Institution
Osaka University
Education•Osaka, Japan•
About: Osaka University is a education organization based out in Osaka, Japan. It is known for research contribution in the topics: Laser & Catalysis. The organization has 83778 authors who have published 185669 publications receiving 5158122 citations. The organization is also known as: Ōsaka daigaku.
Topics: Laser, Catalysis, Population, Gene, Thin film
Papers published on a yearly basis
Papers
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TL;DR: The Bcl‐2 family of proteins are focused on, which control the permeability of mitochondrial membrane during apoptosis and are implicated in apoptotic nuclear changes that occur in a caspase‐independent manner.
Abstract: An increase in the permeability of the outer mitochondrial membrane is central to apoptotic cell death, since it leads to the release of several apoptogenic factors, such as cytochrome c and Smac/Diablo, into the cytoplasm that activate downstream death programs. During apoptosis, the mitochondria also release AIF and endonuclease G, both of which are translocated to the nucleus and are implicated in apoptotic nuclear changes that occur in a caspase-independent manner. Mitochondrial membrane permeability is directly controlled by the major apoptosis regulator, i.e., the Bcl-2 family of proteins, mainly through regulation of the formation of apoptotic protein-conducting pores in the outer mitochondrial membrane, although the precise molecular mechanisms are still not completely understood. Here, I focus on the mechanisms by which Bcl-2 family members control the permeability of mitochondrial membrane during apoptosis.
483 citations
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TL;DR: It is demonstrated that TLR-7 exerts its biological effect in a DC subset-specific manner, and the Th1 cell supporting ability of both DC subsets was enhanced, depending on the cytokines the respective subsets produced.
Abstract: Dendritic cells (DCs) play a crucial role in the immune responses against infections by sensing microbial invasion through toll-like receptors (TLRs). In humans, two distinct DC subsets, CD11c− plasmacytoid DCs (PDCs) and CD11c+ myeloid DCs (MDCs), have been identified and can respond to different TLR ligands, depending on the differential expression of cognate TLRs. In this study, we have examined the effect of TLR-7 ligands on human DC subsets. Both subsets expressed TLR-7 and could respond to TLR-7 ligands, which enhanced the survival of the subsets and upregulated the surface expression of costimulatory molecules such as CD40, CD80, and CD86. However, the cytokine induction pattern was distinct in that PDCs and MDCs produced interferon (IFN)-α and interleukin (IL)-12, respectively. In response to TLR-7 ligands, the Th1 cell supporting ability of both DC subsets was enhanced, depending on the cytokines the respective subsets produced. This study demonstrates that TLR-7 exerts its biological effect in a DC subset-specific manner.
483 citations
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481 citations
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TL;DR: In this article, it was shown that cAMP-GEFII, a cAMP sensor, binds to Rim (Rab3-interacting molecule, Rab3 being a small G protein) and to a new isoform, Rim2, both of which are putative regulators of fusion of vesicles to the plasma membrane.
Abstract: Although cAMP is well known to regulate exocytosis in many secretory cells, its direct target in the exocytotic machinery is not known. Here we show that cAMP-GEFII, a cAMP sensor, binds to Rim (Rab3-interacting molecule, Rab3 being a small G protein) and to a new isoform, Rim2, both of which are putative regulators of fusion of vesicles to the plasma membrane. We also show that cAMP-GEFII, through its interaction with Rim2, mediates cAMP-induced, Ca2+-dependent secretion that is not blocked by an inhibitor of cAMP-dependent protein kinase (PKA). Accordingly, cAMP-GEFII is a direct target of cAMP in regulated exocytosis and is responsible for cAMP-dependent, PKA-independent exocytosis.
481 citations
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TL;DR: Transfected glomerulonephritic rats showed a significant reduction in levels of glomerular TGF–β1 mRNA and TGF-β1 protein, extracellular matrix accumulation and proteinuria, demonstrating the potential of gene therapy as a novel treatment for fibrotic diseases caused by TGF –β1.
Abstract: There are currently no effective therapies for progressive fibrotic diseases. Recent evidence has implicated overproduction of transforming growth factor-beta1 (TGF-beta1) as a major cause of tissue fibrosis. Furthermore, this evidence implies that inhibitors of TGF-beta1 may be clinically useful as antifibrotic agents. The proteoglycan decorin is a known inhibitor of TGF-beta1. In a rat model of glomerulonephritis we have shown that fibrosis is mediated by TGF-beta1. We report here that transfer of decorin cDNA into rat skeletal muscle increases the amount of decorin messenger RNA and protein present in skeletal muscle and decorin present in kidney, where it has a marked therapeutic effect on fibrosis induced by glomerulonephritis. Transfected glomerulonephritic rats showed a significant reduction in levels of glomerular TGF-beta1 mRNA and TGF-beta1 protein, extracellular matrix accumulation and proteinuria. These results demonstrate the potential of gene therapy as a novel treatment for fibrotic diseases caused by TGF-beta1.
481 citations
Authors
Showing all 84130 results
Name | H-index | Papers | Citations |
---|---|---|---|
Shizuo Akira | 261 | 1308 | 320561 |
Thomas C. Südhof | 191 | 653 | 118007 |
Tadamitsu Kishimoto | 181 | 1067 | 130860 |
Yusuke Nakamura | 179 | 2076 | 160313 |
H. S. Chen | 179 | 2401 | 178529 |
Hyun-Chul Kim | 176 | 4076 | 183227 |
Masayuki Yamamoto | 171 | 1576 | 123028 |
Kenji Kangawa | 153 | 1117 | 110059 |
Jongmin Lee | 150 | 2257 | 134772 |
Yoshio Bando | 147 | 1234 | 80883 |
Takeo Kanade | 147 | 799 | 103237 |
Olaf Reimer | 144 | 716 | 74359 |
Yuji Matsuzawa | 143 | 836 | 116711 |
Kim Nasmyth | 142 | 294 | 59231 |
Tasuku Honjo | 141 | 712 | 88428 |