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  • Mice  (105)
  • Meteorology and Climatology
  • Nature Publishing Group (NPG)  (105)
  • 2005-2009  (105)
  • 1950-1954
  • 2008  (105)
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  • 2005-2009  (105)
  • 1950-1954
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  • 1
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    Cutaneous cancer stem cell maintenance is dependent on beta-catenin signalling (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-04
    Description: Continuous turnover of epithelia is ensured by the extensive self-renewal capacity of tissue-specific stem cells. Similarly, epithelial tumour maintenance relies on cancer stem cells (CSCs), which co-opt stem cell properties. For most tumours, the cellular origin of these CSCs and regulatory pathways essential for sustaining stemness have not been identified. In murine skin, follicular morphogenesis is driven by bulge stem cells that specifically express CD34. Here we identify a population of cells in early epidermal tumours characterized by phenotypic and functional similarities to normal bulge skin stem cells. This population contains CSCs, which are the only cells with tumour initiation properties. Transplants derived from these CSCs preserve the hierarchical organization of the primary tumour. We describe beta-catenin signalling as being essential in sustaining the CSC phenotype. Ablation of the beta-catenin gene results in the loss of CSCs and complete tumour regression. In addition, we provide evidence for the involvement of increased beta-catenin signalling in malignant human squamous cell carcinomas. Because Wnt/beta-catenin signalling is not essential for normal epidermal homeostasis, such a mechanistic difference may thus be targeted to eliminate CSCs and consequently eradicate squamous cell carcinomas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malanchi, Ilaria -- Peinado, Hector -- Kassen, Deepika -- Hussenet, Thomas -- Metzger, Daniel -- Chambon, Pierre -- Huber, Marcel -- Hohl, Daniel -- Cano, Amparo -- Birchmeier, Walter -- Huelsken, Joerg -- England -- Nature. 2008 Apr 3;452(7187):650-3. doi: 10.1038/nature06835.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Ecole Polytechnique Federale de Lausanne/ISREC (Swiss Institute for Experimental Cancer Research) and National Center of Competence in Research Molecular Oncology, Chemin des Boveresses 155, 1066 Epalinges, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18385740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/metabolism ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Cells, Cultured ; Epidermis/pathology ; Humans ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplastic Stem Cells/*metabolism/*pathology ; *Signal Transduction ; Skin Neoplasms/*pathology ; beta Catenin/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Proteomic analysis of active multiple sclerosis lesions reveals therapeutic targets (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-02-19
    Description: Understanding the neuropathology of multiple sclerosis (MS) is essential for improved therapies. Therefore, identification of targets specific to pathological types of MS may have therapeutic benefits. Here we identify, by laser-capture microdissection and proteomics, proteins unique to three major types of MS lesions: acute plaque, chronic active plaque and chronic plaque. Comparative proteomic profiles identified tissue factor and protein C inhibitor within chronic active plaque samples, suggesting dysregulation of molecules associated with coagulation. In vivo administration of hirudin or recombinant activated protein C reduced disease severity in experimental autoimmune encephalomyelitis and suppressed Th1 and Th17 cytokines in astrocytes and immune cells. Administration of mutant forms of recombinant activated protein C showed that both its anticoagulant and its signalling functions were essential for optimal amelioration of experimental autoimmune encephalomyelitis. A proteomic approach illuminated potential therapeutic targets selective for specific pathological stages of MS and implicated participation of the coagulation cascade.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, May H -- Hwang, Sun-Il -- Roy, Dolly B -- Lundgren, Deborah H -- Price, Jordan V -- Ousman, Shalina S -- Fernald, Guy Haskin -- Gerlitz, Bruce -- Robinson, William H -- Baranzini, Sergio E -- Grinnell, Brian W -- Raine, Cedric S -- Sobel, Raymond A -- Han, David K -- Steinman, Lawrence -- T32 AI007290/AI/NIAID NIH HHS/ -- England -- Nature. 2008 Feb 28;451(7182):1076-81. doi: 10.1038/nature06559. Epub 2008 Feb 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18278032" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Blood Coagulation ; Encephalomyelitis, Autoimmune, Experimental/immunology/metabolism/pathology ; Female ; *Gene Expression Profiling ; Humans ; Inflammation/metabolism/pathology ; Male ; Mice ; Middle Aged ; Multiple Sclerosis/classification/drug therapy/*metabolism/*pathology ; Protein C/genetics/metabolism/pharmacology ; *Proteomics ; Th1 Cells/immunology ; Th2 Cells/immunology ; Thrombin/antagonists & inhibitors/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    The impact of microRNAs on protein output (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-08-01
    Description: MicroRNAs are endogenous approximately 23-nucleotide RNAs that can pair to sites in the messenger RNAs of protein-coding genes to downregulate the expression from these messages. MicroRNAs are known to influence the evolution and stability of many mRNAs, but their global impact on protein output had not been examined. Here we use quantitative mass spectrometry to measure the response of thousands of proteins after introducing microRNAs into cultured cells and after deleting mir-223 in mouse neutrophils. The identities of the responsive proteins indicate that targeting is primarily through seed-matched sites located within favourable predicted contexts in 3' untranslated regions. Hundreds of genes were directly repressed, albeit each to a modest degree, by individual microRNAs. Although some targets were repressed without detectable changes in mRNA levels, those translationally repressed by more than a third also displayed detectable mRNA destabilization, and, for the more highly repressed targets, mRNA destabilization usually comprised the major component of repression. The impact of microRNAs on the proteome indicated that for most interactions microRNAs act as rheostats to make fine-scale adjustments to protein output.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2745094/" 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/PMC2745094/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baek, Daehyun -- Villen, Judit -- Shin, Chanseok -- Camargo, Fernando D -- Gygi, Steven P -- Bartel, David P -- R01 GM067031/GM/NIGMS NIH HHS/ -- R01 HG003456/HG/NHGRI NIH HHS/ -- R01 HG003456-04A1/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Sep 4;455(7209):64-71. doi: 10.1038/nature07242. Epub 2008 Jul 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18668037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; HeLa Cells ; Humans ; Isotope Labeling ; Male ; Mice ; MicroRNAs/*genetics/*metabolism ; Neutrophils/metabolism ; Oligonucleotide Array Sequence Analysis ; *Protein Biosynthesis ; Proteomics ; Transfection
    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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    Live-animal tracking of individual haematopoietic stem/progenitor cells in their niche (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-12-05
    Description: Stem cells reside in a specialized, regulatory environment termed the niche that dictates how they generate, maintain and repair tissues. We have previously documented that transplanted haematopoietic stem and progenitor cell populations localize to subdomains of bone-marrow microvessels where the chemokine CXCL12 is particularly abundant. Using a combination of high-resolution confocal microscopy and two-photon video imaging of individual haematopoietic cells in the calvarium bone marrow of living mice over time, we examine the relationship of haematopoietic stem and progenitor cells to blood vessels, osteoblasts and endosteal surface as they home and engraft in irradiated and c-Kit-receptor-deficient recipient mice. Osteoblasts were enmeshed in microvessels and relative positioning of stem/progenitor cells within this complex tissue was nonrandom and dynamic. Both cell autonomous and non-autonomous factors influenced primitive cell localization. Different haematopoietic cell subsets localized to distinct locations according to the stage of differentiation. When physiological challenges drove either engraftment or expansion, bone-marrow stem/progenitor cells assumed positions in close proximity to bone and osteoblasts. Our analysis permits observing in real time, at a single cell level, processes that previously have been studied only by their long-term outcome at the organismal level.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2820276/" 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/PMC2820276/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lo Celso, Cristina -- Fleming, Heather E -- Wu, Juwell W -- Zhao, Cher X -- Miake-Lye, Sam -- Fujisaki, Joji -- Cote, Daniel -- Rowe, David W -- Lin, Charles P -- Scadden, David T -- R01 EY014106/EY/NEI NIH HHS/ -- R01 EY014106-05/EY/NEI NIH HHS/ -- England -- Nature. 2009 Jan 1;457(7225):92-6. doi: 10.1038/nature07434. Epub 2008 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Regenerative Medicine, Massachusetts General Hospital, 185 Cambridge Street, Boston, Massachusetts 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19052546" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Vessels/cytology ; Bone Marrow ; Cell Division ; Cell Separation ; Hematopoietic Stem Cells/*cytology ; Mice ; Mice, Inbred C57BL ; Osteoblasts/cytology ; Proto-Oncogene Proteins c-kit/genetics/metabolism ; Skull/cytology ; Stem Cell Niche/*cytology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    WSTF regulates the H2A.X DNA damage response via a novel tyrosine kinase activity (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-12-19
    Description: DNA double-stranded breaks present a serious challenge for eukaryotic cells. The inability to repair breaks leads to genomic instability, carcinogenesis and cell death. During the double-strand break response, mammalian chromatin undergoes reorganization demarcated by H2A.X Ser 139 phosphorylation (gamma-H2A.X). However, the regulation of gamma-H2A.X phosphorylation and its precise role in chromatin remodelling during the repair process remain unclear. Here we report a new regulatory mechanism mediated by WSTF (Williams-Beuren syndrome transcription factor, also known as BAZ1B)-a component of the WICH complex (WSTF-ISWI ATP-dependent chromatin-remodelling complex). We show that WSTF has intrinsic tyrosine kinase activity by means of a domain that shares no sequence homology to any known kinase fold. We show that WSTF phosphorylates Tyr 142 of H2A.X, and that WSTF activity has an important role in regulating several events that are critical for the DNA damage response. Our work demonstrates a new mechanism that regulates the DNA damage response and expands our knowledge of domains that contain intrinsic tyrosine kinase activity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854499/" 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/PMC2854499/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiao, Andrew -- Li, Haitao -- Shechter, David -- Ahn, Sung Hee -- Fabrizio, Laura A -- Erdjument-Bromage, Hediye -- Ishibe-Murakami, Satoko -- Wang, Bin -- Tempst, Paul -- Hofmann, Kay -- Patel, Dinshaw J -- Elledge, Stephen J -- Allis, C David -- F32 GM075486/GM/NIGMS NIH HHS/ -- P30 CA08748/CA/NCI NIH HHS/ -- R01 GM040922/GM/NIGMS NIH HHS/ -- R01 GM040922-24/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jan 1;457(7225):57-62. doi: 10.1038/nature07668. Epub 2008 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chromatin Biology, The Rockefeller University, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19092802" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Animals ; Chromatin Assembly and Disassembly ; Chromosomal Proteins, Non-Histone/metabolism ; *DNA Damage ; Histones/genetics/*metabolism ; Humans ; Mice ; NIH 3T3 Cells ; Nucleosomes/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/*metabolism ; Transcription Factors/chemistry/deficiency/genetics/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Endothelins are vascular-derived axonal guidance cues for developing sympathetic neurons (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-04-11
    Description: During development, sympathetic neurons extend axons along a myriad of distinct trajectories, often consisting of arteries, to innervate one of a large variety of distinct final target tissues. Whether or not subsets of neurons within complex sympathetic ganglia are predetermined to innervate select end-organs is unknown. Here we demonstrate in mouse embryos that the endothelin family member Edn3 (ref. 1), acting through the endothelin receptor EdnrA (refs 2, 3), directs extension of axons of a subset of sympathetic neurons from the superior cervical ganglion to a preferred intermediate target, the external carotid artery, which serves as the gateway to select targets, including the salivary glands. These findings establish a previously unknown mechanism of axonal pathfinding involving vascular-derived endothelins, and have broad implications for endothelins as general mediators of axonal growth and guidance in the developing nervous system. Moreover, they suggest a model in which newborn sympathetic neurons distinguish and choose between distinct vascular trajectories to innervate their appropriate end organs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2713667/" 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/PMC2713667/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makita, Takako -- Sucov, Henry M -- Gariepy, Cheryl E -- Yanagisawa, Masashi -- Ginty, David D -- R01 HL078891/HL/NHLBI NIH HHS/ -- R01 HL078891-01A1/HL/NHLBI NIH HHS/ -- R01 HL078891-02/HL/NHLBI NIH HHS/ -- R01 HL078891-03/HL/NHLBI NIH HHS/ -- R37 NS034814/NS/NINDS NIH HHS/ -- R37 NS034814-11/NS/NINDS NIH HHS/ -- R37 NS034814-11S1/NS/NINDS NIH HHS/ -- R37 NS034814-12/NS/NINDS NIH HHS/ -- R37 NS034814-13/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Apr 10;452(7188):759-63. doi: 10.1038/nature06859.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Solomon H. Snyder Department of Neuroscience, Howard Hughes Medical Institute, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18401410" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Carotid Arteries/cytology/*metabolism ; Cues ; Embryo, Mammalian/blood supply/cytology ; Endothelin-3/metabolism ; Endothelins/*metabolism ; Mice ; Neurites/physiology ; Receptors, Endothelin/metabolism ; Salivary Glands/innervation ; *Signal Transduction ; Superior Cervical Ganglion/*cytology/metabolism
    Print ISSN: 0028-0836
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  • 7
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    Regulation of progenitor cell proliferation and granulocyte function by microRNA-223 (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-02-19
    Description: MicroRNAs are abundant in animal genomes and have been predicted to have important roles in a broad range of gene expression programmes. Despite this prominence, there is a dearth of functional knowledge regarding individual mammalian microRNAs. Using a loss-of-function allele in mice, we report here that the myeloid-specific microRNA-223 (miR-223) negatively regulates progenitor proliferation and granulocyte differentiation and activation. miR-223 (also called Mirn223) mutant mice have an expanded granulocytic compartment resulting from a cell-autonomous increase in the number of granulocyte progenitors. We show that Mef2c, a transcription factor that promotes myeloid progenitor proliferation, is a target of miR-223, and that genetic ablation of Mef2c suppresses progenitor expansion and corrects the neutrophilic phenotype in miR-223 null mice. In addition, granulocytes lacking miR-223 are hypermature, hypersensitive to activating stimuli and display increased fungicidal activity. As a consequence of this neutrophil hyperactivity, miR-223 mutant mice spontaneously develop inflammatory lung pathology and exhibit exaggerated tissue destruction after endotoxin challenge. Our data support a model in which miR-223 acts as a fine-tuner of granulocyte production and the inflammatory response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnnidis, Jonathan B -- Harris, Marian H -- Wheeler, Robert T -- Stehling-Sun, Sandra -- Lam, Michael H -- Kirak, Oktay -- Brummelkamp, Thijn R -- Fleming, Mark D -- Camargo, Fernando D -- England -- Nature. 2008 Feb 28;451(7182):1125-9. doi: 10.1038/nature06607. Epub 2008 Feb 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18278031" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Cell Differentiation ; *Cell Proliferation ; Gene Deletion ; Granulocytes/*cytology/immunology/pathology/*physiology ; Inflammation/genetics/immunology/pathology ; Lung/pathology ; MEF2 Transcription Factors ; Mice ; Mice, Knockout ; MicroRNAs/*genetics/*metabolism ; Myogenic Regulatory Factors/genetics/metabolism ; Neutrophils/physiology ; Phenotype ; Stem Cells/*cytology
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  • 8
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    A role for VEGF as a negative regulator of pericyte function and vessel maturation (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-11-11
    Description: Angiogenesis does not only depend on endothelial cell invasion and proliferation: it also requires pericyte coverage of vascular sprouts for vessel stabilization. These processes are coordinated by vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) through their cognate receptors on endothelial cells and vascular smooth muscle cells (VSMCs), respectively. PDGF induces neovascularization by priming VSMCs/pericytes to release pro-angiogenic mediators. Although VEGF directly stimulates endothelial cell proliferation and migration, its role in pericyte biology is less clear. Here we define a role for VEGF as an inhibitor of neovascularization on the basis of its capacity to disrupt VSMC function. Specifically, under conditions of PDGF-mediated angiogenesis, VEGF ablates pericyte coverage of nascent vascular sprouts, leading to vessel destabilization. At the molecular level, VEGF-mediated activation of VEGF-R2 suppresses PDGF-Rbeta signalling in VSMCs through the assembly of a previously undescribed receptor complex consisting of PDGF-Rbeta and VEGF-R2. Inhibition of VEGF-R2 not only prevents assembly of this receptor complex but also restores angiogenesis in tissues exposed to both VEGF and PDGF. Finally, genetic deletion of tumour cell VEGF disrupts PDGF-Rbeta/VEGF-R2 complex formation and increases tumour vessel maturation. These findings underscore the importance of VSMCs/pericytes in neovascularization and reveal a dichotomous role for VEGF and VEGF-R2 signalling as both a promoter of endothelial cell function and a negative regulator of VSMCs and vessel maturation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605188/" 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/PMC2605188/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greenberg, Joshua I -- Shields, David J -- Barillas, Samuel G -- Acevedo, Lisette M -- Murphy, Eric -- Huang, Jianhua -- Scheppke, Lea -- Stockmann, Christian -- Johnson, Randall S -- Angle, Niren -- Cheresh, David A -- GM 68524/GM/NIGMS NIH HHS/ -- P01 CA078045/CA/NCI NIH HHS/ -- P01 CA078045-050004/CA/NCI NIH HHS/ -- P01 CA078045-100004/CA/NCI NIH HHS/ -- P01 CA078045-109001/CA/NCI NIH HHS/ -- R01 CA095262/CA/NCI NIH HHS/ -- R01 CA095262-06/CA/NCI NIH HHS/ -- R01 CA118165/CA/NCI NIH HHS/ -- R01 HL078912/HL/NHLBI NIH HHS/ -- R01 HL078912-04/HL/NHLBI NIH HHS/ -- R21 CA129660/CA/NCI NIH HHS/ -- R21 CA129660-02/CA/NCI NIH HHS/ -- R37 CA050286/CA/NCI NIH HHS/ -- R37 CA050286-19/CA/NCI NIH HHS/ -- R37 CA050286-20/CA/NCI NIH HHS/ -- R37-CA082515/CA/NCI NIH HHS/ -- R37-CA50286/CA/NCI NIH HHS/ -- England -- Nature. 2008 Dec 11;456(7223):809-13. doi: 10.1038/nature07424. Epub 2008 Nov 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Surgery, School of Medicine, Moore's UCSD Cancer Center, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18997771" target="_blank"〉PubMed〈/a〉
    Keywords: Angiogenesis Inhibitors/pharmacology ; Animals ; Blood Vessels/*metabolism ; Cell Line ; Cells, Cultured ; Fibrosarcoma/blood supply ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Nude ; Neovascularization, Physiologic/drug effects/*physiology ; Pericytes/drug effects/*metabolism ; Platelet-Derived Growth Factor/*metabolism/pharmacology ; Receptor, Platelet-Derived Growth Factor beta/metabolism ; Receptors, Vascular Endothelial Growth Factor/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
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    Pluripotent stem cells induced from adult neural stem cells by reprogramming with two factors (2008)
    Nature Publishing Group (NPG)
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    Publication Date: 2008-07-03
    Description: Reprogramming of somatic cells is a valuable tool to understand the mechanisms of regaining pluripotency and further opens up the possibility of generating patient-specific pluripotent stem cells. Reprogramming of mouse and human somatic cells into pluripotent stem cells, designated as induced pluripotent stem (iPS) cells, has been possible with the expression of the transcription factor quartet Oct4 (also known as Pou5f1), Sox2, c-Myc and Klf4 (refs 1-11). Considering that ectopic expression of c-Myc causes tumorigenicity in offspring and that retroviruses themselves can cause insertional mutagenesis, the generation of iPS cells with a minimal number of factors may hasten the clinical application of this approach. Here we show that adult mouse neural stem cells express higher endogenous levels of Sox2 and c-Myc than embryonic stem cells, and that exogenous Oct4 together with either Klf4 or c-Myc is sufficient to generate iPS cells from neural stem cells. These two-factor iPS cells are similar to embryonic stem cells at the molecular level, contribute to development of the germ line, and form chimaeras. We propose that, in inducing pluripotency, the number of reprogramming factors can be reduced when using somatic cells that endogenously express appropriate levels of complementing factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Jeong Beom -- Zaehres, Holm -- Wu, Guangming -- Gentile, Luca -- Ko, Kinarm -- Sebastiano, Vittorio -- Arauzo-Bravo, Marcos J -- Ruau, David -- Han, Dong Wook -- Zenke, Martin -- Scholer, Hans R -- England -- Nature. 2008 Jul 31;454(7204):646-50. doi: 10.1038/nature07061. Epub 2008 Jun 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Rontgenstrasse 20, 48149 Munster, NRW, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18594515" target="_blank"〉PubMed〈/a〉
    Keywords: Adult Stem Cells/*cytology/metabolism ; Animals ; Cell Differentiation/genetics ; Cells, Cultured ; *Cellular Reprogramming ; Chimera ; DNA-Binding Proteins/genetics/metabolism ; Female ; Gene Expression Profiling ; Genes, myc/genetics ; HMGB Proteins/genetics/metabolism ; Homeodomain Proteins/genetics ; Kruppel-Like Transcription Factors/genetics/metabolism ; Male ; Mice ; Mice, Nude ; Mice, Transgenic ; Neurons/*cytology ; Octamer Transcription Factor-3/genetics/metabolism ; Pluripotent Stem Cells/*cytology/*metabolism ; Proteins/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Untranslated ; SOXB1 Transcription Factors ; Transcription Factors/genetics/metabolism ; Transduction, Genetic
    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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    Melanopsin cells are the principal conduits for rod-cone input to non-image-forming vision (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-04-25
    Description: Rod and cone photoreceptors detect light and relay this information through a multisynaptic pathway to the brain by means of retinal ganglion cells (RGCs). These retinal outputs support not only pattern vision but also non-image-forming (NIF) functions, which include circadian photoentrainment and pupillary light reflex (PLR). In mammals, NIF functions are mediated by rods, cones and the melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs). Rod-cone photoreceptors and ipRGCs are complementary in signalling light intensity for NIF functions. The ipRGCs, in addition to being directly photosensitive, also receive synaptic input from rod-cone networks. To determine how the ipRGCs relay rod-cone light information for both image-forming and non-image-forming functions, we genetically ablated ipRGCs in mice. Here we show that animals lacking ipRGCs retain pattern vision but have deficits in both PLR and circadian photoentrainment that are more extensive than those observed in melanopsin knockouts. The defects in PLR and photoentrainment resemble those observed in animals that lack phototransduction in all three photoreceptor classes. These results indicate that light signals for irradiance detection are dissociated from pattern vision at the retinal ganglion cell level, and animals that cannot detect light for NIF functions are still capable of image formation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2871301/" 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/PMC2871301/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guler, Ali D -- Ecker, Jennifer L -- Lall, Gurprit S -- Haq, Shafiqul -- Altimus, Cara M -- Liao, Hsi-Wen -- Barnard, Alun R -- Cahill, Hugh -- Badea, Tudor C -- Zhao, Haiqing -- Hankins, Mark W -- Berson, David M -- Lucas, Robert J -- Yau, King-Wai -- Hattar, Samer -- R01 DC006904/DC/NIDCD NIH HHS/ -- R01 DC006904-01/DC/NIDCD NIH HHS/ -- R01 DC006904-02/DC/NIDCD NIH HHS/ -- R01 DC006904-03/DC/NIDCD NIH HHS/ -- R01 DC006904-04/DC/NIDCD NIH HHS/ -- R01 EY006837/EY/NEI NIH HHS/ -- R01 EY006837-16A1/EY/NEI NIH HHS/ -- R01 EY006837-18/EY/NEI NIH HHS/ -- R01 EY006837-20A1/EY/NEI NIH HHS/ -- R01 EY006837-21/EY/NEI NIH HHS/ -- R01 EY014596/EY/NEI NIH HHS/ -- R01 EY014596-01/EY/NEI NIH HHS/ -- R01 EY014596-02/EY/NEI NIH HHS/ -- R01 EY014596-03/EY/NEI NIH HHS/ -- R01 EY014596-04/EY/NEI NIH HHS/ -- R01 EY014596-05/EY/NEI NIH HHS/ -- R01 EY014596-06/EY/NEI NIH HHS/ -- R01 EY017137/EY/NEI NIH HHS/ -- R01 GM076430/GM/NIGMS NIH HHS/ -- R01 GM076430-01/GM/NIGMS NIH HHS/ -- R01 GM076430-02/GM/NIGMS NIH HHS/ -- R01 GM076430-03/GM/NIGMS NIH HHS/ -- R01 GM076430-04/GM/NIGMS NIH HHS/ -- R01 GM076430-05/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 May 1;453(7191):102-5. doi: 10.1038/nature06829. Epub 2008 Apr 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Johns Hopkins University, Baltimore, Maryland 21218, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18432195" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/cytology/metabolism ; Circadian Rhythm/physiology/radiation effects ; Cues ; Electroretinography ; Light ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity/physiology ; Pupil/physiology/radiation effects ; Reflex/physiology/radiation effects ; Retinal Cone Photoreceptor Cells/*metabolism ; Retinal Ganglion Cells/*cytology/*metabolism ; Retinal Rod Photoreceptor Cells/*metabolism ; Rod Opsins/deficiency/genetics/*metabolism ; Vision, Ocular/*physiology/radiation effects ; Visual Acuity/physiology
    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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