Author Report for: Okazaki YNo contact information in database for Okazaki Y
Hashimoto T, Yang B, Okazaki Y, Yoshizawa I, Kajihara K, Kato N, Wada M, Yanaka N Ref: PLoS ONE, 11:e0163299, 2016 : PubMed ESTHER: Hashimoto_2016_PLoS.One_11_e0163299 PubMedSearch: Hashimoto 2016 PLoS.One 11 e0163299 PubMedID: 27658304 Abstract Glycerophosphodiesterase 5 (GDE5) selectively hydrolyses glycerophosphocholine to choline and is highly expressed in type II fiber-rich skeletal muscles. We have previously generated that a truncated mutant of GDE5 (GDE5dC471) that lacks phosphodiesterase activity and shown that transgenic mice overexpressing GDE5dC471 in skeletal muscles show less skeletal muscle mass than control mice. However, the molecular mechanism and pathophysiological features underlying decreased skeletal muscle mass in GDE5dC471 mice remain unclear. In this study, we characterized the skeletal muscle disorder throughout development and investigated the primary cause of muscle atrophy. While type I fiber-rich soleus muscle mass was not altered in GDE5dC471 mice, type II fiber-rich muscle mass was reduced in 8-week-old GDE5dC471 mice. Type II fiber-rich muscle mass continued to decrease irreversibly in 1-year-old transgenic mice with an increase in apoptotic cell. Adipose tissue weight and blood triglyceride levels in 8-week-old and 1-year-old transgenic mice were higher than those in control mice. This study also demonstrated compensatory mRNA expression of neuromuscular junction (NMJ) components, including nicotinic acetylcholine receptors (alpha1, gamma, and epsilon subunits) and acetylcholinesterase in type II fiber-rich quadriceps muscles in GDE5dC471 mice. However, we did not observe morphological changes in NMJs associated with skeletal muscle atrophy in GDE5dC471 mice. We also found that HSP70 protein levels are significantly increased in the skeletal muscles of 2-week-old GDE5dC471 mice and in mouse myoblastic C2C12 cells overexpressing GDE5dC471. These findings suggest that GDE5dC471 mouse is a novel model of early-onset irreversible type II fiber-rich myopathy associated with cellular stress. Title: Donepezil prevents RANK-induced bone loss via inhibition of osteoclast differentiation by downregulating acetylcholinesterase Sato T, Enoki Y, Sakamoto Y, Yokota K, Okubo M, Matsumoto M, Hayashi N, Usui M, Kokabu S and Yoda T <7 more author(s)> Sato T, Enoki Y, Sakamoto Y, Yokota K, Okubo M, Matsumoto M, Hayashi N, Usui M, Kokabu S, Mimura T, Nakazato Y, Araki N, Fukuda T, Okazaki Y, Suda T, Takeda S, Yoda T (- 7) Ref: Heliyon, 1:e00013, 2015 : PubMed ESTHER: Sato_2015_Heliyon_1_e00013 PubMedSearch: Sato 2015 Heliyon 1 e00013 PubMedID: 27441211 Abstract OBJECTIVE: Donepezil, an inhibitor of acetylcholinesterase (AChE) targeting the brain, is a common medication for Alzheimer's disease. Interestingly, a recent clinical study found that administration of this agent is associated with lower risk of hip fracture independently of falling, suggesting its direct effect on bone tissues as well. AChE has been reported to be involved in osteoblast function, but the role of AChE on osteoclastogenesis still remains unclear. We analyzed the effect of AChE and donepezil on osteoclastogenesis in vivo and in vitro. Title: Effect of the cholinesterase inhibitor donepezil on cardiac remodeling and autonomic balance in rats with heart failure Okazaki Y, Zheng C, Li M, Sugimachi M Ref: Journal de Physiologie Sci, 60:67, 2010 : PubMed ESTHER: Okazaki_2010_J.Physiol.Sci_60_67 PubMedSearch: Okazaki 2010 J.Physiol.Sci 60 67 PubMedID: 19949913 Abstract In an earlier study we demonstrated the beneficial effect of direct vagal electrical stimulation on cardiac remodeling and survival. In the study reported here, we attempted to reproduce the effect of vagal enhancement through the administration of an acetylcholinesterase inhibitor, donepezil. A rat model of heart failure following extensive healed myocardial infarction was used. Compared to their nontreated counterparts, rats given donepezil (5 mg/kg/day) in their drinking water had a smaller biventricular weight (3.40 +/- 0.13 vs. 3.02 +/- 0.21 g/kg body weight, P < 0.05), and maximal rate of rise (3256 +/- 955 vs. 3822 +/- 389 mmHg/s, P < 0.05) and the end-diastolic value (30.1 +/- 5.6 vs. 23.2 +/- 5.7 mmHg, P < 0.05) of left ventricular pressure were improved. Neurohumoral factors were suppressed in donepezil-treated rats (norepinephrine 1885 +/- 1423 vs. 316 +/- 248 pg/ml, P < 0.01; brain natriuretic peptide 457 +/- 68 vs. 362 +/- 80 ng/ml, P < 0.05), and the high-frequency component of heart rate variability showed a nocturnal increase. These findings indicated that donepezil reproduced the anti-remodeling effect of electrical vagal stimulation. Further studies are warranted to evaluate the clinical usefulness of donepezil in heart failure. Title: The transcriptional landscape of the mammalian genome Carninci P, Kasukawa T, Katayama S, Gough J, Frith MC, Maeda N, Oyama R, Ravasi T, Lenhard B and Hayashizaki Y <184 more author(s)> Carninci P, Kasukawa T, Katayama S, Gough J, Frith MC, Maeda N, Oyama R, Ravasi T, Lenhard B, Wells C, Kodzius R, Shimokawa K, Bajic VB, Brenner SE, Batalov S, Forrest AR, Zavolan M, Davis MJ, Wilming LG, Aidinis V, Allen JE, Ambesi-Impiombato A, Apweiler R, Aturaliya RN, Bailey TL, Bansal M, Baxter L, Beisel KW, Bersano T, Bono H, Chalk AM, Chiu KP, Choudhary V, Christoffels A, Clutterbuck DR, Crowe ML, Dalla E, Dalrymple BP, de Bono B, Della Gatta G, di Bernardo D, Down T, Engstrom P, Fagiolini M, Faulkner G, Fletcher CF, Fukushima T, Furuno M, Futaki S, Gariboldi M, Georgii-Hemming P, Gingeras TR, Gojobori T, Green RE, Gustincich S, Harbers M, Hayashi Y, Hensch TK, Hirokawa N, Hill D, Huminiecki L, Iacono M, Ikeo K, Iwama A, Ishikawa T, Jakt M, Kanapin A, Katoh M, Kawasawa Y, Kelso J, Kitamura H, Kitano H, Kollias G, Krishnan SP, Kruger A, Kummerfeld SK, Kurochkin IV, Lareau LF, Lazarevic D, Lipovich L, Liu J, Liuni S, McWilliam S, Madan Babu M, Madera M, Marchionni L, Matsuda H, Matsuzawa S, Miki H, Mignone F, Miyake S, Morris K, Mottagui-Tabar S, Mulder N, Nakano N, Nakauchi H, Ng P, Nilsson R, Nishiguchi S, Nishikawa S, Nori F, Ohara O, Okazaki Y, Orlando V, Pang KC, Pavan WJ, Pavesi G, Pesole G, Petrovsky N, Piazza S, Reed J, Reid JF, Ring BZ, Ringwald M, Rost B, Ruan Y, Salzberg SL, Sandelin A, Schneider C, Schonbach C, Sekiguchi K, Semple CA, Seno S, Sessa L, Sheng Y, Shibata Y, Shimada H, Shimada K, Silva D, Sinclair B, Sperling S, Stupka E, Sugiura K, Sultana R, Takenaka Y, Taki K, Tammoja K, Tan SL, Tang S, Taylor MS, Tegner J, Teichmann SA, Ueda HR, van Nimwegen E, Verardo R, Wei CL, Yagi K, Yamanishi H, Zabarovsky E, Zhu S, Zimmer A, Hide W, Bult C, Grimmond SM, Teasdale RD, Liu ET, Brusic V, Quackenbush J, Wahlestedt C, Mattick JS, Hume DA, Kai C, Sasaki D, Tomaru Y, Fukuda S, Kanamori-Katayama M, Suzuki M, Aoki J, Arakawa T, Iida J, Imamura K, Itoh M, Kato T, Kawaji H, Kawagashira N, Kawashima T, Kojima M, Kondo S, Konno H, Nakano K, Ninomiya N, Nishio T, Okada M, Plessy C, Shibata K, Shiraki T, Suzuki S, Tagami M, Waki K, Watahiki A, Okamura-Oho Y, Suzuki H, Kawai J, Hayashizaki Y (- 184) Ref: Science, 309:1559, 2005 : PubMed ESTHER: Carninci_2005_Science_309_1559 PubMedSearch: Carninci 2005 Science 309 1559 PubMedID: 16141072 Gene_locus related to this paper: mouse-abhd1, mouse-abhd3, mouse-abhd4, mouse-acot4, mouse-adcl4, mouse-DGLB, mouse-ephx3, mouse-Kansl3, mouse-lipli, mouse-LIPN, mouse-Ppgb, mouse-q3uuq7, mouse-srac1, mouse-Tex30, mouse-tmco4, mouse-tmm53, mouse-f172a Abstract This study describes comprehensive polling of transcription start and termination sites and analysis of previously unidentified full-length complementary DNAs derived from the mouse genome. We identify the 5' and 3' boundaries of 181,047 transcripts with extensive variation in transcripts arising from alternative promoter usage, splicing, and polyadenylation. There are 16,247 new mouse protein-coding transcripts, including 5154 encoding previously unidentified proteins. Genomic mapping of the transcriptome reveals transcriptional forests, with overlapping transcription on both strands, separated by deserts in which few transcripts are observed. The data provide a comprehensive platform for the comparative analysis of mammalian transcriptional regulation in differentiation and development. Title: Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs Okazaki Y, Furuno M, Kasukawa T, Adachi J, Bono H, Kondo S, Nikaido I, Osato N, Saito R and Hayashizaki Y <127 more author(s)> Okazaki Y, Furuno M, Kasukawa T, Adachi J, Bono H, Kondo S, Nikaido I, Osato N, Saito R, Suzuki H, Yamanaka I, Kiyosawa H, Yagi K, Tomaru Y, Hasegawa Y, Nogami A, Schonbach C, Gojobori T, Baldarelli R, Hill DP, Bult C, Hume DA, Quackenbush J, Schriml LM, Kanapin A, Matsuda H, Batalov S, Beisel KW, Blake JA, Bradt D, Brusic V, Chothia C, Corbani LE, Cousins S, Dalla E, Dragani TA, Fletcher CF, Forrest A, Frazer KS, Gaasterland T, Gariboldi M, Gissi C, Godzik A, Gough J, Grimmond S, Gustincich S, Hirokawa N, Jackson IJ, Jarvis ED, Kanai A, Kawaji H, Kawasawa Y, Kedzierski RM, King BL, Konagaya A, Kurochkin IV, Lee Y, Lenhard B, Lyons PA, Maglott DR, Maltais L, Marchionni L, McKenzie L, Miki H, Nagashima T, Numata K, Okido T, Pavan WJ, Pertea G, Pesole G, Petrovsky N, Pillai R, Pontius JU, Qi D, Ramachandran S, Ravasi T, Reed JC, Reed DJ, Reid J, Ring BZ, Ringwald M, Sandelin A, Schneider C, Semple CA, Setou M, Shimada K, Sultana R, Takenaka Y, Taylor MS, Teasdale RD, Tomita M, Verardo R, Wagner L, Wahlestedt C, Wang Y, Watanabe Y, Wells C, Wilming LG, Wynshaw-Boris A, Yanagisawa M, Yang I, Yang L, Yuan Z, Zavolan M, Zhu Y, Zimmer A, Carninci P, Hayatsu N, Hirozane-Kishikawa T, Konno H, Nakamura M, Sakazume N, Sato K, Shiraki T, Waki K, Kawai J, Aizawa K, Arakawa T, Fukuda S, Hara A, Hashizume W, Imotani K, Ishii Y, Itoh M, Kagawa I, Miyazaki A, Sakai K, Sasaki D, Shibata K, Shinagawa A, Yasunishi A, Yoshino M, Waterston R, Lander ES, Rogers J, Birney E, Hayashizaki Y (- 127) Ref: Nature, 420:563, 2002 : PubMed ESTHER: Okazaki_2002_Nature_420_563 PubMedSearch: Okazaki 2002 Nature 420 563 PubMedID: 12466851 Gene_locus related to this paper: mouse-1lipg, mouse-1llip, mouse-1plrp, mouse-3neur, mouse-ABH15, mouse-abhd4, mouse-abhd5, mouse-Abhd8, mouse-Abhd11, mouse-abhda, mouse-acot4, mouse-adcl4, mouse-AI607300, mouse-BAAT, mouse-bphl, mouse-C87498, mouse-Ldah, mouse-Ces1d, mouse-Ces2e, mouse-CMBL, mouse-DGLB, mouse-dpp9, mouse-ES10, mouse-F135A, mouse-FASN, mouse-hslip, mouse-hyes, mouse-Kansl3, mouse-LIPH, mouse-LIPK, mouse-lipli, mouse-LIPM, mouse-lypla1, mouse-lypla2, mouse-MEST, mouse-MGLL, mouse-ndr4, mouse-OVCA2, mouse-pafa, mouse-pcp, mouse-ppce, mouse-Ppgb, mouse-PPME1, mouse-q3uuq7, mouse-Q8BLF1, mouse-ACOT6, mouse-Q8C1A9, mouse-Q9DAI6, mouse-Q80UX8, mouse-Q8BGG9, mouse-Q8C167, mouse-rbbp9, mouse-SERHL, mouse-tssp Abstract Only a small proportion of the mouse genome is transcribed into mature messenger RNA transcripts. There is an international collaborative effort to identify all full-length mRNA transcripts from the mouse, and to ensure that each is represented in a physical collection of clones. Here we report the manual annotation of 60,770 full-length mouse complementary DNA sequences. These are clustered into 33,409 'transcriptional units', contributing 90.1% of a newly established mouse transcriptome database. Of these transcriptional units, 4,258 are new protein-coding and 11,665 are new non-coding messages, indicating that non-coding RNA is a major component of the transcriptome. 41% of all transcriptional units showed evidence of alternative splicing. In protein-coding transcripts, 79% of splice variations altered the protein product. Whole-transcriptome analyses resulted in the identification of 2,431 sense-antisense pairs. The present work, completely supported by physical clones, provides the most comprehensive survey of a mammalian transcriptome so far, and is a valuable resource for functional genomics. Title: Functional annotation of a full-length mouse cDNA collection Kawai J, Shinagawa A, Shibata K, Yoshino M, Itoh M, Ishii Y, Arakawa T, Hara A, Fukunishi Y and Hayashizaki Y <86 more author(s)> Kawai J, Shinagawa A, Shibata K, Yoshino M, Itoh M, Ishii Y, Arakawa T, Hara A, Fukunishi Y, Konno H, Adachi J, Fukuda S, Aizawa K, Izawa M, Nishi K, Kiyosawa H, Kondo S, Yamanaka I, Saito T, Okazaki Y, Gojobori T, Bono H, Kasukawa T, Saito R, Kadota K, Matsuda H, Ashburner M, Batalov S, Casavant T, Fleischmann W, Gaasterland T, Gissi C, King B, Kochiwa H, Kuehl P, Lewis S, Matsuo Y, Nikaido I, Pesole G, Quackenbush J, Schriml LM, Staubli F, Suzuki R, Tomita M, Wagner L, Washio T, Sakai K, Okido T, Furuno M, Aono H, Baldarelli R, Barsh G, Blake J, Boffelli D, Bojunga N, Carninci P, de Bonaldo MF, Brownstein MJ, Bult C, Fletcher C, Fujita M, Gariboldi M, Gustincich S, Hill D, Hofmann M, Hume DA, Kamiya M, Lee NH, Lyons P, Marchionni L, Mashima J, Mazzarelli J, Mombaerts P, Nordone P, Ring B, Ringwald M, Rodriguez I, Sakamoto N, Sasaki H, Sato K, Schonbach C, Seya T, Shibata Y, Storch KF, Suzuki H, Toyo-oka K, Wang KH, Weitz C, Whittaker C, Wilming L, Wynshaw-Boris A, Yoshida K, Hasegawa Y, Kawaji H, Kohtsuki S, Hayashizaki Y (- 86) Ref: Nature, 409:685, 2001 : PubMed ESTHER: Kawai_2001_Nature_409_685 PubMedSearch: Kawai 2001 Nature 409 685 PubMedID: 11217851 Gene_locus related to this paper: mouse-1lipg, mouse-1plip, mouse-1plrp, mouse-ABH15, mouse-abhd5, mouse-ABHD6, mouse-Abhd8, mouse-aryla, mouse-bphl, mouse-cauxin, mouse-Ces1g, mouse-CPMac, mouse-dpp8, mouse-EPHX1, mouse-ES10, mouse-hslip, mouse-hyes, mouse-ABHD2, mouse-lcat, mouse-lipli, mouse-LIPN, mouse-lypla1, mouse-lypla2, mouse-OVCA2, mouse-pafa, mouse-pcp, mouse-Ppgb, mouse-PPME1, mouse-ppt, mouse-q3uuq7, mouse-Q9DAI6, mouse-Q80UX8, mouse-RISC, mouse-SERHL, mouse-SPG21, mouse-Tex30 Abstract The RIKEN Mouse Gene Encyclopaedia Project, a systematic approach to determining the full coding potential of the mouse genome, involves collection and sequencing of full-length complementary DNAs and physical mapping of the corresponding genes to the mouse genome. We organized an international functional annotation meeting (FANTOM) to annotate the first 21,076 cDNAs to be analysed in this project. Here we describe the first RIKEN clone collection, which is one of the largest described for any organism. Analysis of these cDNAs extends known gene families and identifies new ones. Title: Normalization and subtraction of cap-trapper-selected cDNAs to prepare full-length cDNA libraries for rapid discovery of new genes Carninci P, Shibata Y, Hayatsu N, Sugahara Y, Shibata K, Itoh M, Konno H, Okazaki Y, Muramatsu M, Hayashizaki Y Ref: Genome Res, 10:1617, 2000 : PubMed ESTHER: Carninci_2000_Genome.Res_10_1617 PubMedSearch: Carninci 2000 Genome.Res 10 1617 PubMedID: 11042159 Gene_locus related to this paper: mouse-1plip, mouse-1plrp, mouse-abhd5, mouse-Abhd8, mouse-cauxin, mouse-Ces1g, mouse-CPMac, mouse-dpp8, mouse-hslip, mouse-hyes, mouse-lipli, mouse-LIPN, mouse-pafa, mouse-Ppgb, mouse-q3uuq7, mouse-Q9DAI6, mouse-RISC Abstract In the effort to prepare the mouse full-length cDNA encyclopedia, we previously developed several techniques to prepare and select full-length cDNAs. To increase the number of different cDNAs, we introduce here a strategy to prepare normalized and subtracted cDNA libraries in a single step. The method is based on hybridization of the first-strand, full-length cDNA with several RNA drivers, including starting mRNA as the normalizing driver and run-off transcripts from minilibraries containing highly expressed genes, rearrayed clones, and previously sequenced cDNAs as subtracting drivers. Our method keeps the proportion of full-length cDNAs in the subtracted/normalized library high. Moreover, our method dramatically enhances the discovery of new genes as compared to results obtained by using standard, full-length cDNA libraries. This procedure can be extended to the preparation of full-length cDNA encyclopedias from other organisms. Title: Pharmacological and biochemical assessment of SM-10888, a novel cholinesterase inhibitor Natori K, Okazaki Y, Irie T, Katsube J Ref: Japanese Journal of Pharmacology, 53:145, 1990 : PubMed ESTHER: Natori_1990_Jpn.J.Pharmacol_53_145 PubMedSearch: Natori 1990 Jpn.J.Pharmacol 53 145 PubMedID: 2385001 Inhibitor(s) related to this paper: SM-10888, Velnacrine Abstract The effects of the compound SM-10888 (9-amino-8-fluoro-1,2,3,4-tetrahydro-2,4-methanoacridine citrate) in a number of pharmacological and biochemical tests were studied and compared to those of tacrine (THA), amiridin, HP-029 and physostigmine. SM-10888 inhibited cholinesterase activity (IC50: 2.3 x 10(-7) M) in rat cortical P2 fraction with almost the same potency as THA, while SM-10888 was 2-4 times more potent than amiridin and HP-029, but about 10 times less potent than physostigmine. When given to mice p.o., SM-10888 induced central (hypothermia) and peripheral (salivation) cholinergic effects. When the ratio of the ED50 value for hypothermia to that for salivation was regarded as the index of the selectivity to the central nervous system (CNS), SM-10888 was shown to be about 3 times more selective to the CNS than the other four drugs in mice. The minimum effective dose of SM-10888 for its increasing effect on acetylcholine (ACh) content in the mouse cerebral cortex was about 10 times higher than that of physostigmine, but 5-10 times lower than those of THA, amiridin and HP-029. These results suggest that SM-10888 is an adequate drug for increasing the brain ACh content with less peripheral cholinergic side effects than THA, amiridin, HP-029 and physostigmine. Title: Effect of a novel CNS-selective cholinesterase inhibitor, SM-10888, on habituation and passive avoidance responses in mice Okazaki Y, Natori K, Irie T, Katsube J Ref: Japanese Journal of Pharmacology, 53:211, 1990 : PubMed ESTHER: Okazaki_1990_Jpn.J.Pharmacol_53_211 PubMedSearch: Okazaki 1990 Jpn.J.Pharmacol 53 211 PubMedID: 2385006 Inhibitor(s) related to this paper: SM-10888 Abstract The effects of the tacrine (THA) derivative SM-10888 (9-amino-8-fluoro-1,2,3,4-tetrahydro-2,4-methanoacridine citrate) on habituation and passive avoidance responses were studied in mice. We examined its effects on habituation of exploratory activity, measured by photo-cell beam interruptions in a small, simple cage and cycloheximide (CXM)- or electroconvulsive shock (ECS)-induced stepdown type passive avoidance response (PAR) failures in comparison with those of THA, amiridin, HP-029 and physostigmine. SM-10888 (6 mg/kg, p.o.) administered post-acquisition session enhanced the retention of habituation. CXM- and ECS-induced PAR failures were improved by SM-10888 (6 mg/kg, p.o.) administered at pre-training or post-training, respectively. THA enhanced the retention of habituation and improved CXM-induced PAR failure at 30 mg/kg, p.o., but did not affect ECS-induced PAR failure at 1-15 mg/kg, p.o. Amiridin and HP-029 were also effective on habituation and CXM-induced PAR failure at 40-50 mg/kg, p.o., but did not affect ECS-induced PAR failure at the tested doses. Physostigmine showed a moderate improvement only in CXM-induced PAR failure. The results indicate that SM-10888 enhanced habituation and improved PAR failures at much lower doses than THA. This seems to depend on its high selectivity to the central nervous system. | |||||||
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