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  • Mice  (137)
  • 2005-2009  (137)
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  • 2008  (137)
  • 1
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    Pyogenic bacterial infections in humans with MyD88 deficiency (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-08-02
    Description: MyD88 is a key downstream adapter for most Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection. We describe a distinct situation in a natural setting of human infection. Nine children with autosomal recessive MyD88 deficiency suffered from life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease. However, these patients were otherwise healthy, with normal resistance to other microbes. Their clinical status improved with age, but not due to any cellular leakiness in MyD88 deficiency. The MyD88-dependent TLRs and IL-1Rs are therefore essential for protective immunity to a small number of pyogenic bacteria, but redundant for host defense to most natural infections.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688396/" 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/PMC2688396/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉von Bernuth, Horst -- Picard, Capucine -- Jin, Zhongbo -- Pankla, Rungnapa -- Xiao, Hui -- Ku, Cheng-Lung -- Chrabieh, Maya -- Mustapha, Imen Ben -- Ghandil, Pegah -- Camcioglu, Yildiz -- Vasconcelos, Julia -- Sirvent, Nicolas -- Guedes, Margarida -- Vitor, Artur Bonito -- Herrero-Mata, Maria Jose -- Arostegui, Juan Ignacio -- Rodrigo, Carlos -- Alsina, Laia -- Ruiz-Ortiz, Estibaliz -- Juan, Manel -- Fortuny, Claudia -- Yague, Jordi -- Anton, Jordi -- Pascal, Mariona -- Chang, Huey-Hsuan -- Janniere, Lucile -- Rose, Yoann -- Garty, Ben-Zion -- Chapel, Helen -- Issekutz, Andrew -- Marodi, Laszlo -- Rodriguez-Gallego, Carlos -- Banchereau, Jacques -- Abel, Laurent -- Li, Xiaoxia -- Chaussabel, Damien -- Puel, Anne -- Casanova, Jean-Laurent -- U19 AI057234/AI/NIAID NIH HHS/ -- U19 AI057234-02/AI/NIAID NIH HHS/ -- U19 AIO57234-02/PHS HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2008 Aug 1;321(5889):691-6. doi: 10.1126/science.1158298.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Human Genetics of Infectious Diseases, INSERM U550, Paris, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18669862" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Animals ; Bacterial Infections/*genetics/*immunology ; Cell Line, Transformed ; Child ; Child, Preschool ; Cytokines/metabolism ; Disease Susceptibility ; Female ; Gene Deletion ; Humans ; Immunity, Innate ; Male ; Mice ; Mutation, Missense ; Myeloid Differentiation Factor 88/*deficiency/genetics/metabolism ; Pneumococcal Infections/genetics/immunology ; Pseudomonas Infections/genetics/immunology ; Receptors, Interleukin-1/immunology/metabolism ; Signal Transduction ; Staphylococcal Infections/genetics/immunology ; Toll-Like Receptors/immunology/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    DNA double-strand breaks activate a multi-functional genetic program in developing lymphocytes (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-14
    Description: DNA double-strand breaks are generated by genotoxic agents and by cellular endonucleases as intermediates of several important physiological processes. The cellular response to genotoxic DNA breaks includes the activation of transcriptional programs known primarily to regulate cell-cycle checkpoints and cell survival. DNA double-strand breaks are generated in all developing lymphocytes during the assembly of antigen receptor genes, a process that is essential for normal lymphocyte development. Here we show that in murine lymphocytes these physiological DNA breaks activate a broad transcriptional program. This program transcends the canonical DNA double-strand break response and includes many genes that regulate diverse cellular processes important for lymphocyte development. Moreover, the expression of several of these genes is regulated similarly in response to genotoxic DNA damage. Thus, physiological DNA double-strand breaks provide cues that can regulate cell-type-specific processes not directly involved in maintaining the integrity of the genome, and genotoxic DNA breaks could disrupt normal cellular functions by corrupting these processes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605662/" 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/PMC2605662/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bredemeyer, Andrea L -- Helmink, Beth A -- Innes, Cynthia L -- Calderon, Boris -- McGinnis, Lisa M -- Mahowald, Grace K -- Gapud, Eric J -- Walker, Laura M -- Collins, Jennifer B -- Weaver, Brian K -- Mandik-Nayak, Laura -- Schreiber, Robert D -- Allen, Paul M -- May, Michael J -- Paules, Richard S -- Bassing, Craig H -- Sleckman, Barry P -- R01 AI047829/AI/NIAID NIH HHS/ -- R01 AI047829-09/AI/NIAID NIH HHS/ -- R01 CA125195/CA/NCI NIH HHS/ -- R01 CA125195-02/CA/NCI NIH HHS/ -- England -- Nature. 2008 Dec 11;456(7223):819-23. doi: 10.1038/nature07392. Epub 2008 Oct 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18849970" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/drug effects/*metabolism ; Cell Cycle Proteins/drug effects ; Cell Line ; *DNA Breaks, Double-Stranded ; DNA-Binding Proteins/drug effects ; Enzyme Inhibitors/pharmacology ; Gene Expression Profiling ; Gene Expression Regulation, Developmental/drug effects/*genetics ; Homeodomain Proteins/metabolism ; Mice ; Mice, Knockout ; Mice, SCID ; NF-kappa B/metabolism ; Protein-Serine-Threonine Kinases/drug effects ; Tumor Suppressor Proteins/drug effects
    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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  • 3
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    A myocardial lineage derives from Tbx18 epicardial cells (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-05-16
    Description: Understanding the origins and roles of cardiac progenitor cells is important for elucidating the pathogenesis of congenital and acquired heart diseases. Moreover, manipulation of cardiac myocyte progenitors has potential for cell-based repair strategies for various myocardial disorders. Here we report the identification in mouse of a previously unknown cardiac myocyte lineage that derives from the proepicardial organ. These progenitor cells, which express the T-box transcription factor Tbx18, migrate onto the outer cardiac surface to form the epicardium, and then make a substantial contribution to myocytes in the ventricular septum and the atrial and ventricular walls. Tbx18-expressing cardiac progenitors also give rise to cardiac fibroblasts and coronary smooth muscle cells. The pluripotency of Tbx18 proepicardial cells provides a theoretical framework for applying these progenitors to effect cardiac repair and regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cai, Chen-Leng -- Martin, Jody C -- Sun, Yunfu -- Cui, Li -- Wang, Lianchun -- Ouyang, Kunfu -- Yang, Lei -- Bu, Lei -- Liang, Xingqun -- Zhang, Xiaoxue -- Stallcup, William B -- Denton, Christopher P -- McCulloch, Andrew -- Chen, Ju -- Evans, Sylvia M -- P41 RR005351/RR/NCRR NIH HHS/ -- T32 HL007444/HL/NHLBI NIH HHS/ -- England -- Nature. 2008 Jul 3;454(7200):104-8. doi: 10.1038/nature06969. Epub 2008 May 14.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Skaggs School of Pharmacy, University of California, San Diego, La Jolla, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18480752" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; *Cell Lineage ; Gene Expression Regulation, Developmental ; Heart/growth & development ; Lac Operon/genetics ; Mice ; Myocardium/*cytology/metabolism ; Myocytes, Cardiac/*cytology/metabolism ; Myocytes, Smooth Muscle/metabolism ; Pericardium/*cytology/*metabolism ; Stem Cells/*cytology/metabolism ; T-Box Domain Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    A paracrine requirement for hedgehog signalling in cancer (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-30
    Description: Ligand-dependent activation of the hedgehog (Hh) signalling pathway has been associated with tumorigenesis in a number of human tissues. Here we show that, although previous reports have described a cell-autonomous role for Hh signalling in these tumours, Hh ligands fail to activate signalling in tumour epithelial cells. In contrast, our data support ligand-dependent activation of the Hh pathway in the stromal microenvironment. Specific inhibition of Hh signalling using small molecule inhibitors, a neutralizing anti-Hh antibody or genetic deletion of smoothened (Smo) in the mouse stroma results in growth inhibition in xenograft tumour models. Taken together, these studies demonstrate a paracrine requirement for Hh ligand signalling in the tumorigenesis of Hh-expressing cancers and have important implications for the development of Hh pathway antagonists in cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yauch, Robert L -- Gould, Stephen E -- Scales, Suzie J -- Tang, Tracy -- Tian, Hua -- Ahn, Christina P -- Marshall, Derek -- Fu, Ling -- Januario, Thomas -- Kallop, Dara -- Nannini-Pepe, Michelle -- Kotkow, Karen -- Marsters, James C -- Rubin, Lee L -- de Sauvage, Frederic J -- England -- Nature. 2008 Sep 18;455(7211):406-10. doi: 10.1038/nature07275. Epub 2008 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genentech Inc., 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18754008" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Hedgehog Proteins/*metabolism ; Humans ; Ligands ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplasms/genetics/*metabolism ; Paracrine Communication/*physiology ; Receptors, G-Protein-Coupled/deficiency/genetics/metabolism ; Stromal Cells/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Wnt3a-mediated formation of phosphatidylinositol 4,5-bisphosphate regulates LRP6 phosphorylation (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-09-06
    Description: The canonical Wnt-beta-catenin signaling pathway is initiated by inducing phosphorylation of one of the Wnt receptors, low-density lipoprotein receptor-related protein 6 (LRP6), at threonine residue 1479 (Thr1479) and serine residue 1490 (Ser1490). By screening a human kinase small interfering RNA library, we identified phosphatidylinositol 4-kinase type II alpha and phosphatidylinositol-4-phosphate 5-kinase type I (PIP5KI) as required for Wnt3a-induced LRP6 phosphorylation at Ser1490 in mammalian cells and confirmed that these kinases are important for Wnt signaling in Xenopus embryos. Wnt3a stimulates the formation of phosphatidylinositol 4,5-bisphosphates [PtdIns (4,5)P2] through frizzled and dishevelled, the latter of which directly interacted with and activated PIP5KI. In turn, PtdIns (4,5)P2 regulated phosphorylation of LRP6 at Thr1479 and Ser1490. Therefore, our study reveals a signaling mechanism for Wnt to regulate LRP6 phosphorylation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532521/" 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/PMC2532521/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pan, Weijun -- Choi, Sun-Cheol -- Wang, He -- Qin, Yuanbo -- Volpicelli-Daley, Laura -- Swan, Laura -- Lucast, Louise -- Khoo, Cynthia -- Zhang, Xiaowu -- Li, Lin -- Abrams, Charles S -- Sokol, Sergei Y -- Wu, Dianqing -- AR051476/AR/NIAMS NIH HHS/ -- CA132317/CA/NCI NIH HHS/ -- DA018343/DA/NIDA NIH HHS/ -- HL080706/HL/NHLBI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- P30 DA018343/DA/NIDA NIH HHS/ -- R01 AR051476/AR/NIAMS NIH HHS/ -- R01 AR051476-01A1/AR/NIAMS NIH HHS/ -- R01 AR051476-02/AR/NIAMS NIH HHS/ -- R01 AR051476-03/AR/NIAMS NIH HHS/ -- R01 CA132317/CA/NCI NIH HHS/ -- R01 CA132317-01A2/CA/NCI NIH HHS/ -- R01 CA139395/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Sep 5;321(5894):1350-3. doi: 10.1126/science.1160741.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18772438" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Axin Protein ; Cell Line ; Frizzled Receptors/metabolism ; Humans ; LDL-Receptor Related Proteins/*metabolism ; Low Density Lipoprotein Receptor-Related Protein-6 ; Mice ; Models, Biological ; Phosphatidylinositol 4,5-Diphosphate/*metabolism ; Phosphoproteins/metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; RNA, Small Interfering ; Recombinant Proteins/metabolism ; Repressor Proteins/metabolism ; Serine/metabolism ; Signal Transduction ; Threonine/metabolism ; Wnt Proteins/*metabolism ; Wnt3 Protein ; Wnt3A Protein ; Xenopus/embryology ; Xenopus Proteins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    IRF4 addiction in multiple myeloma (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-06-24
    Description: The transcription factor IRF4 (interferon regulatory factor 4) is required during an immune response for lymphocyte activation and the generation of immunoglobulin-secreting plasma cells. Multiple myeloma, a malignancy of plasma cells, has a complex molecular aetiology with several subgroups defined by gene expression profiling and recurrent chromosomal translocations. Moreover, the malignant clone can sustain multiple oncogenic lesions, accumulating genetic damage as the disease progresses. Current therapies for myeloma can extend survival but are not curative. Hence, new therapeutic strategies are needed that target molecular pathways shared by all subtypes of myeloma. Here we show, using a loss-of-function, RNA-interference-based genetic screen, that IRF4 inhibition is toxic to myeloma cell lines, regardless of transforming oncogenic mechanism. Gene expression profiling and genome-wide chromatin immunoprecipitation analysis uncovered an extensive network of IRF4 target genes and identified MYC as a direct target of IRF4 in activated B cells and myeloma. Unexpectedly, IRF4 was itself a direct target of MYC transactivation, generating an autoregulatory circuit in myeloma cells. Although IRF4 is not genetically altered in most myelomas, they are nonetheless addicted to an aberrant IRF4 regulatory network that fuses the gene expression programmes of normal plasma cells and activated B cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2542904/" 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/PMC2542904/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shaffer, Arthur L -- Emre, N C Tolga -- Lamy, Laurence -- Ngo, Vu N -- Wright, George -- Xiao, Wenming -- Powell, John -- Dave, Sandeep -- Yu, Xin -- Zhao, Hong -- Zeng, Yuxin -- Chen, Bangzheng -- Epstein, Joshua -- Staudt, Louis M -- CA113992/CA/NCI NIH HHS/ -- CA97513/CA/NCI NIH HHS/ -- R01 CA113992/CA/NCI NIH HHS/ -- R01 CA113992-02/CA/NCI NIH HHS/ -- R33 CA097513-03/CA/NCI NIH HHS/ -- Z99 CA999999/Intramural NIH HHS/ -- England -- Nature. 2008 Jul 10;454(7201):226-31. doi: 10.1038/nature07064. Epub 2008 Jun 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18568025" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/metabolism/pathology ; Cell Survival ; Cell Transformation, Neoplastic/genetics ; Cells, Cultured ; Chromatin Immunoprecipitation ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, myc/genetics ; Humans ; Interferon Regulatory Factors/deficiency/genetics/*metabolism ; Mice ; Multiple Myeloma/genetics/*metabolism/*pathology ; Proto-Oncogene Proteins c-myc/metabolism ; RNA Interference ; Transcriptional Activation
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Innate immunity and intestinal microbiota in the development of Type 1 diabetes (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-09-23
    Description: Type 1 diabetes (T1D) is a debilitating autoimmune disease that results from T-cell-mediated destruction of insulin-producing beta-cells. Its incidence has increased during the past several decades in developed countries, suggesting that changes in the environment (including the human microbial environment) may influence disease pathogenesis. The incidence of spontaneous T1D in non-obese diabetic (NOD) mice can be affected by the microbial environment in the animal housing facility or by exposure to microbial stimuli, such as injection with mycobacteria or various microbial products. Here we show that specific pathogen-free NOD mice lacking MyD88 protein (an adaptor for multiple innate immune receptors that recognize microbial stimuli) do not develop T1D. The effect is dependent on commensal microbes because germ-free MyD88-negative NOD mice develop robust diabetes, whereas colonization of these germ-free MyD88-negative NOD mice with a defined microbial consortium (representing bacterial phyla normally present in human gut) attenuates T1D. We also find that MyD88 deficiency changes the composition of the distal gut microbiota, and that exposure to the microbiota of specific pathogen-free MyD88-negative NOD donors attenuates T1D in germ-free NOD recipients. Together, these findings indicate that interaction of the intestinal microbes with the innate immune system is a critical epigenetic factor modifying T1D predisposition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2574766/" 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/PMC2574766/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wen, Li -- Ley, Ruth E -- Volchkov, Pavel Yu -- Stranges, Peter B -- Avanesyan, Lia -- Stonebraker, Austin C -- Hu, Changyun -- Wong, F Susan -- Szot, Gregory L -- Bluestone, Jeffrey A -- Gordon, Jeffrey I -- Chervonsky, Alexander V -- DK063452/DK/NIDDK NIH HHS/ -- DK30292/DK/NIDDK NIH HHS/ -- DK42086/DK/NIDDK NIH HHS/ -- DK45735/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- P30 DK042086/DK/NIDDK NIH HHS/ -- P30 DK042086-16/DK/NIDDK NIH HHS/ -- P30 DK045735/DK/NIDDK NIH HHS/ -- P30 DK045735-10/DK/NIDDK NIH HHS/ -- P30 DK045735-119006/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30 DK056341-07/DK/NIDDK NIH HHS/ -- P30 DK056341-08/DK/NIDDK NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- P30 DK063720-01/DK/NIDDK NIH HHS/ -- P30 DK63720/DK/NIDDK NIH HHS/ -- R01 DK030292/DK/NIDDK NIH HHS/ -- R01 DK030292-24/DK/NIDDK NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK070977-04/DK/NIDDK NIH HHS/ -- R21 DK063452/DK/NIDDK NIH HHS/ -- R21 DK063452-02/DK/NIDDK NIH HHS/ -- R37 AI046643/AI/NIAID NIH HHS/ -- R37 AI046643-10/AI/NIAID NIH HHS/ -- R37 AI46643/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1109-13. doi: 10.1038/nature07336. Epub 2008 Sep 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18806780" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/classification/genetics/*immunology/isolation & purification ; CD8-Positive T-Lymphocytes/immunology ; Diabetes Mellitus, Type 1/genetics/*immunology/*microbiology ; Female ; Immunity, Innate/genetics/*immunology ; Interferon-gamma/immunology ; Intestines/*microbiology ; Islets of Langerhans/pathology ; Male ; Mice ; Mice, Inbred NOD ; Mice, Knockout ; Mice, SCID ; Molecular Sequence Data ; Myeloid Differentiation Factor 88/genetics ; Phylogeny ; Specific Pathogen-Free Organisms ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    p53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-10-25
    Description: Glioblastoma (GBM) is a highly lethal brain tumour presenting as one of two subtypes with distinct clinical histories and molecular profiles. The primary GBM subtype presents acutely as a high-grade disease that typically harbours mutations in EGFR, PTEN and INK4A/ARF (also known as CDKN2A), and the secondary GBM subtype evolves from the slow progression of a low-grade disease that classically possesses PDGF and TP53 events. Here we show that concomitant central nervous system (CNS)-specific deletion of p53 and Pten in the mouse CNS generates a penetrant acute-onset high-grade malignant glioma phenotype with notable clinical, pathological and molecular resemblance to primary GBM in humans. This genetic observation prompted TP53 and PTEN mutational analysis in human primary GBM, demonstrating unexpectedly frequent inactivating mutations of TP53 as well as the expected PTEN mutations. Integrated transcriptomic profiling, in silico promoter analysis and functional studies of murine neural stem cells (NSCs) established that dual, but not singular, inactivation of p53 and Pten promotes an undifferentiated state with high renewal potential and drives increased Myc protein levels and its associated signature. Functional studies validated increased Myc activity as a potent contributor to the impaired differentiation and enhanced renewal of NSCs doubly null for p53 and Pten (p53(-/-) Pten(-/-)) as well as tumour neurospheres (TNSs) derived from this model. Myc also serves to maintain robust tumorigenic potential of p53(-/-) Pten(-/-) TNSs. These murine modelling studies, together with confirmatory transcriptomic/promoter studies in human primary GBM, validate a pathogenetic role of a common tumour suppressor mutation profile in human primary GBM and establish Myc as an important target for cooperative actions of p53 and Pten in the regulation of normal and malignant stem/progenitor cell differentiation, self-renewal and tumorigenic potential.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4051433/" 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/PMC4051433/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zheng, Hongwu -- Ying, Haoqiang -- Yan, Haiyan -- Kimmelman, Alec C -- Hiller, David J -- Chen, An-Jou -- Perry, Samuel R -- Tonon, Giovanni -- Chu, Gerald C -- Ding, Zhihu -- Stommel, Jayne M -- Dunn, Katherine L -- Wiedemeyer, Ruprecht -- You, Mingjian J -- Brennan, Cameron -- Wang, Y Alan -- Ligon, Keith L -- Wong, Wing H -- Chin, Lynda -- DePinho, Ronald A -- 5P01CA95616/CA/NCI NIH HHS/ -- P01 CA095616/CA/NCI NIH HHS/ -- P01 CA095616-01A19003/CA/NCI NIH HHS/ -- R01 CA099041/CA/NCI NIH HHS/ -- R01 CA099041-05/CA/NCI NIH HHS/ -- R01CA99041/CA/NCI NIH HHS/ -- U01 CA84313/CA/NCI NIH HHS/ -- England -- Nature. 2008 Oct 23;455(7216):1129-33. doi: 10.1038/nature07443.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18948956" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Neoplasms/genetics/*pathology ; *Cell Differentiation ; Cell Proliferation ; Gene Expression Regulation ; Glioblastoma/genetics/pathology ; Glioma/genetics/*pathology ; Humans ; Immunohistochemistry ; Mice ; Neoplastic Stem Cells/metabolism/*pathology ; Neurons/metabolism/*pathology ; PTEN Phosphohydrolase/genetics/*metabolism ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; Tumor Suppressor Protein p53/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)
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  • 9
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    Activity-dependent regulation of inhibitory synapse development by Npas4 (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-09-26
    Description: Neuronal activity regulates the development and maturation of excitatory and inhibitory synapses in the mammalian brain. Several recent studies have identified signalling networks within neurons that control excitatory synapse development. However, less is known about the molecular mechanisms that regulate the activity-dependent development of GABA (gamma-aminobutyric acid)-releasing inhibitory synapses. Here we report the identification of a transcription factor, Npas4, that plays a role in the development of inhibitory synapses by regulating the expression of activity-dependent genes, which in turn control the number of GABA-releasing synapses that form on excitatory neurons. These findings demonstrate that the activity-dependent gene program regulates inhibitory synapse development, and suggest a new role for this program in controlling the homeostatic balance between synaptic excitation and inhibition.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2637532/" 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/PMC2637532/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lin, Yingxi -- Bloodgood, Brenda L -- Hauser, Jessica L -- Lapan, Ariya D -- Koon, Alex C -- Kim, Tae-Kyung -- Hu, Linda S -- Malik, Athar N -- Greenberg, Michael E -- HD18655/HD/NICHD NIH HHS/ -- NS27572/NS/NINDS NIH HHS/ -- NS48276/NS/NINDS NIH HHS/ -- P01 NS047572/NS/NINDS NIH HHS/ -- P01 NS047572-01A10001/NS/NINDS NIH HHS/ -- P01 NS047572-020001/NS/NINDS NIH HHS/ -- P01 NS047572-030001/NS/NINDS NIH HHS/ -- P01 NS047572-040001/NS/NINDS NIH HHS/ -- P01 NS047572-050001/NS/NINDS NIH HHS/ -- R01 MH091220/MH/NIMH NIH HHS/ -- R01 NS048276/NS/NINDS NIH HHS/ -- R01 NS048276-01/NS/NINDS NIH HHS/ -- R01 NS048276-02/NS/NINDS NIH HHS/ -- R01 NS048276-03/NS/NINDS NIH HHS/ -- R01 NS048276-04/NS/NINDS NIH HHS/ -- R01 NS048276-05/NS/NINDS NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Oct 30;455(7217):1198-204. doi: 10.1038/nature07319. Epub 2008 Sep 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉F. M. Kirby Neurobiology Center, Children's Hospital and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18815592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics/*metabolism ; Brain-Derived Neurotrophic Factor/metabolism ; Cells, Cultured ; Electrophysiology ; Gene Expression Regulation ; Hippocampus/cytology ; Mice ; Neurons/metabolism ; Rats ; Synapses/*metabolism ; Transcription Factors/genetics/*metabolism ; Transfection ; gamma-Aminobutyric Acid/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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  • 10
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    An agonist of toll-like receptor 5 has radioprotective activity in mouse and primate models (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-04-12
    Description: The toxicity of ionizing radiation is associated with massive apoptosis in radiosensitive organs. Here, we investigate whether a drug that activates a signaling mechanism used by tumor cells to suppress apoptosis can protect healthy cells from the harmful effects of radiation. We studied CBLB502, a polypeptide drug derived from Salmonella flagellin that binds to Toll-like receptor 5 (TLR5) and activates nuclear factor-kappaB signaling. A single injection of CBLB502 before lethal total-body irradiation protected mice from both gastrointestinal and hematopoietic acute radiation syndromes and resulted in improved survival. CBLB502 injected after irradiation also enhanced survival, but at lower radiation doses. It is noteworthy that the drug did not decrease tumor radiosensitivity in mouse models. CBLB502 also showed radioprotective activity in lethally irradiated rhesus monkeys. Thus, TLR5 agonists could potentially improve the therapeutic index of cancer radiotherapy and serve as biological protectants in radiation emergencies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4322935/" 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/PMC4322935/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burdelya, Lyudmila G -- Krivokrysenko, Vadim I -- Tallant, Thomas C -- Strom, Evguenia -- Gleiberman, Anatoly S -- Gupta, Damodar -- Kurnasov, Oleg V -- Fort, Farrel L -- Osterman, Andrei L -- Didonato, Joseph A -- Feinstein, Elena -- Gudkov, Andrei V -- AI066497/AI/NIAID NIH HHS/ -- CA75179/CA/NCI NIH HHS/ -- CA84406/CA/NCI NIH HHS/ -- R01 CA084406/CA/NCI NIH HHS/ -- R01 CA084406-01A1/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 11;320(5873):226-30. doi: 10.1126/science.1154986.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Stress Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18403709" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis/drug effects/radiation effects ; Chemotherapy, Adjuvant ; Flagellin/chemistry/pharmacology ; Gamma Rays ; Hematopoietic System/drug effects/radiation effects ; Intestine, Small/cytology/drug effects/radiation effects ; Macaca mulatta ; Mice ; Mice, Inbred ICR ; Molecular Sequence Data ; NF-kappa B/*metabolism ; Neoplasms, Experimental/drug therapy/radiotherapy ; Peptides/administration & dosage/chemistry/*pharmacology/toxicity ; Radiation Dosage ; Radiation Injuries, Experimental/*prevention & control ; Radiation Tolerance/*drug effects ; Radiation-Protective Agents/administration & ; dosage/chemistry/*pharmacology/toxicity ; Salmonella enterica ; Signal Transduction ; Toll-Like Receptor 5/*agonists/metabolism ; Whole-Body Irradiation
    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)
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