義, 松田 外志朗, 足立 孝好, 本多 加津雄, 大阪警察病院医学雑誌, 15, 15, 18,   1991 09
    Summary:1)徐脈性不整脈を合併した急性心筋梗塞例に心室ペーシングを施行し,心不全が遷延する症例に心房心室順次ペーシングを施行した.2)全例において,心室ペーシングに比し心房心室順次ペーシングは,肺動脈拡張末期圧を低下させ,心拍出量の増加を認めた.3)体外式心室ペーシングにて血行動態の改善がみられなかった症例は,改善をみた症例に比し多枝病変例及び非再疎通例が多い傾向があった.4)急性期において再疎通が不成功であった多枝病変例では,徐脈性不整脈に対し心房心室順次ペーシングを考慮すべきであると考えられた
  • 心拍数が冠血流に及ぼす影響 FFT法ドプラーカテーテルによる検討, 松田 外志朗, 日本超音波医学会研究発表会講演論文集, 57回, 577, 578,   1990 10
  • NUCLEOTIDE EXCISION-REPAIR DEFECT AND CARCINOGENESIS IN XPA-KNOCKED OUT MICE, K TANAKA, Y NAKATSU, M SAIJO, KURAOKA, I, T MATSUDA, T KOBAYASHI, H MURAI, H NAKANE, JOURNAL OF CELLULAR BIOCHEMISTRY, 272, 272,   1995 03 , Refereed