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Institution

Osaka University

EducationOsaka, Japan
About: Osaka University is a education organization based out in Osaka, Japan. It is known for research contribution in the topics: Laser & Population. The organization has 83778 authors who have published 185669 publications receiving 5158122 citations. The organization is also known as: Ōsaka daigaku.
Topics: Laser, Population, Catalysis, Thin film, Gene


Papers
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Journal ArticleDOI
TL;DR: A neuron-glia interaction that is indispensable for network formation during a specific period in the developing brain is highlighted, with microglia-derived IGF1 as a trophic factor that maintained neuronal survival.
Abstract: Neurons require trophic support during neural circuit formation; however, how the cellular milieu contributes to neuronal survival remains unclear. We found that layer V cortical neurons require support from microglia for survival during postnatal development. Specifically, we found that microglia accumulated close to the subcerebral and callosal projection axons in the postnatal brain. Inactivation of microglia by minocycline treatment or transient ablation of microglia in CD11b-DTR transgenic mice led to increased apoptosis, specifically in layer V subcerebral and callosal projection neurons. CX3CR1 in microglia was required for the survival of layer V neurons. Microglia consistently promoted the survival of cortical neurons in vitro. In addition, we identified microglia-derived IGF1 as a trophic factor that maintained neuronal survival. Our results highlight a neuron-glia interaction that is indispensable for network formation during a specific period in the developing brain.

581 citations

Journal ArticleDOI
28 Jun 2001-Nature
TL;DR: It is found that Ras at the neurites turned over rapidly; therefore, the sustained Ras activity at neurites was due to high GTP/GDP exchange rate and/or low GTPase activity, but not to the retention of the active Ras.
Abstract: G proteins of the Ras family function as molecular switches in many signalling cascades; however, little is known about where they become activated in living cells. Here we use FRET (fluorescent resonance energy transfer)-based sensors to report on the spatio-temporal images of growth-factor-induced activation of Ras and Rap1. Epidermal growth factor activated Ras at the peripheral plasma membrane and Rap1 at the intracellular perinuclear region of COS-1 cells. In PC12 cells, nerve growth factor-induced activation of Ras was initiated at the plasma membrane and transmitted to the whole cell body. After three hours, high Ras activity was observed at the extending neurites. By using the FRAP (fluorescence recovery after photobleaching) technique, we found that Ras at the neurites turned over rapidly; therefore, the sustained Ras activity at neurites was due to high GTP/GDP exchange rate and/or low GTPase activity, but not to the retention of the active Ras. These observations may resolve long-standing questions as to how Ras and Rap1 induce different cellular responses and how the signals for differentiation and survival are distinguished by neuronal cells.

581 citations

Journal ArticleDOI
TL;DR: IL‐6 generates both growth‐enhancing signals and growth arrest‐ and differentiation‐inducing signals at the same time, suggesting Stat3 may be a key molecule which determines the cellular decision from cell growth to differentiation in M1 cells.
Abstract: Interleukin-6 (IL-6) induces either differentiation or growth of a variety of cells. Little is known about the molecular basis of this cellular decision. The family of signal transducer and activator of transcription (Stat) proteins are involved in signaling through a variety of cytokine and growth factor receptors, although their biological roles have not been established. To address whether Stat proteins play roles in IL-6-induced growth or differentiation, we introduced two types of mutant Stat3 acting in a dominant-negative manner into M1 leukemic cells which respond to IL-6 with growth arrest and terminal differentiation. We show that dominant-negative forms of Stat3 inhibited both IL-6-induced growth arrest at G(0)/G1 and macrophage differentiation in the M1 transformants. Blocking of Stat activation resulted in inhibition of IL-6-induced repression of c-myb and c-myc. Furthermore, IL-6 enhanced the growth of M1 cells primarily through shortening the length of the G1 period when Stat3 was suppressed. Thus IL-6 generates both growth-enhancing signals and growth arrest- and differentiation-inducing signals at the same time. Stat3 may be a key molecule which determines the cellular decision from cell growth to differentiation in M1 cells.

581 citations

Journal ArticleDOI
TL;DR: It is concluded that NF-IL6 is regulated through phosphorylation by MAP kinases in response to activated ras, andutation of Thr-235 abolished the ras-dependent activation of NF- IL6.
Abstract: NF-IL6, a member of the basic leucine zipper (bZIP) family transcription factors, is involved in expression of inducible genes involved in immune and inflammatory responses. We observed that coexpression of oncogenic p21ras stimulated the transactivating activity of NF-IL6 and induced phosphorylation of Thr-235 located just N-terminal to the DNA binding domain of NF-IL6. Recently, mitogen-activated protein (MAP) kinases have been shown to be implicated in the cellular response to activated ras. Purified MAP kinases specifically phosphorylated Thr-235 of NF-IL6 in vitro. Mutation of Thr-235 abolished the ras-dependent activation of NF-IL6. From these results, we conclude that NF-IL6 is regulated through phosphorylation by MAP kinases in response to activated ras.

580 citations

Journal ArticleDOI
TL;DR: Depletion of FOXP3hi Treg cells from tumor tissues, which would augment antitumor immunity, could thus be used as an effective treatment strategy for CRCs and other cancers, whereas strategies that locally increase the population ofFOXP3lo non-Treg cells could be used to suppress or prevent tumor formation.
Abstract: Shimon Sakaguchi and colleagues report that FOXP3+CD4+ T cell subsets differ functionally and are associated with distinct prognoses for individuals with colorectal cancer.

579 citations


Authors

Showing all 84130 results

NameH-indexPapersCitations
Shizuo Akira2611308320561
Thomas C. Südhof191653118007
Tadamitsu Kishimoto1811067130860
Yusuke Nakamura1792076160313
H. S. Chen1792401178529
Hyun-Chul Kim1764076183227
Masayuki Yamamoto1711576123028
Kenji Kangawa1531117110059
Jongmin Lee1502257134772
Yoshio Bando147123480883
Takeo Kanade147799103237
Olaf Reimer14471674359
Yuji Matsuzawa143836116711
Kim Nasmyth14229459231
Tasuku Honjo14171288428
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023139
2022637
20216,914
20206,865
20196,462
20186,189