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ROAD 作詞/82スレ10 明日僕が去るのなら 僕は君に想いを伝えられるのか 明日君が去るのなら 笑顔で手を振る事ができるのか 僕の道 君の道 全く同じ風など吹いてはこない だけど僕が君とすれ違うことを望むのは 君が好きなんだよ その女らしい声や長く綺麗な髪 全てが好きなんだよ だからこそ進めない道もある 消したい道もある 後ろを向かなきゃ見えない道もある だけど 君が好きだから 進めるんだよ どんな茨の道も 全てが好きなんだよ 君を見るほど僕は自信を無くしてゆく 君が好きなんだよ たとえ周りが敵だらけであっても 全てが好きなんだよ 君だけを包んであげたい
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tysP つよしひい【登録タグ クリエイター 作つ】 曲一覧 Invisible Tears Whisper/tysP Loose Change Rainbow Road Runner コメント 名前 コメント
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このページはこちらに移転しました No-sleeping roads 作詞/287スレ246 No-sleeping roads Take me home, to the place I m rubbing Natural virgine, the innocent boy Take me home, no-sleeping road Almost hell, west school Hopeless scineries, Fucking me Life is dead there, more than hell I m tired so get the fuck me back to the house No-sleeping roads Take me home, to the place I m sleeping Natural virgine, the innocent boy Take me home, no-sleeping road oh yea No-sleeping roads Take me home, to the place I m staying up all night Natural virgine, the innocent boy Take me home, no-sleeping road
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スカイガーデン (Cloudtop Cruise) ホネホネ砂漠 (Bone-Dry Dunes) クッパキャッスル (Bowser s Castle) レインボーロード (Rainbow Road)
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http //www.k4.dion.ne.jp/~korekata/ member tamKore CDLive Of Life Korekata Fish Dance LiveLive @ Hey-Joe, Yokohama April 19th 2013 fri Live @ Motion Blue, Minatomirai, Yokohama June 8th 2010 Thu Live @ Jaynepal, Makuhari, Chiba June 14th 2009 Sunday tamKore / sa・Ku・ra ( 2008年4月7日 ) DVD - た tamKore / 音旅 - ototabi - ( 2009年4月15日 ) CD Live Of Life March 6th 2013 1. Aurora Aura / 2. マンモス / 3. Journey to the mind [ feat. 杉山清貴 ] / 4. Gifted spiders [ feat. 田村直美 ] / 5. Good times Good things / 6. The wonderland of peace [ feat. 田村直美 ] / 7. Joro [ feat. 杉山清貴 ] / 8. 想い出の街 / 9. フレ フレ シャッフレ! / 10. Blue Mirage [ feat. ACE ] / 11. Romancing Bird II [ feat. 石井一孝 ] / 12. Over The Rainbow Ikuo (#2) Korekata May 21th 1999 1. Heart Of Earth / 2. Orangoutan Twist / 3. Whale / 4. Puma Gang / 5. Silver Cat / 6. Penguin / 7. Zoo-Zoo-Zoo / 8. Purplesaurus / 9. Romancing Birds Fish Dance August 25th 1987 1. Darts / 2. Fish Dance / 3. Show Boat / 4. So Long ... Kimmie / 5. Final Shot / 6. プリシア / 7. Gold Rush / 8. キティ快適 / 9. Jumpin Duck Flash! / 10. Earth Walker / 11. Goodbye Yellow Brick Road Live Live @ Hey-Joe, Yokohama April 19th 2013 fri "Rainbow Jam" 是方博邦 (g), Ikuo (b), 山崎慶 (ds) Live @ Motion Blue, Minatomirai, Yokohama June 8th 2010 Thu 是方博邦 Rock Unit ( 是方博邦 (g), 杉山清貴 (vo), 長谷川浩二 (ds), バーべQ和佐田 (b) ) Live @ Jaynepal, Makuhari, Chiba June 14th 2009 Sunday tamKore ( 田村直美 (vo,g), 是方博邦 (g,cho) )
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今日 - 合計 - 筋肉番付～ROAD TO SASUKEの攻略ページ 目次 基本情報 [部分編集] ストーリー [部分編集] 攻略情報 [部分編集] Tips [部分編集] プチ情報 [部分編集] 関連動画 [部分編集] 参考文献、参考サイト [部分編集] 感想・レビュー 基本情報 [部分編集] ストーリー [部分編集] 攻略情報 [部分編集] Tips [部分編集] プチ情報 [部分編集] 関連動画 [部分編集] 参考文献、参考サイト [部分編集] 感想・レビュー 名前 コメント 選択肢 投票 役に立った (0) 2020年09月24日 (木) 18時38分07秒 [部分編集] ページごとのメニューの編集はこちらの部分編集から行ってください [部分編集] 編集に関して
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Go Loco Railroad 概要 日本語 ゴー ロコ レールロード 訳：キ○ガイ鉄道 業種：鉄道利用運送事業 所在地 解説 貨物列車でサンアンドレアス州の各地に貨物を運搬する運送会社。モデルはUnion Pacific Railroad 。 機関車に「ゴー・ポスタル 」と同じロゴが表記されているため、同社の子会社もしくはグループ企業であると思われる。 ロスサントス港から採石場やパレト・ベイなどを結ぶ路線を運行している。 また、ノースヤンクトン州にも本社の路線が存在する。 ちなみに、イーストロスサントスには本線と分断された廃線が存在しており、古びた貨車が放置されている。 Locoは｢機関車｣を意味するLocomotiveの略称である…が、スペイン語で「キ○ガイ」（英語のcrazyと同義）という意味があり、GTA流に考えれば恐らくは後者のほうが正しいのだろう。 オフライン 多くのミッションに登場する。 大列車強盗inサンアンドレアスではメリーウェザーの貨物列車を乗っ取られ、運転士の殺害、衝突事故、貨物の盗難と散々な目に遭う。 強盗 パレトでは通過中の貨物列車に銀行強盗犯が逃走する。 さらに大強盗ミッション(派手)ではなんと列車を盗まれ、金塊の回収に使われる。 オフィス 保有車両 Train
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SOS1-/- mice impair Cdc42 activation in PC12 cells. SOS-/- fly impair the development of eyes. Overexpression of GAB1 exhibit neurite outgrowth, DNA synthesis and survival in PC12 cells. SHCB-deficient animals exhibit a loss of peptidergic and nonpeptidergic nociceptive sensory neurons, Hippocampal long-term potentiation in ShcC mutant mice is significantly enhanced. SHCA controls the size of brain. Cbl-b null mice exhibit the enhancement of long-term memory. SOS1-/- mice impair Cdc42 activation in PC12 cells. 1 Mol Biol Cell. 2005 May;16(5) 2207-17. Epub 2005 Feb 23. Local phosphatidylinositol 3,4,5-trisphosphate accumulation recruits Vav2 and Vav3 to activate Rac1/Cdc42 and initiate neurite outgrowth in nerve growth factor-stimulated PC12 cells. Aoki K, Nakamura T, Fujikawa K, Matsuda M. Department of Tumor Virology, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan. Neurite outgrowth is an important process in the formation of neuronal networks. Rac1 and Cdc42, members of the Rho-family GTPases, positively regulate neurite extension through reorganization of the actin cytoskeleton. Here, we examine the dynamic linkage between Rac1/Cdc42 and phosphatidylinositol 3-kinase (PI3-kinase) during nerve growth factor (NGF)-induced neurite outgrowth in PC12 cells. Activity imaging using fluorescence resonance energy transfer probes showed that PI3-kinase as well as Rac1/Cdc42 was transiently activated in broad areas of the cell periphery immediately after NGF addition. Subsequently, local and repetitive activation of PI3-kinase and Rac1/Cdc42 was observed at the protruding sites. Depletion of Vav2 and Vav3 by RNA interference significantly inhibited both Rac1/Cdc42 activation and the formation of short processes leading to neurite outgrowth. At the NGF-induced protrusions, local phosphatidylinositol 3,4,5-trisphosphate accumulation recruited Vav2 and Vav3 to activate Rac1 and Cdc42, and conversely, Vav2 and Vav3 were required for the local activation of PI3-kinase. These observations demonstrated for the first time that Vav2 and Vav3 are essential constituents of the positive feedback loop that is comprised of PI3-kinase and Rac1/Cdc42 and cycles locally with morphological changes. Publication Types Research Support, Non-U.S. Gov t PMID 15728722 [PubMed - indexed for MEDLINE] SOS-/- fly impair the development of eyes. 1 Cell. 1991 Jan 11;64(1) 39-48. Genetic dissection of a neurodevelopmental pathway Son of sevenless functions downstream of the sevenless and EGF receptor tyrosine kinases. Rogge RD, Karlovich CA, Banerjee U. Department of Biology, University of California, Los Angeles 90024. We have isolated a dominant mutation in a gene called Son of sevenless (Sos) that is an allele-specific suppressor of the sevenless phenotype. This suppressor function is autonomously required in R7 and is sensitive to the dosage of the Sos and bride of sevenless genes. Loss-of-function alleles of Sos are recessive lethals, but in the eye Sos has a role in R cell development. Mutations in Sos also interact with the Ellipse allele of the Drosophila EGF receptor. We propose a model suggesting that the Sos product is downstream of sevenless and the EGF receptor, and that the dominant suppression results from the overexpression or increased activity of the gene product. Publication Types Research Support, Non-U.S. Gov t Research Support, U.S. Gov t, P.H.S. PMID 1846090 [PubMed - indexed for MEDLINE] Overexpression of GAB1 exhibit neurite outgrowth, DNA synthesis and survival in PC12 cells. 1 J Biol Chem. 1999 Dec 24;274(52) 37307-14. Gab1 mediates neurite outgrowth, DNA synthesis, and survival in PC12 cells. Korhonen JM, Said FA, Wong AJ, Kaplan DR. Montreal Neurological Institute, Brain Tumor Research Centre, Montreal, Quebec H3A 2B4, Canada. The Gab1-docking protein has been shown to regulate phosphatidylinositol 3-kinase PI3K activity and potentiate nerve growth factor (NGF)-induced survival in PC12 cells. Here, we investigated the potential of Gab1 to induce neurite outgrowth and DNA synthesis, two other important aspects of NGF-induced neuronal differentiation of PC12 cells and NGF-independent survival. We generated a recombinant adenovirus encoding hemagglutinin (HA)-epitope-tagged Gab1 and expressed this protein in PC12 cells. HA-Gab1 was constitutively tyrosine-phosphorylated in PC12 cells and induced the phosphorylation of Akt/protein kinase B and p44/42 mitogen-activated protein kinase. HA-Gab1-stimulated a 10-fold increase in neurite outgrowth in the absence of NGF and a 5-fold increase in NGF-induced neurite outgrowth. HA-Gab1 also stimulated DNA synthesis and caused NGF-independent survival in PC12 cells. Finally, we found that HA-Gab1-induced neuritogenesis was completely suppressed by pharmacological inhibition of mitogen-activated protein kinase kinase (MEK) activity and 50% suppressed by inhibition of PI3K activity. In contrast, HA-Gab1-stimulated cell survival was efficiently suppressed only by inhibition of both PI3K and MEK activities. These results indicate that Gab1 is capable of mediating differentiation, DNA synthesis, and cell survival and uses both PI3K and MEK signaling pathways to achieve its effects. Publication Types Research Support, Non-U.S. Gov t PMID 10601297 [PubMed - indexed for MEDLINE] SHCB-deficient animals exhibit a loss of peptidergic and nonpeptidergic nociceptive sensory neurons, 1 Neuron. 2000 Dec;28(3) 819-33. The mammalian ShcB and ShcC phosphotyrosine docking proteins function in the maturation of sensory and sympathetic neurons. Sakai R, Henderson JT, O Bryan JP, Elia AJ, Saxton TM, Pawson T. Program in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, M5G 1X5, Toronto, Ontario, Canada. Shc proteins possess SH2 and PTB domains and serve a scaffolding function in signaling by a variety of receptor tyrosine kinases. There are three known mammalian Shc genes, of which ShcB and ShcC are primarily expressed in the nervous system. We have generated null mutations in ShcB and ShcC and have obtained mice lacking either ShcB or ShcC or both gene products. ShcB-deficient animals exhibit a loss of peptidergic and nonpeptidergic nociceptive sensory neurons, which is not enhanced by additional loss of ShcC. Mice lacking both ShcB and ShcC exhibit a significant loss of neurons within the superior cervical ganglia, which is not observed in either mutant alone. The results indicate that these Shc family members possess both unique and overlapping functions in regulating neural development and suggest physiological roles for ShcB/ShcC in TrkA signaling. PMID 11163269 [PubMed - indexed for MEDLINE] Hippocampal long-term potentiation in ShcC mutant mice is significantly enhanced. 1 J Neurosci. 2005 Feb 16;25(7) 1826-35. Hippocampal synaptic modulation by the phosphotyrosine adapter protein ShcC/N-Shc via interaction with the NMDA receptor. Miyamoto Y, Chen L, Sato M, Sokabe M, Nabeshima T, Pawson T, Sakai R, Mori N. Department of Molecular Genetics, National Institute for Longevity Sciences, Oobu 474-8522, Japan. N-Shc (neural Shc) (also ShcC), an adapter protein possessing two phosphotyrosine binding motifs [PTB (phosphotyrosine binding) and SH2 (Src homology 2) domains], is predominantly expressed in mature neurons of the CNS and transmits neurotrophin signals from the TrkB receptor to the Ras/mitogen-activated protein kinase (MAPK) pathway, leading to cellular growth, differentiation, or survival. Here, we demonstrate a novel role of ShcC, the modulation of NMDA receptor function in the hippocampus, using ShcC gene-deficient mice. In behavioral analyses such as the Morris water maze, contextual fear conditioning, and novel object recognition tasks, ShcC mutant mice exhibited superior ability in hippocampus-dependent spatial and nonspatial learning and memory. Consistent with this finding, electrophysiological analyses revealed that hippocampal long-term potentiation in ShcC mutant mice was significantly enhanced, with no alteration of presynaptic function, and the effect of an NMDA receptor antagonist on its expression in the mutant mice was notably attenuated. The tyrosine phosphorylation of NMDA receptor subunits NR2A and NR2B was also increased, suggesting that ShcC mutant mice have enhanced NMDA receptor function in the hippocampus. These results indicate that ShcC not only mediates TrkB-Ras/MAPK signaling but also is involved in the regulation of NMDA receptor function in the hippocampus via interaction with phosphotyrosine residues on the receptor subunits and serves as a modulator of hippocampal synaptic plasticity underlying learning and memory. PMID 15716419 [PubMed - indexed for MEDLINE] SHCA controls the size of brain. 1 J Neurosci. 2006 Jul 26;26(30) 7885-97. Neural-specific inactivation of ShcA results in increased embryonic neural progenitor apoptosis and microencephaly. McFarland KN, Wilkes SR, Koss SE, Ravichandran KS, Mandell JW. Department of Pathology (Neuropathology), Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Virginia 22908, USA. Brain size is precisely regulated during development and involves coordination of neural progenitor cell proliferation, differentiation, and survival. The adapter protein ShcA transmits signals from receptor tyrosine kinases via MAPK (mitogen-activated protein kinase)/ERK (extracellular signal-regulated kinase) and PI3K (phosphatidylinositol 3-kinase)/Akt signaling pathways. In the CNS, ShcA expression is high during embryonic development but diminishes as cells differentiate and switches to ShcB/Sck/Sli and ShcC/N-Shc/Rai. To directly test ShcA function in brain development, we used Cre/lox technology to express a dominant-negative form of ShcA (ShcFFF) in nestin-expressing neural progenitors. ShcFFF-expressing mice display microencephaly with brain weights reduced to 50% of littermate controls throughout postnatal and adult life. The cerebrum appeared most severely affected, but the gross architecture of the brain is normal. Body weight was mildly affected with a delay in reaching mature weight. At a mechanistic level, the ShcFFF microencephaly phenotype appears to be primarily attributable to elevated apoptosis levels throughout the brain from embryonic day 10.5 (E10.5) to E12, which declined by E14.5. Apoptosis remained at normal basal levels throughout postnatal development. Proliferation indices were not significantly altered in the embryonic neuroepithelium or within the postnatal subventricular zone. In another approach with the same nestin-Cre transgene, conditional deletion of ShcA in mice with a homozygous floxed shc1 locus also showed a similar microencephaly phenotype. Together, these data suggest a critical role for ShcA in neural progenitor survival signaling and in regulating brain size. PMID 16870734 [PubMed - indexed for MEDLINE] Cbl-b null mice exhibit the enhancement of long-term memory. 1 Proc Natl Acad Sci U S A. 2006 Mar 28;103(13) 5125-30. Epub 2006 Mar 20. Enhancement of long-term memory retention and short-term synaptic plasticity in cbl-b null mice. Tan DP, Liu QY, Koshiya N, Gu H, Alkon D. Blanchette Rockefeller Neurosciences Institute, Rockville, MD 20850, USA. dptan@brni-jhu.org The cbl-b gene is a member of the cbl protooncogene family. It encodes a protein with multiple domains, which can interact with other proteins in a variety of signaling pathways. The functions of cbl family genes in the brain are unknown. In this report, we used genetic, immunohistochemical, behavioral, and electrophysiological approaches to study the role of cbl-b in learning and memory. Cbl-b null mice developed normally and had no abnormalities in their locomotor performance. In spatial learning and memory studies, cbl-b null and WT mice performed similarly during training. To test memory retention, two probe trials were used. cbl-b null mice performed slightly better 1 day after training. However, in the probe trial 45 days after training, the cbl-b null group showed significantly higher memory retention than WT mice, suggesting an enhancement of long-term memory. Using electrophysiological approaches, we found there was enhanced paired-pulse facilitation in the Schaffer Collateral-CA1 glutamatergic synapses of the cbl-b null mice. On the other hand, there was no difference in long-term potentiation between the two groups of mice. In summary, we provide evidence that (i) cbl-b protein is concentrated in the synaptic regions of CA1, CA3, and the dentate gyrus of the hippocampus; (ii) cbl-b null mice have enhanced long-term memory; and (iii) cbl-b null mice show an enhancement in short-term plasticity. These results indicate that cbl-b is a negative regulator of long-term memory, and its neuronal mechanism regulates synaptic transmission in the hippocampus. PMID 16549761 [PubMed - indexed for MEDLINE]
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今日 - 合計 - モノクローム・ファクター cross roadの攻略ページ 目次 基本情報 [部分編集] ストーリー [部分編集] 攻略情報 [部分編集] Tips [部分編集] プチ情報 [部分編集] 関連動画 [部分編集] 参考文献、参考サイト [部分編集] 感想・レビュー 基本情報 [部分編集] ストーリー [部分編集] 攻略情報 [部分編集] Tips [部分編集] プチ情報 [部分編集] 関連動画 [部分編集] 参考文献、参考サイト [部分編集] 感想・レビュー 名前 コメント 選択肢 投票 役に立った (0) 2012年10月09日 (火) 14時33分15秒 [部分編集] ページごとのメニューの編集はこちらの部分編集から行ってください [部分編集] 編集に関して
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_*rio*_さん ご紹介 このページへのコメントは以下へどうぞ☆ リオさん、はじめまして（*＾＾*）よろしくお願いします＾＾ -- †ミホ† (2010-08-24 21 54 42) 半年以上LHおやすみしていたので、何が何だかさっぱりです。よろしくお願いします。 -- _*rio*_ (2010-08-25 10 55 00) 3get 時間帯なかなか合わないっぽいけどよろしくです～ -- 徳之輔 (2010-08-25 22 26 25) ４ゲト。よろしゅう -- 神騎 (2010-08-27 11 35 09) 名前 コメント