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  • 1
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    Expression of RASSF6 in kidney and the implication of RASSF6 and the Hippo pathway in the sorbitol-induced apoptosis in renal proximal tubular epithelial cells (2012)
    Oxford University Press
    Details
    Publication Date: 2012-07-05
    Description: RASSF6, a member of RASSF tumour suppressor proteins, binds to mammalian Ste20-like kinases (MST1/2), core kinases of the proapoptotic Hippo pathway and cooperates with the Hippo pathway to induce apoptosis. We originally identified RASSF6 as a putative interactor of membrane-associated guanylate kinase inverted (MAGI)-1 by the yeast two-hybrid screening. We used human kidney cDNA library for the screening. MAGI-1 is abundantly expressed in kidney and is a core component of the slit diaphragm. These findings suggest that RASSF6 is expressed in kidney. However, the function of RASSF6 in kidney is not yet studied. We performed this study to confirm the interaction of RASSF6 with MAGI-1, to analyse the expression of RASSF6 in kidney and to gain insight into the function of RASSF6 in kidney. RASSF6 binds to PDZ domains of MAGI-1 through its C-terminal PDZ-binding motif and is coimmunoprecipitated with MAGI-1 from rat liver. RASSF6 is localized in normal kidney glomerulus but disappears when the slit diaphragm is disrupted in nephrotic kidney. RASSF6 is also localized on apical membranes in renal proximal tubular epithelial cells. We demonstrated that RASSF6 as well as the Hippo pathway are involved in the sorbitol-induced apoptosis in immortalized human proximal renal tubular epithelial HK-2 cells.
    Print ISSN: 0021-924X
    Electronic ISSN: 1756-2651
    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of The Japanese Biochemical Society (JBS).
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  • 2
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    SC3-seq: a method for highly parallel and quantitative measurement of single-cell gene expression (2015)
    Oxford University Press
    Details
    Publication Date: 2015-05-20
    Description: Single-cell mRNA sequencing (RNA-seq) methods have undergone rapid development in recent years, and transcriptome analysis of relevant cell populations at single-cell resolution has become a key research area of biomedical sciences. We here present s ingle- c ell mRNA 3 -prime end seq uencing (SC3-seq), a practical methodology based on PCR amplification followed by 3-prime-end enrichment for highly quantitative, parallel and cost-effective measurement of gene expression in single cells. The SC3-seq allows excellent quantitative measurement of mRNAs ranging from the 10,000-cell to 1-cell level, and accordingly, allows an accurate estimate of the transcript levels by a regression of the read counts of spike-in RNAs with defined copy numbers. The SC3-seq has clear advantages over other typical single-cell RNA-seq methodologies for the quantitative measurement of transcript levels and at a sequence depth required for the saturation of transcript detection. The SC3-seq distinguishes four distinct cell types in the peri-implantation mouse blastocysts. Furthermore, the SC3-seq reveals the heterogeneity in human-induced pluripotent stem cells (hiPSCs) cultured under on-feeder as well as feeder-free conditions, demonstrating a more homogeneous property of the feeder-free hiPSCs. We propose that SC3-seq might be used as a powerful strategy for single-cell transcriptome analysis in a broad range of investigations in biomedical sciences.
    Keywords: Massively Parallel (Deep) Sequencing
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 3
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    N-terminal phosphorylation of HP1{alpha} increases its nucleosome-binding specificity (2014)
    Oxford University Press
    Details
    Publication Date: 2014-11-12
    Description: Heterochromatin protein 1 (HP1) is an evolutionarily conserved chromosomal protein that binds to lysine 9-methylated histone H3 (H3K9me), a hallmark of heterochromatin. Although HP1 phosphorylation has been described in several organisms, the biological implications of this modification remain largely elusive. Here we show that HP1's phosphorylation has a critical effect on its nucleosome binding properties. By in vitro phosphorylation assays and conventional chromatography, we demonstrated that casein kinase II (CK2) is the kinase primarily responsible for phosphorylating the N-terminus of human HP1α. Pull-down assays using in vitro -reconstituted nucleosomes showed that unmodified HP1α bound H3K9-methylated and H3K9-unmethylated nucleosomes with comparable affinity, whereas CK2-phosphorylated HP1α showed a high specificity for H3K9me3-modified nucleosomes. Electrophoretic mobility shift assays showed that CK2-mediated phosphorylation diminished HP1α's intrinsic DNA binding, which contributed to its H3K9me-independent nucleosome binding. CK2-mediated phosphorylation had a similar effect on the nucleosome-binding specificity of fly HP1a and S. pombe Swi6. These results suggested that HP1 phosphorylation has an evolutionarily conserved role in HP1's recognition of H3K9me-marked nucleosomes.
    Keywords: Protein-protein interaction, Recombinant DNA expression, Chromatin and Epigenetics
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 4
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    Identification of UBIAD1 as a novel human menaquinone-4 biosynthetic enzyme (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-10-19
    Description: Vitamin K occurs in the natural world in several forms, including a plant form, phylloquinone (PK), and a bacterial form, menaquinones (MKs). In many species, including humans, PK is a minor constituent of hepatic vitamin K content, with most hepatic vitamin K content comprising long-chain MKs. Menaquinone-4 (MK-4) is ubiquitously present in extrahepatic tissues, with particularly high concentrations in the brain, kidney and pancreas of humans and rats. It has consistently been shown that PK is endogenously converted to MK-4 (refs 4-8). This occurs either directly within certain tissues or by interconversion to menadione (K(3)), followed by prenylation to MK-4 (refs 9-12). No previous study has sought to identify the human enzyme responsible for MK-4 biosynthesis. Previously we provided evidence for the conversion of PK and K(3) into MK-4 in mouse cerebra. However, the molecular mechanisms for these conversion reactions are unclear. Here we identify a human MK-4 biosynthetic enzyme. We screened the human genome database for prenylation enzymes and found UbiA prenyltransferase containing 1 (UBIAD1), a human homologue of Escherichia coli prenyltransferase menA. We found that short interfering RNA against the UBIAD1 gene inhibited the conversion of deuterium-labelled vitamin K derivatives into deuterium-labelled-MK-4 (MK-4-d(7)) in human cells. We confirmed that the UBIAD1 gene encodes an MK-4 biosynthetic enzyme through its expression and conversion of deuterium-labelled vitamin K derivatives into MK-4-d(7) in insect cells infected with UBIAD1 baculovirus. Converted MK-4-d(7) was chemically identified by (2)H-NMR analysis. MK-4 biosynthesis by UBIAD1 was not affected by the vitamin K antagonist warfarin. UBIAD1 was localized in endoplasmic reticulum and ubiquitously expressed in several tissues of mice. Our results show that UBIAD1 is a human MK-4 biosynthetic enzyme; this identification will permit more effective decisions to be made about vitamin K intake and bone health.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakagawa, Kimie -- Hirota, Yoshihisa -- Sawada, Natsumi -- Yuge, Naohito -- Watanabe, Masato -- Uchino, Yuri -- Okuda, Naoko -- Shimomura, Yuka -- Suhara, Yoshitomo -- Okano, Toshio -- England -- Nature. 2010 Nov 4;468(7320):117-21. doi: 10.1038/nature09464. Epub 2010 Oct 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Hygienic Sciences, Kobe Pharmaceutical University, 4-19-1, Motoyamakita-machi, Higashinada-ku, Kobe 658-8558, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20953171" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Baculoviridae/genetics/physiology ; Bone and Bones/metabolism ; Cell Line ; Dimethylallyltranstransferase ; Humans ; Magnetic Resonance Imaging ; Mice ; Osteoblasts ; Proteins/genetics/*metabolism ; RNA, Small Interfering/genetics/metabolism ; Spodoptera/cytology/virology ; Vitamin K/antagonists & inhibitors/metabolism ; Vitamin K 1/metabolism ; Vitamin K 2/*analogs & derivatives/analysis/chemistry/metabolism ; Warfarin/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Critical role of Trib1 in differentiation of tissue-resident M2-like macrophages (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-03-22
    Description: Macrophages consist of at least two subgroups, M1 and M2 (refs 1-3). Whereas M1 macrophages are proinflammatory and have a central role in host defence against bacterial and viral infections, M2 macrophages are associated with responses to anti-inflammatory reactions, helminth infection, tissue remodelling, fibrosis and tumour progression. Trib1 is an adaptor protein involved in protein degradation by interacting with COP1 ubiquitin ligase. Genome-wide association studies in humans have implicated TRIB1 in lipid metabolism. Here we show that Trib1 is critical for the differentiation of F4/80(+)MR(+) tissue-resident macrophages--that share characteristics with M2 macrophages (which we term M2-like macrophages)--and eosinophils but not for the differentiation of M1 myeloid cells. Trib1 deficiency results in a severe reduction of M2-like macrophages in various organs, including bone marrow, spleen, lung and adipose tissues. Aberrant expression of C/EBPalpha in Trib1-deficient bone marrow cells is responsible for the defects in macrophage differentiation. Unexpectedly, mice lacking Trib1 in haematopoietic cells show diminished adipose tissue mass accompanied by evidence of increased lipolysis, even when fed a normal diet. Supplementation of M2-like macrophages rescues the pathophysiology, indicating that a lack of these macrophages is the cause of lipolysis. In response to a high-fat diet, mice lacking Trib1 in haematopoietic cells develop hypertriglyceridaemia and insulin resistance, together with increased proinflammatory cytokine gene induction. Collectively, these results demonstrate that Trib1 is critical for adipose tissue maintenance and suppression of metabolic disorders by controlling the differentiation of tissue-resident M2-like macrophages.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Satoh, Takashi -- Kidoya, Hiroyasu -- Naito, Hisamichi -- Yamamoto, Masahiro -- Takemura, Naoki -- Nakagawa, Katsuhiro -- Yoshioka, Yoshichika -- Morii, Eiichi -- Takakura, Nobuyuki -- Takeuchi, Osamu -- Akira, Shizuo -- P01 AI070167/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Mar 28;495(7442):524-8. doi: 10.1038/nature11930. Epub 2013 Mar 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Host Defense, WPI Immunology Frontier Research Center, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23515163" target="_blank"〉PubMed〈/a〉
    Keywords: Adipose Tissue/*cytology/metabolism/pathology ; Animals ; Bone Marrow Cells/cytology/metabolism ; CCAAT-Enhancer-Binding Protein-alpha/metabolism ; Cell Count ; Cell Cycle Proteins/deficiency/genetics/metabolism ; *Cell Differentiation ; Cytokines/genetics ; Diet, High-Fat/adverse effects ; Eosinophils/cytology/metabolism ; Female ; Hypertriglyceridemia/chemically induced/genetics ; Inflammation Mediators/metabolism ; Insulin Resistance/genetics ; Intracellular Signaling Peptides and ; Proteins/chemistry/deficiency/genetics/*metabolism ; Lipodystrophy/chemically induced/metabolism/pathology ; Lipolysis ; Lung/cytology ; Macrophages/classification/*cytology/*metabolism ; Male ; Mice ; Neutrophils/cytology/metabolism ; Organ Specificity ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/*antagonists & ; inhibitors/chemistry/deficiency/genetics/metabolism ; Spleen/cytology ; Ubiquitin/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 6
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    c-Jun N-terminal phosphorylation antagonises recruitment of the Mbd3/NuRD repressor complex (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-01-05
    Description: AP-1 (activator protein 1) activity is strongly induced in response to numerous signals, including growth factors, cytokines and extracellular stresses. The proto-oncoprotein c-Jun belongs to the AP-1 group of transcription factors and it is a crucial regulator of intestinal progenitor proliferation and tumorigenesis. An important mechanism of AP-1 stimulation is phosphorylation of c-Jun by the Jun amino-terminal kinases (JNKs). N-terminal phosphorylation of the c-Jun transactivation domain increases target gene transcription, but a molecular explanation was elusive. Here we show that unphosphorylated, but not N-terminally phosphorylated c-Jun, interacts with Mbd3 and thereby recruits the nucleosome remodelling and histone deacetylation (NuRD) repressor complex. Mbd3 depletion in colon cancer cells increased histone acetylation at AP-1-dependent promoters, which resulted in increased target gene expression. The intestinal stem cell marker lgr5 was identified as a novel target gene controlled by c-Jun/Mbd3. Gut-specific conditional deletion of mbd3 (mbd3(DeltaG/DeltaG) mice) stimulated c-Jun activity and increased progenitor cell proliferation. In response to inflammation, mdb3 deficiency resulted in colonic hyperproliferation and mbd3(DeltaG/DeltaG) mice showed markedly increased susceptibility to colitis-induced tumorigenesis. Notably, concomitant inactivation of a single allele of c-jun reverted physiological and pathological hyperproliferation, as well as the increased tumorigenesis in mbd3(DeltaG/DeltaG) mice. Thus the transactivation domain of c-Jun recruits Mbd3/NuRD to AP-1 target genes to mediate gene repression, and this repression is relieved by JNK-mediated c-Jun N-terminal phosphorylation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aguilera, Cristina -- Nakagawa, Kentaro -- Sancho, Rocio -- Chakraborty, Atanu -- Hendrich, Brian -- Behrens, Axel -- 081816/Wellcome Trust/United Kingdom -- 098021/Wellcome Trust/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 Jan 13;469(7329):231-5. doi: 10.1038/nature09607. Epub 2011 Jan 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mammalian Genetics Laboratory, Cancer Research UK London Research Institute, Lincoln's Inn Fields Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21196933" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Cell Line, Tumor ; Cell Proliferation ; Colonic Neoplasms/metabolism/pathology ; DNA-Binding Proteins/*antagonists & inhibitors/deficiency/*metabolism ; Gene Expression Regulation, Neoplastic ; Histones/metabolism ; Intestines/cytology ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mi-2 Nucleosome Remodeling and Deacetylase Complex/*antagonists & ; inhibitors/chemistry/*metabolism ; Mice ; Phosphorylation ; Promoter Regions, Genetic/genetics ; Protein Binding ; Proto-Oncogene Proteins c-jun/*chemistry/*metabolism ; Receptors, G-Protein-Coupled/genetics ; Stem Cells/cytology ; Transcription Factors/*antagonists & inhibitors/deficiency/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 7
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    Three-dimensional electronic structures and the metal-insulator transition in Ruddlesden-Popper iridates (2016)
    American Physical Society (APS)
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    Publication Date: 2016-09-03
    Description: Author(s): A. Yamasaki, H. Fujiwara, S. Tachibana, D. Iwasaki, Y. Higashino, C. Yoshimi, K. Nakagawa, Y. Nakatani, K. Yamagami, H. Aratani, O. Kirilmaz, M. Sing, R. Claessen, H. Watanabe, T. Shirakawa, S. Yunoki, A. Naitoh, K. Takase, J. Matsuno, H. Takagi, A. Sekiyama, and Y. Saitoh In this study, we systematically investigate three-dimensional (3D) momentum ( ℏ k )-resolved electronic structures of Ruddlesden-Popper-type iridium oxides Sr n + 1 Ir n O 3 n + 1 using soft-x-ray (SX) angle-resolved photoemission spectroscopy (ARPES). Our results provide direct evidence of an insulator-to-meta… [Phys. Rev. B 94, 115103] Published Fri Sep 02, 2016
    Keywords: Electronic structure and strongly correlated systems
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
    Published by American Physical Society (APS)
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  • 8
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    Photoinduced phase separation with local structural ordering in organic molecular conductors (2017)
    American Physical Society (APS)
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    Publication Date: 2017-10-28
    Description: Author(s): S. Tsuchiya, K. Nakagawa, J. Yamada, H. Taniguchi, and Y. Toda In this work, polarized pump-probe spectroscopy was carried out to investigate the effects of a structural ordering of molecules on photoinduced phase separation (PIPS) in the organic conductors κ − ( BEDT − TTF ) 2 X [ X = Cu [ N ( CN ) 2 ] Br   ( κ − B r ) and Cu ( NCS ) 2 ( κ -NCS)]. We found that the anisotropic response for t... [Phys. Rev. B 96, 134311] Published Fri Oct 27, 2017
    Keywords: Dynamics, dynamical systems, lattice effects
    Print ISSN: 1098-0121
    Electronic ISSN: 1095-3795
    Topics: Physics
    Published by American Physical Society (APS)
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  • 9
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    Comparison of the kinetic disposition of and serum gastrin change by lansoprazole versus rabeprazole during an 8-day dosing scheme in relation to CYP2C19 polymorphism (2001)
    Springer
    Details
    Publication Date: 2001-09-01
    Print ISSN: 0031-6970
    Electronic ISSN: 1432-1041
    Topics: Chemistry and Pharmacology , Medicine
    Published by Springer
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  • 10
    Electronic Resource
    Electronic Resource
    Photoionization processes in nonpolar media: Density effect
    Amsterdam : Elsevier
    International Journal of Radiation Applications & Instrumentation. Part C, 37 (1991), S. 643-651 
    Details
    ISSN: 1359-0197
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering , Physics
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/1359-0197(91)90162-U
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    Paper (German National Licenses)
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