48 research outputs found
Who wrote “Takekawa” in The Tale of Genji : Examining special words in “Takekawa”
No full textapplication/pdf『源氏物語』五四帖は誰の手によって書かれたものであろうか。匂宮三帖、とりわけ竹河巻は古来より他の巻とは別筆ではないかと疑われてきた。最近ではこの論争は沈静化されているが、本稿では敢えてこの問題に取り組んでみた。 研究史の中には物語内の語彙の用法に着目して、その用法の違いを分析することにより、別筆説を導き出そうとする作業もあるが、本稿は語彙そのものに焦点を当てた。﹃源氏物語﹄は、その場の自然の状況や登場人物の心の動きなどを表現するために、実に多彩な複合語を駆使していて、それらの複合語は源氏以前には用例のない源氏固有の造語が多い。これらの固有語を調べ出して、その造語方法の特徴や巻ごとの分布などを把握して、竹河巻の語彙と比較した。果たして別筆の可能性はありやなしや。Many researchers of The Tale of Genji have long suspected the writer of “Takekawa” could not be Murasaki Shikibu, because the writing style in “Takekawa” is poor and childish, and the story of “Takekawa” is not possible. Recently, students of Genji have chosen not to take up this question because of the difficulties involved, but, in this paper, I attempt to answer this question by examining special words, namely, those words that were not found in The Tale of Genji. Murasaki Sikibu created many new words in The Tale of Genji. In this paper, I find all of the special words in Genji and compare them with the special words of “Takekawa”. In doing so, I am convinced that this is an innovative way of dealing with the problem of identifying the author of the latter.departmental bulletin pape
A Family of Stress-Inducible GADD45-like Proteins Mediate Activation of the Stress-Responsive MTK1/MEKK4 MAPKKK
No full textAbstractThe stress-responsive p38 and JNK MAPK pathways regulate cell cycle and apoptosis. A human MAPKKK, MTK1 (= MEKK4), mediates activation of both p38 and JNK in response to environmental stresses. Using a yeast two-hybrid method, three related proteins, GADD45α (= GADD45), GADD45β (= MyD118), and GADD45γ, were identified that bound to an N-terminal domain of MTK1. These proteins activated MTK1 kinase activity, both in vivo and in vitro. The GADD45-like genes are induced by environmental stresses, including MMS, UV, and γ irradiation. Expression of the GADD45-like genes induces p38/JNK activation and apoptosis, which can be partially suppressed by coexpression of a dominant inhibitory MTK1 mutant protein. We propose that the GADD45-like proteins mediate activation of the p38/JNK pathway, via MTK1/MEKK4, in response to environmental stresses
SAPK pathways and p53 cooperatively regulate PLK4 activity and centrosome integrity under stress
No full textWGA-based lectin affinity gel electrophoresis: A novel method for the detection of O-GlcNAc-modified proteins.
No full textPost-translational modification with O-linked β-N-acetylglucosamine (O-GlcNAc) occurs selectively on serine and/or threonine residues of cytoplasmic and nuclear proteins, and dynamically regulates their molecular functions. Since conventional strategies to evaluate the O-GlcNAcylation level of a specific protein require time-consuming steps, the development of a rapid and easy method for the detection and quantification of an O-GlcNAcylated protein has been a challenging issue. Here, we describe a novel method in which O-GlcNAcylated and non-O-GlcNAcylated forms of proteins are separated by lectin affinity gel electrophoresis using wheat germ agglutinin (WGA), which primarily binds to N-acetylglucosamine residues. Electrophoresis of cell lysates through a gel containing copolymerized WGA selectively induced retardation of the mobility of O-GlcNAcylated proteins, thereby allowing the simultaneous visualization of both the O-GlcNAcylated and the unmodified forms of proteins. This method is therefore useful for the quantitative detection of O-GlcNAcylated proteins
REGULATION OF STRESS-ACTIVATED MAP KINASE PATHWAYS DURING CELL FATE DECISIONS
No full text2011-02Mammalian cells are frequently exposed to a variety of environmental stresses, such as ultraviolet rays, ionizing radiation, genotoxins, heat shock, and oxidative stress. In coping with the barrage of these and other stresses, multi-cellular eukaryotic organisms have developed a strategy as to how damaged cells will respond to stresses. In general, if the intensity of the damage is moderate, the cell will seek to repair the damage. If, however, the damage to a cell is too severe to be repaired, the affected cells are eliminated by apoptosis. This cell death reduces the risk to the organism as a whole, such as development of a cancer. Such a crucial decision between survival and death is, at least in part, mediated by the stress-activated MAP kinase (SAPK) pathways. SAPKs are a group of serine/threonine protein kinases that convert extracellular stress stimuli into diverse cellular responses, including cell cycle arrest, apoptotic cell death, and cytokine production, through phosphorylation of specific target proteins. Recent progress in the identification of molecules that participate in the SAPK pathways, such as GADD45 proteins and Wip1, has provided new insights, not only into the molecular basis of the cellular response to environmental stress, but also into the etiology of human diseases including cancer.departmental bulletin pape
REGULATION OF STRESS-ACTIVATED MAP KINASE PATHWAYS DURING CELL FATE DECISIONS
No full textMammalian cells are frequently exposed to a variety of environmental stresses, such as ultraviolet rays, ionizing radiation, genotoxins, heat shock, and oxidative stress. In coping with the barrage of these and other stresses, multi-cellular eukaryotic organisms have developed a strategy as to how damaged cells will respond to stresses. In general, if the intensity of the damage is moderate, the cell will seek to repair the damage. If, however, the damage to a cell is too severe to be repaired, the affected cells are eliminated by apoptosis. This cell death reduces the risk to the organism as a whole, such as development of a cancer. Such a crucial decision between survival and death is, at least in part, mediated by the stress-activated MAP kinase (SAPK) pathways. SAPKs are a group of serine/threonine protein kinases that convert extracellular stress stimuli into diverse cellular responses, including cell cycle arrest, apoptotic cell death, and cytokine production, through phosphorylation of specific target proteins. Recent progress in the identification of molecules that participate in the SAPK pathways, such as GADD45 proteins and Wip1, has provided new insights, not only into the molecular basis of the cellular response to environmental stress, but also into the etiology of human diseases including cancer
Oncogenic Ras abrogates MEK SUMOylation that suppresses the ERK pathway and cell transformation
No full textMolecular dynamics simulations of a multicellular model with cell-cell interactions and Hippo signaling pathway
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