九州大学 研究者情報
研究者情報 (研究者の方へ)入力に際してお困りですか?
基本情報 研究活動 教育活動 社会活動
柴田 弘紀(しばた ひろき) データ更新日:2019.06.26

准教授 /  生体防御医学研究所 附属トランスオミクス医学研究センター システム生命科学府 生命医科学講座


主な研究テーマ
ハブの島嶼集団間の毒液タンパク質多様性の解析
キーワード:ハブ、トカラハブ、サキシマハブ、ミトゲノム、毒液タンパク質、遺伝的分化、遺伝的多様性、南西諸島
2012.04.
痙性対麻痺の責任遺伝子DDHD1のマウスモデル作製と発症機序解明
キーワード:痙性対麻痺、DDHD1、ゲノム編集マウス、RNA-seq、メタボローム解析
2015.04.
日本固有の毒蛇ハブの島嶼集団間のミトゲノム多様性解析
キーワード:ハブ、トカラハブ、サキシマハブ、ミトゲノム、マイクロサテライトマーカー、遺伝的分化、遺伝的多様性、南西諸島
2012.04.
日本固有の毒蛇ハブの全遺伝子カタログ作成
キーワード:ハブ、次世代シークエンサ、cDNA、毒腺、蛇毒
2011.09.
日本固有の毒蛇ハブの全ゲノム配列決定
キーワード:ハブ、次世代シークエンサ、新規アセンブリ、スキャッフォールディング、遺伝子予測、蛇毒
2012.04.
家族性痙性対麻痺の遺伝解析
キーワード:痙性対麻痺、次世代シークエンサ、エクソーム解析、ゲノム編集マウス
2014.04.
脊髄小脳変性症の遺伝解析
キーワード:脊髄小脳変性症、連鎖解析、次世代シークエンサ、エクソーム解析
2014.04.
家族性てんかんの遺伝解析
キーワード:ミオクロヌスてんかん、連鎖解析、次世代シークエンサ、エクソーム解析
2011.04.
連鎖解析とエクソーム解析による家族性ニューロパチーの責任変異同定
キーワード:家族性運動感覚ニューロパチー、連鎖解析、次世代シークエンサ、エクソーム解析
2010.04.
統合失調症関連遺伝子としてのグルタミン酸受容体遺伝子群の進化学的解析
キーワード:統合失調症、グルタミン酸伝達系、分子進化、遺伝子多型、自然選択
2004.04~2013.03.
統合失調症とグルタミン酸受容体遺伝子群の関連解析
キーワード:統合失調症 関連解析 SNP 連鎖不平衡 ハプロタイプ グルタミン酸受容体
1999.05.
脊髄小脳失調症16型の原因遺伝子探索
キーワード:SCA16、小脳、運動失調、全ゲノムスキャン
2002.04~2006.03.
統合失調症の全ゲノム罹患同胞対解析
キーワード:統合失調症 ノンパラメトリック連鎖解析 罹患同胞対 マイクロサテライトマーカー
1999.05~2004.01.
従事しているプロジェクト研究
痙性対麻痺のモデルマウスの解析
2014.04, 代表者:柴田弘紀, 九州大学生体防御医学研究所, 九州大学生体防御医学研究所.
日本固有の毒蛇ハブの島嶼集団間の多様性解析
2012.04, 代表者:柴田弘紀, 九州大学生体防御医学研究所, 九州大学生体防御医学研究所.
毒蛇ハブとその近縁種の全ゲノム解析
2012.04, 代表者:柴田弘紀, 九州大学生体防御医学研究所, 九州大学生体防御医学研究所.
連鎖解析と次世代シークエンサによるターゲッテドリシークエンスによる疾患責任変異探索
2010.04, 代表者:柴田弘紀, 九州大学生体防御医学研究所, 九州大学生体防御医学研究所.
日本固有の毒蛇ハブの全遺伝子カタログ作成
2011.09, 代表者:柴田弘紀, 九州大学生体防御医学研究所, 九州大学生体防御医学研究所.
精神疾患関連遺伝子群の分子進化学的研究
2007.04, 代表者:柴田弘紀, 九州大学生体防御医学研究所.
グルタミン酸受容体遺伝子群のチンパンジー配列の決定と比較解析
2004.04, 代表者:柴田弘紀, 九州大学生体防御医学研究所, 九州大学 生体防御医学研究所 遺伝情報実験センター ゲノム機能学 (日本).
精神分裂病感受性遺伝子としてのグルタミン酸受容体遺伝子群の包括的研究
2002.04, 代表者:柴田弘紀, 九州大学生体防御医学研究所, 九州大学 生体防御医学研究所 遺伝情報実験センター ゲノム機能学(日本).
統合失調症モデル動物脳における遺伝子発現:DNA microarrayによる解析
2003.04, 代表者:黒木俊秀, 九州大学医学研究院, 国立肥前療養所(日本).
グルタミン酸受容体遺伝子群の多型検索及び精神分裂病との相関解析
2000.04~2002.03, 代表者:服巻保幸, 九州大学生体防御医学研究所, 九州大学 生体防御医学研究所 遺伝情報実験センター ゲノム機能学 (日本).
研究業績
主要著書
主要原著論文
1. Hiroki Shibata, Takahito Chijiwa, Naoko Oda-Ueda, Hitomi Nakamura, Kazuaki Yamaguchi, Shousaku Hattori, Kazumi Matsubara, Yoichi Matsuda, Akifumi Yamashita, Akiko Isomoto, Kazuki Mori, Kosuke Tashiro, Satoru Kuhara, Shinichi Yamasaki, Manabu Fujie, Hiroki Goto, Ryo Koyanagi, Takeshi Takeuchi, Yasuyuki Fukumaki, Motonori Ohno, Eiichi Shoguchi, Kanako Hisata, Noriyuki Satoh, Tomohisa Ogawa, The habu genome reveals an evolutionary background of venom protein genes., Sceintific Reports, 8: 11300., 2018.07, Evolution of novel traits is a challenging subject in biological research. Several snake lineages developed elaborate venom systems to deliver complex protein mixtures for prey capture. To understand mechanisms involved in snake venom evolution, we decoded here the ~1.4-Gb genome of a habu, Protobothrops flavoviridis. We identified 60 snake venom protein genes (SV) and 224 nonvenom paralogs (NV), belonging to 18 gene families. Molecular phylogeny reveals early divergence of SV and NV genes, suggesting that one of the four copies generated through two rounds of whole genome duplication was modified for use as a toxin. Among them, both SV and NV genes in four major components were extensively duplicated after their diversification, but accelerated evolution is evident exclusively in the SV genes. Both venom-related SV and NV genes are significantly enriched in microchromosomes. The present study thus provides a genetic background for evolution of snake venom composition..
2. Hiroki Shibata, Shuichi Sakata, Yuzo Hirano, Eiji Nitasaka, Ai Sakabe. , Facultative parthenogenesis validated by DNA analyses in the green anaconda (Eunectes murinus)., Plos ONE, 12, 12, e0189654, 2017.12, In reptiles, the mode of reproduction is typically sexual. However, facultative parthenogenesis occurs in some Squamata, such as Komodo dragon (Varanus komodoensis) and Burmese python (Python bivittatus). Here, we report facultative parthenogenesis in the green anaconda (Eunectes murinus). We found two fully developed female neonates and 17 undeveloped eggs in the oviduct of a female anaconda isolated from other individuals for eight years and two months at Ueno Zoo, Japan. To clarify the zygosity of the neonates, we analyzed 18 microsatellite markers of which 16 were informative. We observed only maternal alleles and no paternal alleles for all 16 markers. To examine the possibility of the long-term sperm storage, we estimated allele frequencies in a putative parental stock by genotyping five unrelated founders. If all founders, including the mother, are originated from a single Mendelian population, then the probability that the neonates were produced by sexual reproduction with an unrelated male via long-term sperm storage was infinitesimally small (2.31E-32 per clutch). We also examined samples from two additional offspring that the mother delivered eight years before her death. We consistently observed paternal alleles in these elder offspring, indicating that the mother had switched from sexual reproduction to asexual reproduction during the eight years of isolation. This is the first case of parthenogenesis in Eunectes to be validated by DNA analysis, and suggests that facultative parthenogenesis is widespread in the Boidae..
3. Shiroh Miura, Takuya Morikawa, Ryuta Fujioka, Kazuhito Noda, Kengo Kosaka, Takayuki Taniwaki, Hiroki Shibata, A novel missense variation (Q220R) of GNB4 encoding a guanine nucleotide-binding protein, beta-4 in a Japanese autosomal dominant motor and sensory neuropathy family., European Journal of Medical Genetics, 60, 9, 474-478, 2016.06, Dominant intermediate CharcoteMarieeTooth disease F (CMTDIF) is an autosomal dominant hereditary form of CharcoteMarieeTooth disease (CMT) caused by variations in the guanine nucleotide-binding protein, subunit beta-4 gene (GNB4). We examined two Japanese familial cases with CMT. Case 1 was a 49-year-old male whose chief complaint was slowly progressive gait disturbance and limb dysesthesia that appeared at the age of 47. On neurological examination, he showed hyporeflexia or areflexia, distal limb muscle weakness, and distal sensory impairment with lower dominancy. Nerve conduction studies demonstrated demyelinating sensorimotor neuropathy with reduced action potentials in the lower limbs. Case 2 was an 80-year-old man, Case 1's father, who reported difficulty in riding a bicycle at the age of 76. On neurological examination, he showed areflexia in the upper and lower limbs. Distal sensory
impairment in the lower limbs was also observed. Nerve conduction studies revealed mainly axonal involvement. Exome sequencing identified a novel heterozygous nonsynonymous variant (NM_021629.3:c.659T > C [p.Gln220Arg]) in GNB4 exon 8, which is known to be responsible for CMT. Sanger sequencing confirmed that both patients are heterozygous for the variation, which causes an amino acid substitution, Gln220Arg, in the highly conserved region of the WD40 domain of GNB4. The frequency of this variant in the Exome Aggregation Consortium Database was 0.000008247, and we confirmed its absence in 502 Japanese control subjects. We conclude that this novel GNB4 variant is causative for CMTDIF in these patients, who represent the first record of the disease in the Japanese
population..
4. Shiroh Miura, Takuya Morikawa, Ryuta Fujioka, Kengo Kosaka, Kohei Yamada, Kazuhito Noda, Gohsuke Hattori, Manabu Motomura, Takayuki Taniwaki, Hiroki Shibata, A novel frameshift mutation of DDHD1 in a Japanese patient with autosomal recessive spastic paraplegia., European Journal of Medical Genetics, 10.1016/j.ejmg.2016.05.010, 59, 8, 413-416, 2016.05, Spastic paraplegia (SPG) type 28 is an autosomal recessive SPG caused by mutations in the DDHD1 gene. We examined a Japanese 54-years-old male patient with autosomal recessive SPG. His parents were consanguineous. He needed a wheelchair for transfer due to spastic paraplegia. There was a history of operations for bilateral hallux valgus, thoracic ossification of the yellow ligament, bilateral carpal tunnel syndrome, bilateral ankle contracture, and lumbar spinal canal stenosis. He noticed gait disturbance at age 14. He used a cane for walking in his 40s. On neurological examination, he showed hyperreflexia, spasticity, and weakness in the lower extremities and bilateral Babinski reflexes. Urinary dysfunctions and impaired vibration sense in the lower limbs were observed. By exome sequencing analysis using Agilent SureSelect and Illumina MiSeq, we identified 17,248 homozygous nucleotide variants in the patient. Through the examination of 48 candidate genes known to be responsible for autosomal recessive SPG, we identified a novel homozygous 4-bp deletion, c.914_917delGTAA, p.Ser305Ilefs*2 in exon2 of the DDHD1 gene encoding phosphatidic acid-preferring phospholipase A1 (PA-PLA1). The mutation is expected to cause a frameshift generating a premature stop codon 3-bp downstream from the deletion. In consequence, the DDHD domain that is known to be critical for PLA1 activity is completely depleted in the mutated DDHD1 protein, predicted to be a functionally null mutation of the DDHD1 gene. By Sanger sequencing, we confirmed that both parents are heterozygous for the mutation. This variation was not detected in 474 Japanese control subjects as well as the data of the 1,000G Project. We conclude that the novel mutation in DDHD1 is the causative variant for the SPG28 patient that is the first record of the disease in Japanese population..
5. Hiroki Shibata, Takahito Chijiwa, Shosaku Hattori, Koki Terada, Motonori Ohno, Yasuyuki Fukumaki, The taxonomic position and the unexpected divergence of the Habu viper, Protobothrops among Japanese subtropical islands., Molecular Phylogenetics and Evolution, 10.1016/j.ympev.2016.04.027, 101, 91-100, 2016.04, There are four Habu species currently recognized in Japan: Protobothrops flavoviridis from the Amami Islands and the Okinawa Islands, P. tokarensis from the Tokara Islands, P. elegans from the Yaeyama Islands and Ovophis okinabvensis from the Amami Islands and the Okinawa Islands. To clarify their taxonomic positions, we determined the complete mitochondria genome sequence (approx. 17 kb) from two specimens from two different islands each for P. flavoviridis, P. tokarensis and P. elegans as well as one specimen of O. okinavensis and reconstructed the molecular phylogeny of Protobothrops using the published sequences of related species. The maximum likelihood tree showed four major species groups within Protbothrops: Group I consisting of P. cornutus, P. dabieshanensis, P. jerdonii and P. xiangchengensis; Group II consisting of P. flavoviridis and P. tokarensis; Group III consisting of P. maolensis, P. mucrosquamatus and P. elegans; Group IV consisting of P. himalayanus and P. kaubacki. Since we observed an unexpected divergence and the paraphyly of the two samples of P. flavoviridis collected from different islands, Amami-Oshima and Okinawajima within the Group II, we expanded the analysis by increasing the number of P. flavoviridis and P. tokarensis collected from 10 islands: Amami-Oshima (5 specimens), Kakeromajima (4) and Tokunoshima (4) from the Amami Islands, Okinawajima (4), Iheyajima (4), Iejima (4), Tokashikijima (4) and Kumejima (4) from the Okinawa Islands, Kodakarajima (P. tokarensis) (4) and Takarajima (P. tokarensis) (4) from the Tokara Islands. The maximum likelihood tree of the 44 samples replicated the significant divergence of P. flavoviridis between the Amami Clade including Amami-Oshima, Kakeromajima and Tokunoshima and the Okinawa Clade including Okinawajima, Iheyajima, Iejima, Tokashikijima and Kumejima. The Amami Clade also include all specimens from the Tokara Islands currently known as an independent species, P. tokarensis, suggesting the paraphyly of the taxon, P. flavoviridis. In contrast, we observed a distinct lineage of the two specimens from the Yaeyama Islands, supporting the validity of the taxon, P. elegans as an independent species. By MCMC method, we estimated the divergence time between the Amami Clade and the Okinawa Clade to be 6.51 MYA, suggesting that the vicariance of the two clades preceded the geological separation of the Amami Islands and the Okinawa Islands (~1.5 MYA). As expected from the limited mobility of terrestrial reptiles including snakes, we observed high genetic divergence in Habu mtDNA among Japanese subtropical island populations..
6. Ken Sano, Shiroh Miura, Toshiya Fujiwara, Ryuta Fujioka, Akiko Yorita, Kazuhito Noda, Hiroshi Kida, Koichi Azuma, Shinjiro Kaieda, Ken Yamamoto, Takayuki Taniwaki, Yasuyuki Fukumaki, Hiroki Shibata, A novel missense mutation of RYR1 in familial idiopathic hyper CK-emia, Journal of Neurological Sciences, 10.1016/j.jns.2015.06.035, 356, 1-2, 142-147, 2015.09, Persistent elevation of serum creatine kinase (CK) without any symptoms has been called idiopathic hyper CKemia
(IHCK).We examined a four-generation Japanese pedigree of familial IHCK. Themultipoint linkage analysis
of the pedigree showed seven clear peaks of logarithm of odds (LOD) scores (>1.4). By the exome sequencing
followed bymultiple filtering processes,we identified one novel heterozygous nonsynonymous single nucleotide
variant (SNV), c.7034GNC, p.S2345T in the ryanodine receptor 1 gene, RYR1 cosegregated with IHCK in the pedigree.
Mutation Taster predicted this substitution as “disease causing” (p = 0.999). The PolyPhen-2 and PANTHER
subPSEC scores for the substitution are 0.911 (possibly damaging) and−3.56 (probably damaging), respectively.
We confirmed the absence of the SNV in 511 healthy Japanese individuals excluding the possibility of a normal
variant with a very low frequency. Immunohistochemistry andWestern blotting of biopsy samples consistently
showed the expression level of RYR1 reduced in the patient. In real-time RT-PCR, the mRNA expression level of
RYR1 was also significantly reduced in the patient (p = 0.009). These results suggest that the novel
nonsynonymous SNV contribute to the vulnerability of the RYR1 protein through the dominant negative effect.
We conclude that the SNV in the RYR1 gene is one of the responsible genes of IHCK..
7. Naoki Kubo, Hidehiro Toh, Kenjiro Shirane, Takayuki Shirakawa, Hisato Kobayashi, Sato Tetsuya, Hidetoshi Sone, Yasuyuki Sato, Shin-ichi Tomizawa, Yoshinori Tsurusaki, Hiroki Shibata, Hirotomo Saitsu, Yutaka Suzuki, Naomichi Matsumoto, Tomohiro Kono, Kazuyuki Ohbo, Hiroyuki Sasaki, DNA methylation and gene expression dynamics during spermatogonial stem cell differentiation in the early postnatal mouse testis., BMC Genomics, 10.1186/s12864-015-1833-5, 16, 1, 624-624, 2015.08, Background: In the male germline, neonatal prospermatogonia give rise to spermatogonia, which include stem cell
population (undifferentiated spermatogonia) that supports continuous spermatogenesis in adults. Although the levels of
DNA methyltransferases change dynamically in the neonatal and early postnatal male germ cells, detailed genome-wide
DNA methylation profiles of these cells during the stem cell formation and differentiation have not been reported.
Results: To understand the regulation of spermatogonial stem cell formation and differentiation, we examined the DNA
methylation and gene expression dynamics of male mouse germ cells at the critical stages: neonatal prospermatogonia,
and early postntal (day 7) undifferentiated and differentiating spermatogonia. We found large partially methylated
domains similar to those found in cancer cells and placenta in all these germ cells, and high levels of non-CG
methylation and 5-hydroxymethylcytosines in neonatal prospermatogonia. Although the global CG methylation levels
were stable in early postnatal male germ cells, and despite the reported scarcity of differential methylation in the adult
spermatogonial stem cells, we identified many regions showing stage-specific differential methylation in and around
genes important for stem cell function and spermatogenesis. These regions contained binding sites for specific
transcription factors including the SOX family members.
Conclusions: Our findings show a distinctive and dynamic regulation of DNA methylation during spermatogonial stem
cell formation and differentiation in the neonatal and early postnatal testes. Furthermore, we revealed a unique
accumulation and distribution of non-CG methylation and 5hmC marks in neonatal prospermatogonia. These findings
contrast with the reported scarcity of differential methylation in adult spermatogonial stem cell differentiation and
represent a unique phase of male germ cell development..
8. Hiroki Shibata, Ken Yamamoto, Zhu Sun, Akira Oka, Hidetoshi Inoko, Tadao Arinami, Toshiya Inada, Hiroshi Ujike, Masanari Itokawa, Mamoru Tochigi, Yuichiro Watanabe, Toshiyuki Someya, Hiroshi Kunugi, Tatsuyo Suzuki, Nakao Iwata, Norio Ozaki, Yasuyuki Fukumaki, Genome-wide association study of schizophrenia using microsatellite markers in the Japanese population., Psychiatr Genetics, 23, 3, 117-123, 2013.06, OBJECTIVES: To search for schizophrenia susceptibility loci, we carried out a case-control study using 28601 microsatellite markers distributed across the entire genome.
MATERIALS AND METHODS: To control the highly multiple testing, we designed three sequential steps of screening using three independent sets of pooled samples, followed by the confirmatory step using an independent sample set (>2200 case-control pairs).
RESULTS: The first screening using pooled samples of 157 case-control pairs showed 2966 markers to be significantly associated with the disorder (P<0.05). After the second and the third screening steps using pooled samples of 150 pairs each, 374 markers remained significantly associated with the disorder. We individually genotyped all screening samples using a total of 1536 tag single nucleotide polymorphisms (SNPs) located in the vicinity of ∼200 kb from the 59 positive microsatellite markers. Of the 167 SNPs that replicated the significance, we selected 31 SNPs on the basis of the levels of P values for the confirmatory association test using an independent-sample set. The best association signal was observed in rs13404754, located in the upstream region of SLC23A3. We genotyped six additional SNPs in the vicinity of rs13404754. Significant associations were observed in rs13404754, rs6436122, and rs1043160 in the cumulative samples (2617 cases and 2698 controls) (P=0.005, 0.035, and 0.011, respectively). These SNPs are located in the linkage disequilibrium block of 20 kb in size containing SLC23A3, CNPPD1, and FAM134A genes.
CONCLUSION: Genome-wide association study using microsatellite markers suggested SLC23A3, CNPPD1, and FAM134A genes as candidates for schizophrenia susceptibility in the Japanese population..
9. Hiroki Goto, Kazunori Watanabe, Naozumi Araragi, Rui Kageyama, Kunika Tanaka, Yoko Kuroki, Atsushi Toyoda, Masahira Hattori, Yoshiyuki Sakaki, Asao Fujiyama, Yasuyuki Fukumaki, Hiroki Shibata., The identification and functional implications of human-specific "fixed" amino acid substitutions in the glutamate receptor family., BMC Evolutionary Biology., 9: 224, 2009.09, [URL], Background: The glutamate receptors (GluRs) play a vital role in the mediation of excitatory synaptic transmission in the central nervous system. To clarify the evolutionary dynamics and mechanisms of the GluR genes in the lineage leading to humans, we determined the complete sequences of the coding regions and splice sites of 26 chimpanzee GluR genes.
Results: We found that all of the reading frames and splice sites of these genes reported in humans were completely conserved in chimpanzees, suggesting that there were no gross structural changes in humans after their divergence from the human-chimpanzee common ancestor. We observed low KA/KS ratios in both humans and chimpanzees, and we found no evidence of accelerated evolution. We identified 30 human-specific "fixed" amino acid substitutions in the GluR genes by analyzing 80 human samples of seven different populations worldwide. Grantham's distance analysis showed that GRIN2C and GRIN3A are the most and the second most diverged GluR genes between humans and chimpanzees. However, most of the substitutions are non-radical and are not clustered in any particular region. Protein motif analysis assigned 11 out of these 30 substitutions to functional regions. Two out of these 11 substitutions, D71G in GRIN3A and R727H in GRIN3B, caused differences in the functional assignments of these genes between humans and other apes.
Conclusion: We conclude that the GluR genes did not undergo drastic changes such as accelerated evolution in the human lineage after the divergence of chimpanzees. However, there remains a possibility that two human-specific "fixed" amino acid substitutions, D71G in GRIN3A and R727H in GRIN3B, are related to human-specific brain function.
.
10. Hiroki Shibata, Ayako Tani, Tomoyuki Chikuhara, Rumiko Kikuta, Mayumi Sakai, Hideaki Ninomiya, Nobutada Tashiro, Nakao Iwata, Norio Ozaki and Yasuyuki Fukumaki. , Association study of polymorphisms in the group III metabotropic glutamate receptor genes, GRM4 and GRM7, with schizophrenia. , Psychiatric Res. , 167:88-96., 2009.04, Based on the hypothesis that a glutamatergic dysfunction is involved in the pathophysiology of schizophrenia, we have been conducting systematic studies on the association between glutamate receptor genes and schizophrenia. Here we report association studies of schizophrenia with polymorphisms in group III metabotropic glutamate receptor genes, GRM4 and GRM7. We selected 8 and 43 common SNPs distributed in the entire gene regions of GRM4 (> 111 kb) and GRM7 (> 900 kb), respectively. We scanned significant associations with schizophrenia using 100 case-control pairs of Japanese. We identified two neighboring SNPs (rs12491620 and rs1450099) in GRM7 showing highly significant haplotype association with schizophrenia surviving the FDR correction. We then performed additional typing of the two SNPs using the expanded sample set (404 cases and 420 controls) and confirmed the significant association with the disease. We conclude that at least one susceptibility locus for schizophrenia is located within or nearby GRM7, whereas GRM4 is unlikely to be a major susceptibility gene for schizophrenia in the Japanese population..
11. Shibata H, Aramaki T, Sakai M, Ninomiya H, Tashiro N, Iwata N, Ozaki N and Fukumaki Y., Association study of polymorphisms in the GluR7, KA1 and KA2 kainate receptor genes (GRIK3, GRIK4, GRIK5) with schizophrenia., Psychiatry Res., 141: 39-51, 2006.01.
12. Makino C, Shibata H, Ninomiya H, Tashiro N, Fukumaki Y., Identification of single-nucleotide polymorphisms in the human N-methyl-D-aspartate receptor subunit NR2D gene, GRIN2D, and association study with schizophrenia., Psychiatr Genet., 10.1097/00041444-200509000-00014, 15, 3, 215-221, 15 (3): 215-221., 2005.09.
13. Deng XD, Shibata H, Ninomiya H, Tashiro N, Iwata N, Ozaki N and Fukumaki Y., Association study of polymorphisms in the excitatory amino acid transporter 2 gene (SLC1A2) with schizophrenia., BMC Psychiatry, 10.1186/1471-244X-4-21, 4, 4(1): 21, 2004.08.
14. Takaki H, Kikuta R, Shibata H, Ninomiya H, Tashiro N and Fukumaki Y., Positive associations of polymorphisms in the metabotropic glutamate receptor type 8 gene (GRM8) with schizophrenia., Am J Med Genet., 10.1002/ajmg.b.20108, 128B, 1, 6-14, 128B: 6-14., 2004.07.
15. The Japanese Schizophrenia Sib-pair Linkage Group., Initial genome-wide scan for linkage with schizophrenia in the Japanese Schizophrenia Sib-pair Linkage Group (JSSLG) families., Am J Med Genet., 10.1002/ajmg.b.20022, 120B, 1, 22-28, 120B(1): 22-8., 2003.07.
16. Fujii Y, Shibata H, Kikuta R, Makino C, Tani A, Hirata N, Shibata A, Ninomiya H, Tashiro N, Fukumaki Y., Positive associations of polymorphisms in the metabotropic glutamate receptor type 3 gene (GRM3) with schizophrenia., Psychiatric Genetics., 10.1097/01.ypg.0000056682.82896.b0, 13, 2, 71-76, 13(2):71-6., 2003.06.
17. Makino C, Fujii Y, Kikuta R, Hirata N, Tani A, Shibata A, Ninomiya H, Tashiro N, Shibata H, Fukumaki Y., Positive association of the AMPA receptor subunit GluR4 gene (GRIA4) haplotype with schizophrenia: linkage disequilibrium mapping using SNPs evenly distributed across the gene region., Am J Med Genet., 10.1002/ajmg.b.10041, 116B, 1, 17-22, 116B (1): 17-22., 2003.01.
18. Shibata H, Shibata A, Ninomiya H, Tashiro N, Fukumaki Y., Association study of polymorphisms in the GluR6 kainate receptor gene (GRIK2) with schizophrenia., Psychiatry Res., 10.1016/S0165-1781(02)00231-7, 113, 1-2, 59-67, 113(1-2): 59-67., 2002.12.
19. Tani A, Kikuta R, Itoh K, Joo A, Shibata H, Ninomiya H, Tashiro N and Fukumaki Y., Polymorphism analysis of upstream regions of the human N-methyl-D-aspartate receptor subunit NR1 gene (GRIN1): implications for schizophrenia., Schizophr Research, 10.1016/S0920-9964(02)00161-5, 58, 1, 83-86, 58 (1):83-86., 2002.11.
20. Shibata H, Joo A, Fujii Y, Tani A, Makino C, Hirata N, Kikuta R, Ninomiya H, Tashiro N, Fukumaki Y., Association study of polymorphisms in the coding region of the GluR5 kainate receptor gene (GRIK1) with schizophrenia., Psychiatric Genetics, 10.1097/00041444-200109000-00005, 11, 3, 139-144, 11 (3): 139-144., 2001.09.
21. Kiehl TR, Shibata H, Huynh DP, Vo T, Pulst SM., Identification and expression of a mouse ortholog of A2BP1., Mammalian Genome., 12 (8): 595-601., 2001.08.
22. Shibata H, Huynh DP, Pulst SM., A novel protein with RNA binding motif binds to C-terminal ataxin-2., Human Molecular Genetics, 9 (9): 1303-1313., 2000.05.
23. Shibata H, Tahira T, Hayashi K., RNA-primed PCR., Genome Research, 10.1101/gr.5.4.400, 5, 4, 400-403, 5 (4): 400-403., 1995.11.
24. Shibata H, Yamazaki T., Molecular evolution of the duplicated Amy locus in the Drosophila melanogaster species subgroup: concerted evolution only in coding region and an excess of nonsynonymous substitutions in speciation., Genetics, 141, 1, 223-236, 141 (1): 223-236., 1995.09.
主要総説, 論評, 解説, 書評, 報告書等
主要学会発表等
1. Shiroh Miura, Kengo Kosaka, Ryuta Fujioka, Takayuki Taniwaki, Hiroki Shibata, Genetic analysis of autosomal dominant motor and sensory neuropathy with proximal dominancy in the lower extremities, urinary disturbance, and paroxysmal dry cough., The European Human Genetics Conference 2019, 2019.06.
2. Takuya Morikawa, Shiroh Miura, Hiroaki Ohishi, Kengo Kosaka, Tomofumi Shimojo, Akihiro Nagano, Ryuta Fujioka, Kosei Moriyama, Motoko Unoki, Masatomo Takahashi, Motonao Nakao, Yoshihiro Izumi, Takeshi Bamba, Hiroyuki Sasaki, Hiroki Shibata, Ddhd1 knockout mouse as a model for familial spastic paraplegia., The European Human Genetics Conference 2019, 2019.06.
3. 柴田弘紀, 千々岩崇仁, 小田-上田直子, 服部正策, 松原和純, 松田洋一, 山崎慎一, 藤江学, 後藤大輝, 小柳亮, 竹内猛, 服巻保幸, 大野素徳, 将口栄一, 久田香奈子, 佐藤矩行, 小川智久, ハブ(Protobothrops flavoviridis)の全ゲノム配列決定から明らかになった毒液関連遺伝子群の多重化および加速進化と染色体構造との関係., 日本爬虫両棲類学会第57回大会, 2018.11.
4. Miura S, Shimojo T, Kosaka K, Fujioka R, Taniwaki T, Shibata H., Exome sequencing in sporadic patients with young-onset parkinsonism reveals novel candidates., 2018 American Neurological Association Annual Meeting, 2018.11.
5. Shibata H, Chijiwa T, Oda-Ueda N, Yamaguchi K, Hattori S, Matsubara K, Matsuda Y, Isomoto A, Koyanagi R, Hisata K, Fukumaki Y, Ohno M, Shoguchi E, Satoh N, Ogawa T. , Whole genome sequencing of a Japanese endemic pit viper, habu, Protobothrops flavoviridis reveals accelerated evolution of venom protein genes enriched in microchromosomal regions., The International Society of Toxinology 2018 European Section Congress, 2018.09.
6. Shibata H, Chijiwa T, Oda-Ueda N, Yamaguchi K, Hattori S, Matsubara K, Matsuda Y, Koyanagi R, Hisata K, Fukumaki Y, Ohno M, Shoguchi E, Satoh N, Ogawa T. , Whole genome sequencing of a Japanese endemic pit viper, habu, Protobothrops flavoviridis reveals accelerated evolution of venom protein genes enriched in microchromosomal regions., SMBE 2018, 2018.07.
7. Miura S, Kosaka K, Fujioka R, Uchiyama Y, Taniwaki T, Shimojo T, Shibata H., A novel nonsense variant (Lys177X) of FGF14 in a Japanese patient with autosomal dominant spinocerebellar ataxia., The European Human Genetics Conference 2018, 2018.06.
8. 小川智久, 千々岩崇仁, 小田-上田直子, 中村仁美, 服部正策, 松原和純, 松田洋一, 森一樹, 田代康介, 久原哲, 山崎慎一, 藤江学, 後藤大輝, 小柳亮, 竹内猛, 服巻保幸, 大野素徳, 将口栄一. 久田香奈子, 佐藤矩行, 柴田弘紀, ハブゲノム解読により明らかになった毒関連遺伝子の進化., 第40回日本分子生物学会年会, 2017.12.
9. Shiroh Miura, Takuya Morikawa, Ryuta Fujioka, Kazuhito Noda, Kengo Kosaka, Takayuki Taniwaki, Hiroki Shibata, A novel missense variation (Q220R) of GNB4 encoding a guanine nucleotide-binding protein, beta-4 in a Japanese neuropathy family., The European Human Genetics Conference 2017, 2017.05.
10. Hiroki Shibata, Accelerated evolution of venom protein genes in the habu genome., Global Symposium GEM , 2017.03.
11. Tomohisa Ogawa, Takahito Chijiwa, Naoko Oda-Ueda, Hitomi Nakamura, Shousaku Hattori, Kazumi Matsubara, Yoichi Matsuda, Kazuki Mori, Kosuke Tashiro, Shinichi Yamasaki, Manabu Fujie, Hiroki Goto, Ryo Koyanagi, Yasuyuki Fukumaki, Motonori Ohn, Eiichi Shoguchi, Kanako Hisata, Noriyuki Satoh, Hiroki Shibata, Habu snake genome reveals the evolutionary strategy for generating the venom-related genes., Global Symposium GEM , 2017.03.
12. 柴田弘紀, 千々岩崇仁, 上田直子, 中村仁美, 服部正策, 松原和純, 松田洋一, 森 一樹, 田代 康介, 久原 哲, 山崎慎一, 藤江学, 後藤大輝, 将口栄一, 久田香奈子, 小柳亮, 佐藤矩行, 大野素徳, 服巻保幸, ハブ(Protobothrops flavoviridis)の全ゲノム配列決定から明らかになった毒液関連遺伝子群の多重化と加速進化および染色体構造との関係, 第39回日本分子生物学会年会, 2016.12.
13. 森川拓弥, 三浦史郎, 小坂健悟, 藤岡竜太, 佐野 謙, 頼田章子, 内山雄介, 谷脇考恭, 柴田弘紀, 脊髄小脳変性症に関わる新規責任遺伝子の同定, 第39回日本分子生物学会年会, 2016.12.
14. 柴田弘紀, 千々岩崇仁, 上田直子, 中村仁美, 服部正策, 松原和純, 松田洋一, 森 一樹, 田代 康介, 久原 哲, 山崎慎一, 藤江学, 後藤大輝, 将口栄一, 久田香奈子, 小柳亮, 佐藤矩行, 大野素徳, 服巻保幸, ハブ(Protobothrops flavoviridis)の全ゲノム配列決定から明らかになった毒液関連遺伝子群の多重化と加速進化および染色体構造との関係, 第55回日本爬虫両棲類学会大会, 2016.11.
15. Takuya Morikawa, Shiroh Miura, Kengo Kosaka, Ryuta Fujioka, Ken Sano, Akiko Yorita, Kosuke Aoki, Yusuke Uchiyama, Takayuki Taniwaki, Hiroki Shibata, Heterozygous missense mutation in SEC24A encoding a coat protein complex II vesicle associated with autosomal dominant spinocerebellar ataxia., 66th Annual Meeting of The American Society of Human Genetics, 2016.10.
16. Ryuta Fujioka, Shiroh Miura, Kohei Yamada, Takuya Morikawa, Hiromichi Motooka, Yasuhiro Aso, Noriyuki Kimura, Ken Sano, Ken Yamamoto, Takayuki Taniwaki, Hiroki Shibata, A missense mutation in the PPIG gene encoding the peptidyl-prolyl isomerase G in patients with autosomal dominant benign adult familial myoclonic epilepsy., 66th Annual Meeting of The American Society of Human Genetics, 2016.10.
17. 柴田弘紀, 千々岩崇仁, 上田直子, 中村仁美, 服部正策, 松原和純, 松田洋一, 森 一樹, 田代 康介, 久原 哲, 山崎慎一, 藤江学, 後藤大輝, 将口栄一, 久田香奈子, 小柳亮, 佐藤矩行, 大野素徳, 服巻保幸, 毒蛇ハブ(Protobothrops flavoviridis)の全ゲノム配列決定から明らかになった毒液関連遺伝子群の多重化と染色体構造との関係, 第89回日本生化学会大会, 2016.09.
18. 森川拓弥, 三浦史郎, 藤岡竜太, 小坂健悟, 山田浩平, 服部剛典, 本村学, 谷脇考恭, 柴田弘紀, SPG28の発症に関わるDDHD1内の新規ホモ接合変異の同定, 日本遺伝学会第88回大会, 2016.09.
19. 小坂健悟, 三浦史郎, 佐野謙, 藤岡竜太, 才津浩智, 谷脇考恭, 山本健, 柴田弘紀, 連鎖解析とエクソームシーケンスによる新規ニューロパチー家系の疾患責任遺伝子変異の同定, 日本遺伝学会第88回大会, 2016.09.
20. 柴田弘紀, 千々岩崇仁, 上田直子, 中村仁美, 服部正策, 松原和純, 松田洋一, 森 一樹, 田代 康介, 久原 哲, 山崎慎一, 藤江学, 後藤大輝, 将口栄一, 久田香奈子, 小柳亮, 佐藤矩行, 大野素徳, Yasuyuki Fukumaki, 日本固有の毒蛇ハブ(Protobothrops flavoviridis)の全ゲノム配列決定と遺伝子モデルの作製, 第63回トキシンシンポジウム, 2016.07.
21. 森川拓弥, 三浦史郎, 山田浩平, 服部剛典, 小坂健悟, 藤岡竜太, 本村学, 谷脇考恭, 柴田弘紀, Homozygous 4-bp deletion in the DDHD1 gene, resulting the complete deletion of DDHD domain, as a causative variant in a SPG28 patient., The 13th International Congress of Human Genetics, 2016.04.
22. 柴田弘紀, 千々岩崇仁, 上田直子, 中村仁美, 服部正策, 松原和純, 松田洋一, 森 一樹, 田代 康介, 久原 哲, 山崎慎一, 藤江学, 後藤大輝, 将口栄一, 久田香奈子, 小柳亮, 佐藤矩行, 大野素徳, Yasuyuki Fukumaki, 日本固有の毒蛇ハブ(Protobothrops flavoviridis)の全ゲノム配列決定と遺伝子モデルの作製, 第54回日本爬虫両棲類学会大会, 2015.12.
23. 柴田弘紀, 千々岩崇仁, 上田直子, 中村仁美, 服部正策, 松原和純, 松田洋一, 森 一樹, 田代 康介, 久原 哲, 山崎慎一, 藤江学, 後藤大輝, 将口栄一, 久田香奈子, 小柳亮, 佐藤矩行, 大野素徳, Yasuyuki Fukumaki, 日本固有の毒蛇ハブ(Protobothrops flavoviridis)の全ゲノム配列決定と遺伝子モデルの作製, 第38回日本分子生物学会年会、第88回日本生化学会大会合同大会, 2015.12.
24. 柴田弘紀, 千々岩崇仁, 上田直子, 服部正策, 小柳亮, 久田香奈子, 佐藤矩行, 大野素徳, Yasuyuki Fukumaki, 小川智久, 日本固有の毒蛇ハブ(Protobothrops flavoviridis)の全ゲノム配列決定と遺伝子モデルの作製, 第87回日本遺伝学会大会, 2015.09.
25. 柴田弘紀, 山本真由美, タケット奈々, 小川智久, 森一樹, 千々岩崇仁, 服部正策, 上田直子, 久原 哲, 大野素徳, 服巻保幸, 日本固有の毒蛇ハブ(Protobothrops flavoviridis)の全ゲノムシークエンスと繰り返し配列の解析, 第36回日本分子生物学会年会, 2013.12.
26. 柴田弘紀, 山本真由美, タケット奈々, 小川智久, 森一樹, 千々岩崇仁, 服部正策, 上田直子, 久原 哲, 大野素徳, 服巻保幸, 日本固有の毒蛇ハブ(Protobothrops flavoviridis)の全ゲノムシークエンスと繰り返し配列の解析, 日本爬虫両棲類学会第52回大会, 2013.11.
27. 柴田弘紀, 山本真由美, タケット奈々, 小川智久, 森一樹, 千々岩崇仁, 服部正策, 上田直子, 久原 哲, 大野素徳, 服巻保幸, 日本固有の毒蛇ハブ(Protobothrops flavoviridis)の全ゲノムシークエンスと繰り返し配列の解析, 第85回日本遺伝学会大会, 2013.09.
28. 柴田弘紀, 山本真由美, タケット奈々, 小川智久, 森一樹, 千々岩崇仁, 服部正策, 上田直子, 久原 哲, 大野素徳, 服巻保幸, 日本固有の毒蛇ハブ(Protobothrops flavoviridis)の全ゲノムシークエンスと繰り返し配列の解析, 第15回日本進化学会大会, 2013.08.
29. 柴田 弘紀, 山本真由美, 千々岩崇仁, 服部正策, 上田直子, 大野素徳, 服巻 保幸, Genetic divergence of mitochondria genome sequence among island populations of Japanese Habu snakes, Protobothrops., 第35回日本分子生物学会年会, 2012.12.
30. 藤原敏弥, 柴田 弘紀, 三浦史郎, 山本真由美, 貴田浩志, 野田和人, 加來庸一郎, 岩城 明子, 綾部光芳, 谷脇考恭, 服巻 保幸, Linkage-Exome approach to identify the responsible variant for a novel type of hereditary neuropathy, 第35回日本分子生物学会年会, 2012.12.
31. 藤原敏弥, 柴田 弘紀, 三浦史郎, 山本真由美, 貴田浩志, 野田和人, 加來庸一郎, 岩城 明子, 綾部光芳, 谷脇考恭, 服巻 保幸, 連鎖・エクソームアプローチによる新規家族性ニューロパチーの変異検索, 第84回日本遺伝学会大会, 2012.09.
32. Shibata H, Miura S, Kida H, Noda K, Kaku Y, Iwaki A, Ayabe M, Taniwaki T, Fukumaki Y., Linkage-assisted exome sequencing to identify the responsible variant for a novel type of hereditary motor and sensory neuropathy with proximal dominancy in the lower extremities found in a single Japanese family., Human Genome Meeting 2012, 2012.03.
33. Shibata H, Miura S, Kida H, Noda K, Kaku Y, Iwaki A, Ayabe M, Taniwaki T, Fukumaki Y., Exome sequencing approach to identify the responsible variant for a novel type of hereditary motor and sensory neuropathy with proximal dominancy in the lower extremities found in a Japanese descent., 12th International Congress of Human Genetics / 61st Annual Meeting of The American Society of Human Genetics, Montreal, Canada, 2011.10.
34. Yu Liang, Yasuyuki Fukumaki, Hiroki Shibata, Resequencing of dopamine receptor genes DRD1 and DRD2 as schizophrenia susceptibility genes revealed non-neutral process possibly associated with schizophrenia., 第33回日本分子生物学会年会、第83回日本生化学会大会合同大会, 2010.12.
35. Hiroki Shibata, Maiko Uchida, Hiroki Goto, Shuhei Mano, Osamu Takenaka, Yasuyuki Fukumaki, Resequencing of the catechol-O-methyltransferase gene, COMT revealed non-neutral processes associated with schizophrenia., 60th Annual Meeting of The American Society of Human Genetics, 2010.11.
36. 柴田弘紀、内田麻衣子、後藤大輝、間野修平、竹中 修、服巻保幸, 統合失調症感受性遺伝子COMTに見出される中立進化からの逸脱, 日本人類遺伝学会第55回大会, 2010.10.
37. 鄧 湘東、柴田弘紀、高木宏美、王 麗香、黒木俊秀、中原 辰雄、橋本喜次郎、岩田仲生、尾崎紀夫、有波忠雄、服巻保幸, 統合失調症関連候補遺伝子としてのPCP応答遺伝子探索と関連解析, 日本人類遺伝学会第55回大会, 2010.10.
38. 柴田弘紀、内田麻衣子、後藤大輝、間野修平、竹中 修、服巻保幸, 統合失調症感受性遺伝子COMTに見出される中立進化からの逸脱, 第82回日本遺伝学会大会, 2010.09.
39. 柴田弘紀, 統合失調症の原因を進化的手法で探る〜天才とナントカは紙一重か?〜, 第12回日本進化学会大会, 2010.08.
40. Hiroki Shibata, Kunika Tanaka, Kazunori Watanabe, Hiroki Goto, Shuhei Mano, Osamu Takenaka, Yasuyuki Fukumaki., Molecular evolutionary study of the ionotropic glutamate-receptor gene family as schizophrenia susceptibility genes: human-specific balancing selection in GRIN2B upstream region., International Symposium on Biodiversity Sciences: Genome, Evolution and Environment, 2010.07.
41. 柴田弘紀、田中邦佳、渡邉和典、後藤大輝、間野修平、竹中 修、服巻保幸, 統合失調症感受性遺伝子としてのグルタミン酸受容体遺伝子群の集団遺伝学手法による自然選択の検出, 第5回日本統合失調症学会, 2010.03.
42. 服巻保幸、山本 健、岡 晃、猪子英俊、有波忠雄、岩田仲生、尾崎紀夫、柴田弘紀, マイクロサテライトマーカーを用いた統合失調症のゲノムワイド関連解析, 第5回日本統合失調症学会, 2010.03.
43. 内田麻衣子、服巻保幸、柴田弘紀, 統合失調症感受性遺伝子としてのCOMT遺伝子の分子進化学的解析, 第32回日本分子生物学会年会, 2009.12.
44. Hiroki Shibata, Kazunori Watanabe, Kunika Tanaka, Hiroki Goto, Shuhei Mano, Osamu Takenaka, Yasuyuki Fukumaki., Molecular evolutionary study of the ionotropic glutamate-receptor gene family as schizophrenia susceptibility genes: human-specific balancing selection in the GRIN2B upstream region., 59th Annual Meeting of The American Society of Human Genetics, 2009.10.
45. Yasuyuki Fukumaki Y, Ken Yamamoto, Zhu Sun, Akira Oka, Hidetoshi Inoko, Tadao Arinami, Nakao Iwata, Norio Ozaki, Hiroki Shibata., Genome-wide association study of schizophrenia using STR markers., 59th Annual Meeting of The American Society of Human Genetics, 2009.10.
46. 柴田弘紀、森田 彩、後藤大輝、間野修平、竹中 修、服巻保幸, 高次脳機能関連遺伝子群の分子進化学的解析:代謝調節型グルタミン酸受容体遺伝子群における自然選択の検出, 日本人類遺伝学会第54回大会, 2009.09.
47. 服巻保幸、山本 健、孫 竹、岡 晃、猪子英俊、有波忠雄、岩田仲生、尾崎紀夫、柴田弘紀, 統合失調症のSTRマーカーによるゲノムワイド関連解析, 日本人類遺伝学会第54回大会, 2009.09.
48. 柴田弘紀、森田 彩、後藤大輝、間野修平、竹中 修、服巻保幸, 高次脳機能関連遺伝子群の分子進化学的解析:代謝調節型グルタミン酸受容体遺伝子群における自然選択の検出, 第81回日本遺伝学会大会, 2009.09.
49. 柴田弘紀、森田 彩、後藤大輝、間野修平、竹中 修、服巻保幸, 高次脳機能関連遺伝子群の分子進化学的解析:代謝調節型グルタミン酸受容体遺伝子群における自然選択の検出, 第11回日本進化学会大会, 2009.09.
50. Hiroki Shibata, Kunika Tanaka K, Kazunori Watanabe, Hiroki Goto, Shuhei Mano, Osamu Takenaka, Yasuyuki Fukumaki., Molecular Evolutionary Study Of The Ionotropic Glutamate-Receptor Gene Family As Schizophrenia Susceptibility Genes: Human-Specific Balancing Selection In GRIN2B Upstream Region, The 8th International Workshop on Advanced Genomics: Expansion of Genome Science, Tokyo, Japan., 2009.06.
51. 柴田弘紀、後藤大輝、渡邉和典、黒木陽子、豊田 敦、服部正平、榊 佳之、藤山秋佐夫、服巻保幸, Comparative analysis of glutamate receptor gene family between human and chimpanzee, 第31回日本分子生物学会年会、第81回日本生化学会大会合同大会, 2008.12.
52. Xiangdong Deng, Hiroki Shibata, Toshihide Kuroki, Tatsuo Nakahara, Kijiro Hashimoto, Hideaki Ninomiya, Nakao Iwata, Norio Ozaki, Yasuyuki Fukumaki, Association study of phencyclidine-responsive genes with schizophrenia, 58th Annual Meeting of The American Society of Human Genetics, 2008.11.
53. Hiroki Shibata, Kunika Tanaka, Kazunori Watanabe, Hiroki Goto, Shuhei Mano, Osamu Takenaka, Yasuyuki Fukumaki., Molecular evolutionary study of the ionotropic glutamate-receptor gene family as schizophrenia susceptibility genes: human-specific non-neutral pattern observed in GRIN2B upstream region., XX International Congress of Genetics, 2008.10.
54. Yasuyuki Fukumaki, Xiangdong Deng, Toshihide Kuroki, Tatsuo Nakahara, Kijiro Hashimoto, Hideaki Ninomiya, Nakao Iwata, Norio Ozaki, Hiroki Shibata ., Search for schizophrenia susceptibility loci focusing on PCP-responsive genes as candidates., XX International Congress of Genetics, 2008.10.
55. 柴田弘紀、渡邉和典、田中邦佳、森田 彩、後藤大輝 、間野修平、竹中 修、服巻保幸, 統合失調症感受性遺伝子としてのグルタミン酸受容体遺伝子群の分子進化学的解析 II, 日本人類遺伝学会第53回大会, 2008.09.
56. 柴田弘紀、渡邉和典、田中邦佳、森田 彩、後藤大輝 、間野修平、竹中 修、服巻保幸, 高次脳機能に関連するイオンチャンネル型グルタミン酸受容体遺伝子群14種の上流調節領域における分子進化学的解析, 第80回日本遺伝学会大会, 2008.09.
57. 柴田弘紀, 統合失調症関連遺伝子としてのグルタミン酸受容体遺伝子群の分子進化学的解析, 第10回日本進化学会大会, 2008.08.
58. Hiroki Shibata, Kunika Tanaka, Kazunori Watanabe, Hiroki Goto, Shuhei Mano, Osamu Takenaka, Yasuyuki Fukumaki., Molecular evolutionary study of the ionotropic glutamate-receptor gene family as schizophrenia susceptibility genes: human-specific non-neutral pattern observed in GRIN2B upstream region, XX International Congress of Genetics, 2008.07.
59. 服巻保幸、小林 茂、柴田弘紀, 進化医学序説:なぜ病気は存在するのか?, 第30回日本分子生物学会年会、第80回日本生化学会大会合同大会, 2007.12.
60. Shibata H, Tanaka K, Watanabe K, Goto H, Takenaka O, Fukumaki Y., Molecular evolutionary study of the ionotropic glutamate-receptor gene family as schizophrenia susceptibility genes: human-specific non-neutral pattern observed in GRIN2B upstream region., 57th Annual Meeting of The American Society of Human Genetics, 2007.10.
61. 柴田弘紀, 統合失調症関連遺伝子としてのグルタミン酸受容体遺伝子群の分子進化学的解析, 国立遺伝学研究所研究会シンポジウム「ヒトゲノム多様性に基づく進化医学の発展」, 2007.10.
62. 柴田弘紀、田中邦佳、渡邉和典、後藤大輝、竹中 修、服巻保幸, 統合失調症関連遺伝子としてのグルタミン酸受容体遺伝子群の分子進化学的解析, 日本遺伝学会第79回大会, 2007.09.
63. 柴田弘紀、田中邦佳、渡邉和典、蔭山瑠衣、後藤大輝、蘭 直純、黒木陽子、豊田 敦、服部正平、榊 佳之、藤山秋佐夫、服巻保幸, 統合失調症感受性遺伝子としてのグルタミン酸受容体遺伝子群の分子進化学的解析, 第52回日本人類遺伝学会、, 2007.09.
64. 田中邦佳、渡邉和典、蔭山瑠衣、後藤大輝、蘭 直純、黒木陽子、豊田 敦、服部正平、榊 佳之、藤山秋佐夫、服巻保幸、柴田弘紀, グルタミン酸受容体遺伝子群におけるヒト特異的アミノ酸置換の同定と上流領域の分子進化学的解析, 分子生物学会2006フォーラム, 2006.12.
特許出願・取得
特許出願件数  2件
特許登録件数  1件
学会活動
所属学会名
日本爬虫両棲類学会
日本進化学会
日本遺伝学会
日本分子生物学会
米国人類遺伝学会
日本人類遺伝学会
学会誌・雑誌・著書の編集への参加状況
2012.06, Anthropological Science, 国際, 編集委員.
学術論文等の審査
年度 外国語雑誌査読論文数 日本語雑誌査読論文数 国際会議録査読論文数 国内会議録査読論文数 合計
2019年度      
2018年度      
2017年度      
2016年度      
2014年度      
2013年度      
2012年度      
2011年度      
2010年度      
2009年度      
2008年度      
2007年度      
2006年度      
2005年度      
2004年度      
2003年度      
2001年度      
研究資金
科学研究費補助金の採択状況(文部科学省、日本学術振興会)
2018年度~2021年度, 基盤研究(B), 代表, ゲノム情報を用いたハブ毒タンパク質の包括的多様性および進化過程の解明.
2016年度~2019年度, 基盤研究(C), 分担, 遺伝子間相互作用解析を活用した口唇口蓋裂疾患感受性遺伝子の解明.
2014年度~2016年度, 基盤研究(C), 分担, 第1番染色体に連鎖する新規遺伝性ニューロパチーの分子基盤解明.
2013年度~2015年度, 基盤研究(C), 代表, ミトゲノム解析と核マーカータイピングによる日本産ハブ属3種の遺伝的集団構造の研究.
2009年度~2011年度, 基盤研究(C), 代表, 統合失調症感受性遺伝子多型の進化医学的解析.
2008年度~2009年度, 特定領域研究, 代表, ヒト高次脳機能関連遺伝子群の分子進化学的解析.
2007年度~2008年度, 特定領域研究, 代表, ヒト高次脳機能関連遺伝子群の分子進化学的解析.
2006年度~2007年度, 特定領域研究, 代表, 統合失調症関連遺伝子群を突破口とした”humanness”の起源の解明.
2005年度~2005年度, 特定領域研究, 代表, グルタミン酸受容体遺伝子群のヒト上科における多様性と”humanness”の起源.
2002年度~2004年度, 若手研究(A), 代表, 精神分裂病感受性遺伝子としてのグルタミン酸受容体遺伝子群の包括的研究.
2000年度~2001年度, 奨励研究(A), 代表, グルタミン受容体遺伝子群の多型検索及び精神分裂病との相関解析.
日本学術振興会への採択状況(科学研究費補助金以外)
2016年度~2017年度, 特別研究員, エイジングに伴うエピゲノム変化に注目した糖尿病バイオマーカーの解明(岩谷千寿).
競争的資金(受託研究を含む)の採択状況
2005年度~2005年度, 第37回内藤記念科学奨励金(研究助成), 代表, ローカスワイド関連解析による統合失調症感受性遺伝子の探索と同定〜多面的アプローチによる候補遺伝子探索と大規模検体による関連解析.
寄附金の受入状況
2018年度, 第一三共株式会社, 第一三共奨学寄付プログラム/発作性運動誘発性ジスキネシアの遺伝解析研究.
2017年度, 第一三共株式会社, 第一三共奨学寄付プログラム/発作性運動誘発性ジスキネシアの遺伝解析研究.

九大関連コンテンツ

pure2017年10月2日から、「九州大学研究者情報」を補完するデータベースとして、Elsevier社の「Pure」による研究業績の公開を開始しました。
 
 
九州大学知的財産本部「九州大学Seeds集」