ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Tet-mediated formation of 5-carboxylcytosine and its excision by TDG in mammalian DNA (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-06
    Description: The prevalent DNA modification in higher organisms is the methylation of cytosine to 5-methylcytosine (5mC), which is partially converted to 5-hydroxymethylcytosine (5hmC) by the Tet (ten eleven translocation) family of dioxygenases. Despite their importance in epigenetic regulation, it is unclear how these cytosine modifications are reversed. Here, we demonstrate that 5mC and 5hmC in DNA are oxidized to 5-carboxylcytosine (5caC) by Tet dioxygenases in vitro and in cultured cells. 5caC is specifically recognized and excised by thymine-DNA glycosylase (TDG). Depletion of TDG in mouse embyronic stem cells leads to accumulation of 5caC to a readily detectable level. These data suggest that oxidation of 5mC by Tet proteins followed by TDG-mediated base excision of 5caC constitutes a pathway for active DNA demethylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462231/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3462231/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Yu-Fei -- Li, Bin-Zhong -- Li, Zheng -- Liu, Peng -- Wang, Yang -- Tang, Qingyu -- Ding, Jianping -- Jia, Yingying -- Chen, Zhangcheng -- Li, Lin -- Sun, Yan -- Li, Xiuxue -- Dai, Qing -- Song, Chun-Xiao -- Zhang, Kangling -- He, Chuan -- Xu, Guo-Liang -- 1S10RR027643-01/RR/NCRR NIH HHS/ -- GM071440/GM/NIGMS NIH HHS/ -- R01 GM071440/GM/NIGMS NIH HHS/ -- S10 RR027643/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2011 Sep 2;333(6047):1303-7. doi: 10.1126/science.1210944. Epub 2011 Aug 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Group of DNA Metabolism, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21817016" target="_blank"〉PubMed〈/a〉
    Keywords: 5-Methylcytosine/metabolism ; Animals ; Cell Line ; Cytosine/*analogs & derivatives/metabolism ; DNA/*metabolism ; DNA Methylation ; DNA-Binding Proteins/genetics/*metabolism ; Embryonic Stem Cells ; HEK293 Cells ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mice ; Oxidation-Reduction ; Proto-Oncogene Proteins/genetics/*metabolism ; RNA, Small Interfering ; Thymine DNA Glycosylase/genetics/*metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    The Lkb1 metabolic sensor maintains haematopoietic stem cell survival (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-03
    Description: Haematopoietic stem cells (HSCs) can convert between growth states that have marked differences in bioenergetic needs. Although often quiescent in adults, these cells become proliferative upon physiological demand. Balancing HSC energetics in response to nutrient availability and growth state is poorly understood, yet essential for the dynamism of the haematopoietic system. Here we show that the Lkb1 tumour suppressor is critical for the maintenance of energy homeostasis in haematopoietic cells. Lkb1 inactivation in adult mice causes loss of HSC quiescence followed by rapid depletion of all haematopoietic subpopulations. Lkb1-deficient bone marrow cells exhibit mitochondrial defects, alterations in lipid and nucleotide metabolism, and depletion of cellular ATP. The haematopoietic effects are largely independent of Lkb1 regulation of AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signalling. Instead, these data define a central role for Lkb1 in restricting HSC entry into cell cycle and in broadly maintaining energy homeostasis in haematopoietic cells through a novel metabolic checkpoint.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037591/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3037591/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gurumurthy, Sushma -- Xie, Stephanie Z -- Alagesan, Brinda -- Kim, Judith -- Yusuf, Rushdia Z -- Saez, Borja -- Tzatsos, Alexandros -- Ozsolak, Fatih -- Milos, Patrice -- Ferrari, Francesco -- Park, Peter J -- Shirihai, Orian S -- Scadden, David T -- Bardeesy, Nabeel -- DK050234/DK/NIDDK NIH HHS/ -- R01 DK050234/DK/NIDDK NIH HHS/ -- R01 DK050234-12/DK/NIDDK NIH HHS/ -- R01 DK050234-13/DK/NIDDK NIH HHS/ -- R01 HG005230/HG/NHGRI NIH HHS/ -- R01 HG005230-01/HG/NHGRI NIH HHS/ -- U01 CA141576-01/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 2;468(7324):659-63. doi: 10.1038/nature09572.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cancer Center and Center for Regenerative Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21124451" target="_blank"〉PubMed〈/a〉
    Keywords: AMP-Activated Protein Kinases/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Apoptosis ; Autophagy ; Bone Marrow/metabolism/pathology ; Cell Cycle ; Cell Proliferation ; Cell Survival ; *Energy Metabolism ; Enzyme Activation ; Female ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/*metabolism/pathology ; Homeostasis ; Lipid Metabolism ; Male ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism/pathology ; Multiprotein Complexes ; Protein-Serine-Threonine Kinases/deficiency/genetics/*metabolism ; Proteins/antagonists & inhibitors/metabolism ; TOR Serine-Threonine Kinases/metabolism ; Tumor Suppressor Proteins/deficiency/genetics/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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Trans-endocytosis of CD80 and CD86: a molecular basis for the cell-extrinsic function of CTLA-4 (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-09
    Description: Cytotoxic T lymphocyte antigen 4 (CTLA-4) is an essential negative regulator of T cell immune responses whose mechanism of action is the subject of debate. CTLA-4 shares two ligands (CD80 and CD86) with a stimulatory receptor, CD28. Here, we show that CTLA-4 can capture its ligands from opposing cells by a process of trans-endocytosis. After removal, these costimulatory ligands are degraded inside CTLA-4-expressing cells, resulting in impaired costimulation via CD28. Acquisition of CD86 from antigen-presenting cells is stimulated by T cell receptor engagement and observed in vitro and in vivo. These data reveal a mechanism of immune regulation in which CTLA-4 acts as an effector molecule to inhibit CD28 costimulation by the cell-extrinsic depletion of ligands, accounting for many of the known features of the CD28-CTLA-4 system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3198051/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3198051/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Qureshi, Omar S -- Zheng, Yong -- Nakamura, Kyoko -- Attridge, Kesley -- Manzotti, Claire -- Schmidt, Emily M -- Baker, Jennifer -- Jeffery, Louisa E -- Kaur, Satdip -- Briggs, Zoe -- Hou, Tie Z -- Futter, Clare E -- Anderson, Graham -- Walker, Lucy S K -- Sansom, David M -- 17851/Arthritis Research UK/United Kingdom -- BB/D011000/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/H013598/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- G0400931/Medical Research Council/United Kingdom -- G0401620/Medical Research Council/United Kingdom -- G0802382/Medical Research Council/United Kingdom -- G1000213/Medical Research Council/United Kingdom -- G9818340/Medical Research Council/United Kingdom -- Arthritis Research UK/United Kingdom -- Biotechnology and Biological Sciences Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2011 Apr 29;332(6029):600-3. doi: 10.1126/science.1202947. Epub 2011 Apr 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Centre for Immune Regulation, School of Immunity and Infection, Institute of Biomedical Research, University of Birmingham Medical School, Birmingham B15 2TT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21474713" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/*immunology/metabolism ; Antigens, CD28/*immunology ; Antigens, CD80/*immunology/metabolism ; Antigens, CD86/*immunology/metabolism ; CHO Cells ; CTLA-4 Antigen ; Cricetinae ; Cricetulus ; Dendritic Cells/immunology ; *Endocytosis ; Humans ; Jurkat Cells ; Ligands ; Lymphocyte Activation ; Mice ; Mice, Transgenic ; Models, Biological ; Ovalbumin/immunology ; Receptors, Antigen, T-Cell/immunology ; Recombinant Fusion Proteins/metabolism ; T-Lymphocyte Subsets/*immunology/metabolism ; T-Lymphocytes, Regulatory/immunology/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    Equilibrative nucleoside transporter 3 deficiency perturbs lysosome function and macrophage homeostasis (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-12-17
    Description: Lysosomal storage diseases (LSDs) are a group of heterogeneous disorders caused by defects in lysosomal enzymes or transporters, resulting in accumulation of undegraded macromolecules or metabolites. Macrophage numbers are expanded in several LSDs, leading to histiocytosis of unknown pathophysiology. Here, we found that mice lacking the equilibrative nucleoside transporter 3 (ENT3) developed a spontaneous and progressive macrophage-dominated histiocytosis. In the absence of ENT3, defective apoptotic cell clearance led to lysosomal nucleoside buildup, elevated intralysosomal pH, and altered macrophage function. The macrophage accumulation was partly due to increased macrophage colony-stimulating factor and receptor expression and signaling secondary to the lysosomal defects. These studies suggest a cellular and molecular basis for the development of histiocytosis in several human syndromes associated with ENT3 mutations and potentially other LSDs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, Chia-Lin -- Lin, Weiyu -- Seshasayee, Dhaya -- Chen, Yung-Hsiang -- Ding, Xiao -- Lin, Zhonghua -- Suto, Eric -- Huang, Zhiyu -- Lee, Wyne P -- Park, Hyunjoo -- Xu, Min -- Sun, Mei -- Rangell, Linda -- Lutman, Jeff L -- Ulufatu, Sheila -- Stefanich, Eric -- Chalouni, Cecile -- Sagolla, Meredith -- Diehl, Lauri -- Fielder, Paul -- Dean, Brian -- Balazs, Mercedesz -- Martin, Flavius -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):89-92. doi: 10.1126/science.1213682. Epub 2011 Dec 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Immunology, Genentech Inc., 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22174130" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/metabolism ; Animals ; Apoptosis ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Histiocytosis/*physiopathology ; *Homeostasis ; Humans ; Hydrogen-Ion Concentration ; Listeriosis/immunology/microbiology ; Lysosomal Storage Diseases/physiopathology ; Lysosomes/*physiology/ultrastructure ; Macrophage Colony-Stimulating Factor/metabolism ; Macrophages/immunology/*physiology/ultrastructure ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelopoiesis ; Nucleoside Transport Proteins/genetics/*physiology ; Phagocytosis ; Receptor, Macrophage Colony-Stimulating Factor/metabolism ; Signal Transduction ; Thymocytes/immunology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Akt-mediated regulation of autophagy and tumorigenesis through Beclin 1 phosphorylation (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-11-01
    Description: Aberrant signaling through the class I phosphatidylinositol 3-kinase (PI3K)-Akt axis is frequent in human cancer. Here, we show that Beclin 1, an essential autophagy and tumor suppressor protein, is a target of the protein kinase Akt. Expression of a Beclin 1 mutant resistant to Akt-mediated phosphorylation increased autophagy, reduced anchorage-independent growth, and inhibited Akt-driven tumorigenesis. Akt-mediated phosphorylation of Beclin 1 enhanced its interactions with 14-3-3 and vimentin intermediate filament proteins, and vimentin depletion increased autophagy and inhibited Akt-driven transformation. Thus, Akt-mediated phosphorylation of Beclin 1 functions in autophagy inhibition, oncogenesis, and the formation of an autophagy-inhibitory Beclin 1/14-3-3/vimentin intermediate filament complex. These findings have broad implications for understanding the role of Akt signaling and intermediate filament proteins in autophagy and cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507442/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3507442/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Richard C -- Wei, Yongjie -- An, Zhenyi -- Zou, Zhongju -- Xiao, Guanghua -- Bhagat, Govind -- White, Michael -- Reichelt, Julia -- Levine, Beth -- K08 CA164047/CA/NCI NIH HHS/ -- P30 CA142543/CA/NCI NIH HHS/ -- R01 CA071443/CA/NCI NIH HHS/ -- R01 CA084254/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA129451/CA/NCI NIH HHS/ -- R01 CA84254-S1/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):956-9. doi: 10.1126/science.1225967. Epub 2012 Oct 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23112296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis Regulatory Proteins/genetics/*metabolism ; *Autophagy ; Cell Line, Tumor ; Cell Transformation, Neoplastic/genetics/*metabolism ; Fibroblasts/metabolism/pathology ; HeLa Cells ; Humans ; Membrane Proteins/genetics/*metabolism ; Mice ; Phosphorylation ; Proto-Oncogene Proteins c-akt/genetics/*metabolism ; RNA, Small Interfering/genetics ; Rats ; Transduction, Genetic ; Vimentin/genetics ; Xenograft Model Antitumor Assays
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    CRL4 complex regulates mammalian oocyte survival and reprogramming by activation of TET proteins (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-21
    Description: The duration of a woman's reproductive period is determined by the size and persistence of a dormant oocyte pool. Specific oocyte genes are essential for follicle maintenance and female fertility. The mechanisms that regulate the expression of these genes are poorly understood. We found that a cullin-ring finger ligase-4 (CRL4) complex was crucial in this process. Oocyte-specific deletion of the CRL4 linker protein DDB1 or its substrate adaptor VPRBP (also known as DCAF1) caused rapid oocyte loss, premature ovarian insufficiency, and silencing of fertility maintaining genes. CRL4(VPRBP) activates the TET methylcytosine dioxygenases, which are involved in female germ cell development and zygote genome reprogramming. Hence, CRL4(VPRBP) ubiquitin ligase is a guardian of female reproductive life in germ cells and a maternal reprogramming factor after fertilization.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, Chao -- Zhang, Yin-Li -- Pan, Wei-Wei -- Li, Xiao-Meng -- Wang, Zhong-Wei -- Ge, Zhao-Jia -- Zhou, Jian-Jie -- Cang, Yong -- Tong, Chao -- Sun, Qing-Yuan -- Fan, Heng-Yu -- New York, N.Y. -- Science. 2013 Dec 20;342(6165):1518-21. doi: 10.1126/science.1244587.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Life Sciences Institute and Innovation Center for Cell Biology, Zhejiang University, Hangzhou 310058, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24357321" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/genetics/*metabolism ; Cell Survival/genetics/physiology ; Cellular Reprogramming/*genetics ; Cullin Proteins/genetics/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Dioxygenases/genetics/*metabolism ; Female ; Fertility/*genetics ; Gene Silencing ; Gonadal Dysgenesis/genetics ; HeLa Cells ; Humans ; Mice ; Mice, Knockout ; Oocytes/*physiology ; Ovary/physiopathology ; Proto-Oncogene Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Crystal structure of NLRC4 reveals its autoinhibition mechanism (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-06-15
    Description: Nucleotide-binding and oligomerization domain-like receptor (NLR) proteins oligomerize into multiprotein complexes termed inflammasomes when activated. Their autoinhibition mechanism remains poorly defined. Here, we report the crystal structure of mouse NLRC4 in a closed form. The adenosine diphosphate-mediated interaction between the central nucleotide-binding domain (NBD) and the winged-helix domain (WHD) was critical for stabilizing the closed conformation of NLRC4. The helical domain HD2 repressively contacted a conserved and functionally important alpha-helix of the NBD. The C-terminal leucine-rich repeat (LRR) domain is positioned to sterically occlude one side of the NBD domain and consequently sequester NLRC4 in a monomeric state. Disruption of ADP-mediated NBD-WHD or NBD-HD2/NBD-LRR interactions resulted in constitutive activation of NLRC4. Together, our data reveal the NBD-organized cooperative autoinhibition mechanism of NLRC4 and provide insight into its activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Zehan -- Yan, Chuangye -- Liu, Peiyuan -- Huang, Zhiwei -- Ma, Rui -- Zhang, Chenlu -- Wang, Ruiyong -- Zhang, Yueteng -- Martinon, Fabio -- Miao, Di -- Deng, Haiteng -- Wang, Jiawei -- Chang, Junbiao -- Chai, Jijie -- New York, N.Y. -- Science. 2013 Jul 12;341(6142):172-5. doi: 10.1126/science.1236381. Epub 2013 Jun 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Life Sciences, Tsinghua University, and Tsinghua-Peking Center for Life Sciences, Beijing 100084, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23765277" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Diphosphate/chemistry ; Animals ; Apoptosis Regulatory Proteins/*antagonists & inhibitors/*chemistry ; Calcium-Binding Proteins/*antagonists & inhibitors/*chemistry ; Crystallography, X-Ray ; Mice ; Protein Multimerization ; Protein Structure, Secondary ; Protein Structure, Tertiary
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Viral infection. Prevention and cure of rotavirus infection via TLR5/NLRC4-mediated production of IL-22 and IL-18 (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-15
    Description: Activators of innate immunity may have the potential to combat a broad range of infectious agents. We report that treatment with bacterial flagellin prevented rotavirus (RV) infection in mice and cured chronically RV-infected mice. Protection was independent of adaptive immunity and interferon (IFN, type I and II) and required flagellin receptors Toll-like receptor 5 (TLR5) and NOD-like receptor C4 (NLRC4). Flagellin-induced activation of TLR5 on dendritic cells elicited production of the cytokine interleukin-22 (IL-22), which induced a protective gene expression program in intestinal epithelial cells. Flagellin also induced NLRC4-dependent production of IL-18 and immediate elimination of RV-infected cells. Administration of IL-22 and IL-18 to mice fully recapitulated the capacity of flagellin to prevent or eliminate RV infection and thus holds promise as a broad-spectrum antiviral agent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Benyue -- Chassaing, Benoit -- Shi, Zhenda -- Uchiyama, Robin -- Zhang, Zhan -- Denning, Timothy L -- Crawford, Sue E -- Pruijssers, Andrea J -- Iskarpatyoti, Jason A -- Estes, Mary K -- Dermody, Terence S -- Ouyang, Wenjun -- Williams, Ifor R -- Vijay-Kumar, Matam -- Gewirtz, Andrew T -- AI038296/AI/NIAID NIH HHS/ -- AI080656/AI/NIAID NIH HHS/ -- AI107943/AI/NIAID NIH HHS/ -- DK061417/DK/NIDDK NIH HHS/ -- DK064730/DK/NIDDK NIH HHS/ -- DK56338/DK/NIDDK NIH HHS/ -- R01 AI038296/AI/NIAID NIH HHS/ -- R37 AI038296/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Nov 14;346(6211):861-5. doi: 10.1126/science.1256999.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. ; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. ; Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA. ; Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN, USA. ; Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, TN, USA. Departments of Pediatrics, Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA. ; Department of Immunology, Genentech, South San Francisco, CA, USA. ; Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. ; Department of Nutritional Sciences and Medicine, Pennsylvania State University, University Park, PA 16802, USA. ; Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA. Department of Pathology, Emory University School of Medicine, Atlanta, GA, USA. agewirtz@gsu.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25395539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Diarrhea/immunology/therapy/virology ; Disease Models, Animal ; Feces/virology ; Flagellin/*administration & dosage/immunology ; Homeodomain Proteins/genetics ; *Immunity, Innate ; Interleukin-18/administration & dosage/genetics/*immunology ; Interleukins/administration & dosage/genetics/*immunology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mutation ; Rotavirus Infections/immunology/*prevention & control/therapy ; Toll-Like Receptor 5/genetics/*physiology ; Virus Shedding
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Subtypes of medulloblastoma have distinct developmental origins (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-15
    Description: Medulloblastoma encompasses a collection of clinically and molecularly diverse tumour subtypes that together comprise the most common malignant childhood brain tumour. These tumours are thought to arise within the cerebellum, with approximately 25% originating from granule neuron precursor cells (GNPCs) after aberrant activation of the Sonic Hedgehog pathway (hereafter, SHH subtype). The pathological processes that drive heterogeneity among the other medulloblastoma subtypes are not known, hindering the development of much needed new therapies. Here we provide evidence that a discrete subtype of medulloblastoma that contains activating mutations in the WNT pathway effector CTNNB1 (hereafter, WNT subtype) arises outside the cerebellum from cells of the dorsal brainstem. We found that genes marking human WNT-subtype medulloblastomas are more frequently expressed in the lower rhombic lip (LRL) and embryonic dorsal brainstem than in the upper rhombic lip (URL) and developing cerebellum. Magnetic resonance imaging (MRI) and intra-operative reports showed that human WNT-subtype tumours infiltrate the dorsal brainstem, whereas SHH-subtype tumours are located within the cerebellar hemispheres. Activating mutations in Ctnnb1 had little impact on progenitor cell populations in the cerebellum, but caused the abnormal accumulation of cells on the embryonic dorsal brainstem which included aberrantly proliferating Zic1(+) precursor cells. These lesions persisted in all mutant adult mice; moreover, in 15% of cases in which Tp53 was concurrently deleted, they progressed to form medulloblastomas that recapitulated the anatomy and gene expression profiles of human WNT-subtype medulloblastoma. We provide the first evidence, to our knowledge, that subtypes of medulloblastoma have distinct cellular origins. Our data provide an explanation for the marked molecular and clinical differences between SHH- and WNT-subtype medulloblastomas and have profound implications for future research and treatment of this important childhood cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059767/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059767/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gibson, Paul -- Tong, Yiai -- Robinson, Giles -- Thompson, Margaret C -- Currle, D Spencer -- Eden, Christopher -- Kranenburg, Tanya A -- Hogg, Twala -- Poppleton, Helen -- Martin, Julie -- Finkelstein, David -- Pounds, Stanley -- Weiss, Aaron -- Patay, Zoltan -- Scoggins, Matthew -- Ogg, Robert -- Pei, Yanxin -- Yang, Zeng-Jie -- Brun, Sonja -- Lee, Youngsoo -- Zindy, Frederique -- Lindsey, Janet C -- Taketo, Makoto M -- Boop, Frederick A -- Sanford, Robert A -- Gajjar, Amar -- Clifford, Steven C -- Roussel, Martine F -- McKinnon, Peter J -- Gutmann, David H -- Ellison, David W -- Wechsler-Reya, Robert -- Gilbertson, Richard J -- 01CA96832/CA/NCI NIH HHS/ -- P01 CA096832/CA/NCI NIH HHS/ -- P01 CA096832-06A18120/CA/NCI NIH HHS/ -- P01 CA096832-078120/CA/NCI NIH HHS/ -- P30CA021765/CA/NCI NIH HHS/ -- R01 CA129541/CA/NCI NIH HHS/ -- R01 CA129541-01/CA/NCI NIH HHS/ -- R01 CA129541-02/CA/NCI NIH HHS/ -- R01 CA129541-03/CA/NCI NIH HHS/ -- R01 CA129541-04/CA/NCI NIH HHS/ -- R01 CA129541-05/CA/NCI NIH HHS/ -- R01 NS037956/NS/NINDS NIH HHS/ -- R01 NS037956-13/NS/NINDS NIH HHS/ -- R01CA129541/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1095-9. doi: 10.1038/nature09587. Epub 2010 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Neurobiology, St Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, Tennessee 38105, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21150899" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Stem/*pathology ; Cerebellar Neoplasms/*pathology ; Disease Models, Animal ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Humans ; Medulloblastoma/*pathology ; Mice ; Mice, Transgenic ; Mutation ; beta Catenin/genetics
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 10
    facet.materialart.
    Unknown
    Cortical representations of olfactory input by trans-synaptic tracing (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-24
    Description: In the mouse, each class of olfactory receptor neurons expressing a given odorant receptor has convergent axonal projections to two specific glomeruli in the olfactory bulb, thereby creating an odour map. However, it is unclear how this map is represented in the olfactory cortex. Here we combine rabies-virus-dependent retrograde mono-trans-synaptic labelling with genetics to control the location, number and type of 'starter' cortical neurons, from which we trace their presynaptic neurons. We find that individual cortical neurons receive input from multiple mitral cells representing broadly distributed glomeruli. Different cortical areas represent the olfactory bulb input differently. For example, the cortical amygdala preferentially receives dorsal olfactory bulb input, whereas the piriform cortex samples the whole olfactory bulb without obvious bias. These differences probably reflect different functions of these cortical areas in mediating innate odour preference or associative memory. The trans-synaptic labelling method described here should be widely applicable to mapping connections throughout the mouse nervous system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073090/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyamichi, Kazunari -- Amat, Fernando -- Moussavi, Farshid -- Wang, Chen -- Wickersham, Ian -- Wall, Nicholas R -- Taniguchi, Hiroki -- Tasic, Bosiljka -- Huang, Z Josh -- He, Zhigang -- Callaway, Edward M -- Horowitz, Mark A -- Luo, Liqun -- R01 MH063912/MH/NIMH NIH HHS/ -- R01 NS050835/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 14;472(7342):191-6. doi: 10.1038/nature09714. Epub 2010 Dec 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉HHMI/Department of Biology, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179085" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/anatomy & histology/cytology/physiology ; Animals ; Axons/physiology ; Bias (Epidemiology) ; Brain Mapping ; HEK293 Cells ; Humans ; Mice ; Mice, Transgenic ; *Neuroanatomical Tract-Tracing Techniques ; Odors/analysis ; Olfactory Bulb/anatomy & histology/cytology/physiology ; Olfactory Pathways/anatomy & histology/*cytology/*physiology ; Olfactory Perception/genetics/*physiology ; Olfactory Receptor Neurons/cytology/physiology ; Rabies virus/physiology ; Synapses/genetics/*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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...