排序方式: 共有71条查询结果,搜索用时 46 毫秒
31.
Maruoka M Suzuki J Kawata S Yoshida K Hirao N Sato S Goff SP Takeya T Tani K Shishido T 《FEBS letters》2005,579(14):2986-2990
In previous work we showed that Abl interactor 1 (Abi-1), by linking enzyme and substrate, promotes the phosphorylation of Mammalian Enabled (Mena) by c-Abl. To determine whether this mechanism extends to other c-Abl substrates, we used the yeast two-hybrid system to search for proteins that interact with Abi-1. By screening a human leukocyte cDNA library, we identified BCAP (B-cell adaptor for phosphoinositide 3-kinase) as another Abi-1-interacting protein. Binding experiments revealed that the SH3 domain of Abi-1 and the C-terminal polyproline structure of BCAP are involved in interactions between the two. In cultured cells, Abi-1 promoted phosphorylation of BCAP not only by c-Abl but also by v-Abl. The phosphorylation sites of BCAP by c-Abl were mapped to five tyrosine residues in the C-terminal region that are well conserved in mammals. These results show that Abi-1 promotes Abl-mediated BCAP phosphorylation and suggest that Abi-1 in general coordinates kinase-substrate interactions. 相似文献
32.
Konno D Yoshimura S Hori K Maruoka H Sobue K 《The Journal of biological chemistry》2005,280(6):5082-5088
During cortical development, newly generated neurons migrate radially toward their final positions. Although several candidate genes essential for this radial migration have been reported, the signaling pathways regulating it are largely unclear. Here we studied the role of phosphatidylinositol (PI) 3-kinase and its downstream signaling molecules in the radial migration of cortical neurons in vivo and in vitro. The expression of constitutively active and dominant-negative PI 3-kinases markedly inhibited radial migration. In the neocortical slice culture, a PI 3-kinase inhibitor suppressed the formation of GTP-bound Rac1 and Cdc42 and radial migration. Constitutively active and dominant-negative forms of Rac1 and Cdc42 but not Akt also significantly inhibited radial migration. In migrating neurons, wild-type Rac1 and Cdc42 showed different localizations; Rac1 localized to the plasma membrane and Cdc42 to the perinuclear region on the side of the leading processes. These results suggest that both the PI 3-kinase/Rac1 and Cdc42 pathways are involved in the radial migration of cortical neurons and that they have different roles. 相似文献
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34.
Mizuho Kondo Takako Maruoka Noriyuki Otsuka Jun Kasamatsu Kazunori Fugo Naoto Hanzawa Masanori Kasahara 《Immunogenetics》2010,62(7):441-450
NKG2D is a major activating receptor of natural killer cells. Its ligands are major histocompatibility complex (MHC) class
I-like molecules whose expression is induced by cellular stresses such as infections and tumorigenesis. Humans have two families
of NKG2D ligands (NKG2DL): MHC class I-related chains (MIC) encoded in the MHC and UL16-binding proteins (ULBP) encoded outside
the MHC. By contrast, mice have only the latter family of ligands; instead, they have non-MHC-encoded MILL molecules that
are closely related to MIC, but do not function as NKG2DL. To gain insights into the origin and evolution of MIC, ULBP, and MILL gene families, we conducted comparative genomic analysis of NKG2DL family genes in five mammalian species. In the opossum
MHC, we identified a ULBP-like gene adjacent to a previously described MIC-like gene, suggesting that ULBP genes were originally encoded in the MHC. The opossum genome also contained a transcribed MILL-like gene in a region syntenic to the rodent regions encoding MILL molecules. These observations indicate that MIC-, ULBP-, and MILL-like genes emerged before the divergence of placental and marsupial mammals. Comparison of the human, cattle, rat, mouse,
and opossum genomes indicates that after emigration from the MHC, ULBP genes underwent extensive duplications in each species. In mice, some of the ULBP genes appear to have been translocated telomerically on the same chromosome, forming a major cluster of existent NKG2DL genes. 相似文献
35.
Ishida-Kitagawa N Tanaka K Bao X Kimura T Miura T Kitaoka Y Hayashi K Sato M Maruoka M Ogawa T Miyoshi J Takeya T 《The Journal of biological chemistry》2012,287(21):17493-17502
Osteoclasts are multinucleated giant cells that reside in osseous tissues and resorb bone. Signaling mediated by receptor activator of nuclear factor (NF)-κB (RANK) and its ligand leads to the nuclear factor of activated T cells 2/c1 (NFAT2 or NFATc1) expression, a critical step in the formation of functional osteoclasts. In addition, adaptor proteins harboring immunoreceptor tyrosine-based activation motifs, such as DNAX-activating protein of 12 kDa (DAP12), play essential roles. In this study, we identified the gene encoding the lectin Siglec-15 as NFAT2-inducible, and we found that the protein product links RANK ligand-RANK-NFAT2 and DAP12 signaling in mouse osteoclasts. Both the recognition of sialylated glycans by the Siglec-15 V-set domain and the association with DAP12 through its Lys-272 are essential for its function. When Siglec-15 expression was knocked down, fewer multinucleated cells developed, and those that did were morphologically contracted with disordered actin-ring structures. These changes were accompanied by significantly reduced bone resorption. Siglec-15 formed complexes with Syk through DAP12 in response to vitronectin. Furthermore, chimeric molecules consisting of the extracellular and transmembrane regions of Siglec-15 with a K272A mutation and the cytoplasmic region of DAP12 significantly restored bone resorption in cells with knocked down Siglec-15 expression. Together, these results suggested that the Siglec-15-DAP12-Syk-signaling cascade plays a critical role in functional osteoclast formation. 相似文献
36.
Hui‐Min Qin Akihiro Yamamura Takuya Miyakawa Michihiko Kataoka Shintaro Maruoka Jun Ohtsuka Koji Nagata Sakayu Shimizu Masaru Tanokura 《Proteins》2013,81(11):2059-2063
Conjugated polyketone reductase (CPR‐C1) from Candida parapsilosis IFO 0708 is a member of the aldo–keto reductase (AKR) superfamily and reduces ketopantoyl lactone to d ‐pantoyl lactone in a NADPH‐dependent and stereospecific manner. We determined the crystal structure of CPR‐C1.NADPH complex at 2.20 Å resolution. CPR‐C1 adopted a triose‐phosphate isomerase (TIM) barrel fold at the core of the structure in which Thr25 and Lys26 of the GXGTX motif bind uniquely to the adenosine 2′‐phosphate group of NADPH. This finding provides a novel structural basis for NADPH binding of the AKR superfamily. Proteins 2013; 81:2059–2063. © 2013 Wiley Periodicals, Inc. 相似文献
37.
Masaaki Konishi Naruyuki Maruoka Yoshifumi Furuta Tomotake Morita Tokuma Fukuoka Tomohiro Imura 《Bioscience, biotechnology, and biochemistry》2013,77(3):516-523
The isolation of biosurfactant-producing yeasts from food materials was accomplished. By a combination of a new drop collapse method and thin-layer chromatography, 48 strains were selected as glycolipid biosurfactant producers from 347 strains, which were randomly isolated from various vegetables and fruits. Of the producers, 69% were obtained from vegetables of the Brassica family. Of the 48 producers, 15 strains gave relatively high yields of mannosylerythritol lipids (MELs), and were identified as Pseudozyma yeasts. These strains produced MELs from olive oil at yields ranging from 8.5 to 24.3?g/L. The best yield coefficient reached 0.49?g/g as to the carbon sources added. Accordingly, MEL producers were isolated at high efficiency from various vegetables and fruits, indicating that biosurfactant producers are widely present in foods. The present results should facilitate their application in the food and related industries. 相似文献
38.
Kido M Watanabe N Aoki N Iwamoto S Nishiura H Maruoka R Ikeda A Azuma T Chiba T 《Biochemical and biophysical research communications》2011,412(2):266-272
Cytotoxin-associated gene A (CagA) acts directly on gastric epithelial cells. However, the roles of CagA in host adaptive immunity against Helicobacter pylori (H. pylori) infection are not fully understood. In this study, to investigate the roles of CagA in the development of H. pylori-induced chronic gastritis, we used an adoptive-transfer model in which spleen cells from C57BL/6 mice with or without H. pylori infection were transferred into RAG2−/− mice, with gastric colonization of either CagA+H. pylori or CagA−H. pylori. Colonization of CagA+H. pylori but not CagA−H. pylori in the host gastric mucosa induced severe chronic gastritis in RAG2−/− mice transferred with spleen cells from H. pylori-uninfected mice. In addition, when CagA+H. pylori-primed spleen cells were transferred into RAG2−/− mice, CD4+ T cell infiltration in the host gastric mucosa were observed only in RAG2−/− mice infected with CagA+H. pylori but not CagA−H. pylori, suggesting that colonization of CagA+H. pylori in the host gastric mucosa is essential for the migration of H. pylori-primed CD4+ T cells. On the other hand, transfer of CagA−H. pylori-primed spleen cells into CagA+H. pylori-infected RAG2−/− mice induced more severe chronic gastritis with less Foxp3+ regulatory T-cell infiltration as compared to transfer of CagA+H. pylori-primed spleen cells. In conclusion, CagA in the stomach plays an important role in the migration of H. pylori-primed CD4+ T cells in the gastric mucosa, whereas CagA-dependent T-cell priming induces regulatory T-cell differentiation, suggesting dual roles for CagA in the pathophysiology of H. pylori-induced chronic gastritis. 相似文献
39.
Sato M Maruoka M Yokota N Kuwano M Matsui A Inada M Ogawa T Ishida-Kitagawa N Takeya T 《FEBS letters》2011,585(6):834-840
Abi-1 is an adaptor protein for Abelson kinase (c-Abl), and Abi-1 promotes the Abl-mediated phosphorylation of Mammalian Enabled (Mena) by binding both c-Abl and Mena. Here, we identified a new phosphorylation site (Y398) in the SH3 domain of Abi-1, and disruption of Y398, combined with the previously identified phosphorylation site Y213, significantly weakens the binding of Abi-1 to c-Abl. The SH3 domain of Abi-1 and the proline-rich domain of c-Abl are involved in this interaction. Abi-1 phosphorylation at both sites stimulates the phosphorylation of Mena through the activation of c-Abl kinase. The phosphorylation of Abi-1 also plays a role in enhancing the adhesion of Bcr-Abl-transformed leukemic cells. 相似文献
40.
Shimoke K Matsuki Y Fukunaga K Matsumura Y Fujita E Sugihara K Nobuhara M Maruoka H Ikeuchi T Kudo M 《Cellular and molecular neurobiology》2011,31(5):795-802
Following endoplasmic reticulum (ER) stress, cerebral infarctions have been reported to involve an apoptotic process, including
the activation of the caspase cascade. To confirm whether fragmented caspase-12, which is activated by cleavage and is detectable
during ER stress, is also involved in embolic cerebral infarctions in rats, we adopted an autologous blood clot model for
the analysis of cerebral infarctions. We performed experiments in rats with brain infarctions, which are closely related to
embolic cerebral infarctions. We utilized a homologous blood clot, i.e., natural materials, to form the infarct area. Our
findings reveal that caspase-12 is fragmented when infarct areas form in cerebral cortical neurons. Interestingly, we observed
that these fragments translocated to the nuclei of not only cerebral cortical neurons but hippocampal neurons. We further
found that glucose-regulated protein 78 (GRP78), a marker of ER stress, is up-regulated in both cerebral cortical and hippocampal
neurons during cerebral infarction. This result suggests that the fragmentation of caspase-12 and the subsequent nuclear translocation
of these fragments are involved in the brain infarction process in rats. 相似文献