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  • Mice, Inbred C57BL  (284)
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  • 1
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    Muc5b is required for airway defence (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-12-10
    Description: Respiratory surfaces are exposed to billions of particulates and pathogens daily. A protective mucus barrier traps and eliminates them through mucociliary clearance (MCC). However, excessive mucus contributes to transient respiratory infections and to the pathogenesis of numerous respiratory diseases. MUC5AC and MUC5B are evolutionarily conserved genes that encode structurally related mucin glycoproteins, the principal macromolecules in airway mucus. Genetic variants are linked to diverse lung diseases, but specific roles for MUC5AC and MUC5B in MCC, and the lasting effects of their inhibition, are unknown. Here we show that mouse Muc5b (but not Muc5ac) is required for MCC, for controlling infections in the airways and middle ear, and for maintaining immune homeostasis in mouse lungs, whereas Muc5ac is dispensable. Muc5b deficiency caused materials to accumulate in upper and lower airways. This defect led to chronic infection by multiple bacterial species, including Staphylococcus aureus, and to inflammation that failed to resolve normally. Apoptotic macrophages accumulated, phagocytosis was impaired, and interleukin-23 (IL-23) production was reduced in Muc5b(-/-) mice. By contrast, in mice that transgenically overexpress Muc5b, macrophage functions improved. Existing dogma defines mucous phenotypes in asthma and chronic obstructive pulmonary disease (COPD) as driven by increased MUC5AC, with MUC5B levels either unaffected or increased in expectorated sputum. However, in many patients, MUC5B production at airway surfaces decreases by as much as 90%. By distinguishing a specific role for Muc5b in MCC, and by determining its impact on bacterial infections and inflammation in mice, our results provide a refined framework for designing targeted therapies to control mucin secretion and restore MCC.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4001806/" 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/PMC4001806/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roy, Michelle G -- Livraghi-Butrico, Alessandra -- Fletcher, Ashley A -- McElwee, Melissa M -- Evans, Scott E -- Boerner, Ryan M -- Alexander, Samantha N -- Bellinghausen, Lindsey K -- Song, Alfred S -- Petrova, Youlia M -- Tuvim, Michael J -- Adachi, Roberto -- Romo, Irlanda -- Bordt, Andrea S -- Bowden, M Gabriela -- Sisson, Joseph H -- Woodruff, Prescott G -- Thornton, David J -- Rousseau, Karine -- De la Garza, Maria M -- Moghaddam, Seyed J -- Karmouty-Quintana, Harry -- Blackburn, Michael R -- Drouin, Scott M -- Davis, C William -- Terrell, Kristy A -- Grubb, Barbara R -- O'Neal, Wanda K -- Flores, Sonia C -- Cota-Gomez, Adela -- Lozupone, Catherine A -- Donnelly, Jody M -- Watson, Alan M -- Hennessy, Corinne E -- Keith, Rebecca C -- Yang, Ivana V -- Barthel, Lea -- Henson, Peter M -- Janssen, William J -- Schwartz, David A -- Boucher, Richard C -- Dickey, Burton F -- Evans, Christopher M -- CA016086/CA/NCI NIH HHS/ -- CA016672/CA/NCI NIH HHS/ -- CA046934/CA/NCI NIH HHS/ -- G1000450/Medical Research Council/United Kingdom -- K01 DK090285/DK/NIDDK NIH HHS/ -- P01 HL108808/HL/NHLBI NIH HHS/ -- P01 HL110873/HL/NHLBI NIH HHS/ -- P30 CA016086/CA/NCI NIH HHS/ -- P30 CA016672/CA/NCI NIH HHS/ -- P30 CA046934/CA/NCI NIH HHS/ -- P30 DK065988/DK/NIDDK NIH HHS/ -- P30DK065988/DK/NIDDK NIH HHS/ -- P50 HL107168/HL/NHLBI NIH HHS/ -- R01 AA008769/AA/NIAAA NIH HHS/ -- R01 HL080396/HL/NHLBI NIH HHS/ -- R01 HL097000/HL/NHLBI NIH HHS/ -- R01 HL109517/HL/NHLBI NIH HHS/ -- R01 HL114381/HL/NHLBI NIH HHS/ -- England -- Nature. 2014 Jan 16;505(7483):412-6. doi: 10.1038/nature12807. Epub 2013 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] University of Texas, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2]. ; 1] University of North Carolina-Chapel Hill, 7011 Thurston-Bowles Building, Chapel Hill, North Carolina 27599, USA [2]. ; 1] University of Colorado School of Medicine, 12700 East 19th Avenue, Aurora, Colorado 80045, USA [2]. ; University of Texas, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA. ; University of Texas Health Science Center-Houston Medical School, 6431 Fannin Street, Houston, Texas 77030, USA. ; 1] University of Texas, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2] Instituto Tecnologico y de Estudios Superiores de Monterrey, Avenida Eugenio Garza Sada 2501 Sur Colonia Tecnologico, Monterrey, Nuevo Leon 64849, Mexico. ; Texas A&M Health Science Center, 2121 W. Holcombe Boulevard, Houston, Texas 77030, USA. ; 1] Texas A&M Health Science Center, 2121 W. Holcombe Boulevard, Houston, Texas 77030, USA [2] University of Houston-Downtown, 1 Main Street, Houston, Texas 77002, USA. ; University of Nebraska Medical Center, 985910 Nebraska Medical Center, Omaha, Nebraska 68198, USA. ; University of California San Francisco, 505 Parnassus Avenue, San Francisco, California 27599, USA. ; University of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK. ; University of North Carolina-Chapel Hill, 7011 Thurston-Bowles Building, Chapel Hill, North Carolina 27599, USA. ; University of Colorado School of Medicine, 12700 East 19th Avenue, Aurora, Colorado 80045, USA. ; 1] University of Colorado School of Medicine, 12700 East 19th Avenue, Aurora, Colorado 80045, USA [2] National Jewish Health, Denver, Colorado 80206, USA. ; 1] University of Texas, MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA [2] University of Colorado School of Medicine, 12700 East 19th Avenue, Aurora, Colorado 80045, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24317696" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/immunology/metabolism ; Bacterial Infections/immunology/microbiology ; Cilia/physiology ; Ear, Middle/immunology/microbiology ; Female ; Inflammation/pathology ; Lung/*immunology/metabolism/microbiology ; Macrophages/immunology/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Biological ; Mucin 5AC/deficiency/metabolism ; Mucin-5B/deficiency/genetics/*metabolism/secretion ; Phagocytosis ; Pulmonary Disease, Chronic Obstructive/immunology/microbiology ; Respiratory Mucosa/*immunology/*metabolism ; Staphylococcus aureus/immunology ; Survival Analysis
    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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    Platelet-biased stem cells reside at the apex of the haematopoietic stem-cell hierarchy (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-08-13
    Description: The blood system is maintained by a small pool of haematopoietic stem cells (HSCs), which are required and sufficient for replenishing all human blood cell lineages at millions of cells per second throughout life. Megakaryocytes in the bone marrow are responsible for the continuous production of platelets in the blood, crucial for preventing bleeding--a common and life-threatening side effect of many cancer therapies--and major efforts are focused at identifying the most suitable cellular and molecular targets to enhance platelet production after bone marrow transplantation or chemotherapy. Although it has become clear that distinct HSC subsets exist that are stably biased towards the generation of lymphoid or myeloid blood cells, we are yet to learn whether other types of lineage-biased HSC exist or understand their inter-relationships and how differently lineage-biased HSCs are generated and maintained. The functional relevance of notable phenotypic and molecular similarities between megakaryocytes and bone marrow cells with an HSC cell-surface phenotype remains unclear. Here we identify and prospectively isolate a molecularly and functionally distinct mouse HSC subset primed for platelet-specific gene expression, with enhanced propensity for short- and long-term reconstitution of platelets. Maintenance of platelet-biased HSCs crucially depends on thrombopoietin, the primary extrinsic regulator of platelet development. Platelet-primed HSCs also frequently have a long-term myeloid lineage bias, can self-renew and give rise to lymphoid-biased HSCs. These findings show that HSC subtypes can be organized into a cellular hierarchy, with platelet-primed HSCs at the apex. They also demonstrate that molecular and functional priming for platelet development initiates already in a distinct HSC population. The identification of a platelet-primed HSC population should enable the rational design of therapies enhancing platelet output.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sanjuan-Pla, Alejandra -- Macaulay, Iain C -- Jensen, Christina T -- Woll, Petter S -- Luis, Tiago C -- Mead, Adam -- Moore, Susan -- Carella, Cintia -- Matsuoka, Sahoko -- Bouriez Jones, Tiphaine -- Chowdhury, Onima -- Stenson, Laura -- Lutteropp, Michael -- Green, Joanna C A -- Facchini, Raffaella -- Boukarabila, Hanane -- Grover, Amit -- Gambardella, Adriana -- Thongjuea, Supat -- Carrelha, Joana -- Tarrant, Paul -- Atkinson, Deborah -- Clark, Sally-Ann -- Nerlov, Claus -- Jacobsen, Sten Eirik W -- G0701761/Medical Research Council/United Kingdom -- G0900892/Medical Research Council/United Kingdom -- G84/6443/Medical Research Council/United Kingdom -- H4RPLK0/Medical Research Council/United Kingdom -- England -- Nature. 2013 Oct 10;502(7470):232-6. doi: 10.1038/nature12495. Epub 2013 Aug 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Stem Cell Research and MRC Centre for Regenerative Medicine, University of Edinburgh, Edinburgh EH9 16UU, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23934107" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Platelets/*cytology ; *Cell Differentiation ; Cell Lineage/genetics ; Female ; Gene Expression Regulation, Developmental ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/*cytology/metabolism ; Lymphocytes/cytology ; Male ; Mice ; Mice, Inbred C57BL
    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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    A mesoscale connectome of the mouse brain (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-04-04
    Description: Comprehensive knowledge of the brain's wiring diagram is fundamental for understanding how the nervous system processes information at both local and global scales. However, with the singular exception of the C. elegans microscale connectome, there are no complete connectivity data sets in other species. Here we report a brain-wide, cellular-level, mesoscale connectome for the mouse. The Allen Mouse Brain Connectivity Atlas uses enhanced green fluorescent protein (EGFP)-expressing adeno-associated viral vectors to trace axonal projections from defined regions and cell types, and high-throughput serial two-photon tomography to image the EGFP-labelled axons throughout the brain. This systematic and standardized approach allows spatial registration of individual experiments into a common three dimensional (3D) reference space, resulting in a whole-brain connectivity matrix. A computational model yields insights into connectional strength distribution, symmetry and other network properties. Virtual tractography illustrates 3D topography among interconnected regions. Cortico-thalamic pathway analysis demonstrates segregation and integration of parallel pathways. The Allen Mouse Brain Connectivity Atlas is a freely available, foundational resource for structural and functional investigations into the neural circuits that support behavioural and cognitive processes in health and disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Oh, Seung Wook -- Harris, Julie A -- Ng, Lydia -- Winslow, Brent -- Cain, Nicholas -- Mihalas, Stefan -- Wang, Quanxin -- Lau, Chris -- Kuan, Leonard -- Henry, Alex M -- Mortrud, Marty T -- Ouellette, Benjamin -- Nguyen, Thuc Nghi -- Sorensen, Staci A -- Slaughterbeck, Clifford R -- Wakeman, Wayne -- Li, Yang -- Feng, David -- Ho, Anh -- Nicholas, Eric -- Hirokawa, Karla E -- Bohn, Phillip -- Joines, Kevin M -- Peng, Hanchuan -- Hawrylycz, Michael J -- Phillips, John W -- Hohmann, John G -- Wohnoutka, Paul -- Gerfen, Charles R -- Koch, Christof -- Bernard, Amy -- Dang, Chinh -- Jones, Allan R -- Zeng, Hongkui -- England -- Nature. 2014 Apr 10;508(7495):207-14. doi: 10.1038/nature13186. Epub 2014 Apr 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Allen Institute for Brain Science, Seattle, Washington 98103, USA [2]. ; Allen Institute for Brain Science, Seattle, Washington 98103, USA. ; Laboratory of Systems Neuroscience, National Institute of Mental Health, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24695228" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atlases as Topic ; Axons/physiology ; Brain/*anatomy & histology/*cytology ; Cerebral Cortex/cytology ; *Connectome ; Corpus Striatum/cytology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Neuroanatomical Tract-Tracing Techniques ; Thalamus/cytology
    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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    Gut microbiota from twins discordant for obesity modulate metabolism in mice (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-09-07
    Description: The role of specific gut microbes in shaping body composition remains unclear. We transplanted fecal microbiota from adult female twin pairs discordant for obesity into germ-free mice fed low-fat mouse chow, as well as diets representing different levels of saturated fat and fruit and vegetable consumption typical of the U.S. diet. Increased total body and fat mass, as well as obesity-associated metabolic phenotypes, were transmissible with uncultured fecal communities and with their corresponding fecal bacterial culture collections. Cohousing mice harboring an obese twin's microbiota (Ob) with mice containing the lean co-twin's microbiota (Ln) prevented the development of increased body mass and obesity-associated metabolic phenotypes in Ob cage mates. Rescue correlated with invasion of specific members of Bacteroidetes from the Ln microbiota into Ob microbiota and was diet-dependent. These findings reveal transmissible, rapid, and modifiable effects of diet-by-microbiota interactions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3829625/" 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/PMC3829625/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ridaura, Vanessa K -- Faith, Jeremiah J -- Rey, Federico E -- Cheng, Jiye -- Duncan, Alexis E -- Kau, Andrew L -- Griffin, Nicholas W -- Lombard, Vincent -- Henrissat, Bernard -- Bain, James R -- Muehlbauer, Michael J -- Ilkayeva, Olga -- Semenkovich, Clay F -- Funai, Katsuhiko -- Hayashi, David K -- Lyle, Barbara J -- Martini, Margaret C -- Ursell, Luke K -- Clemente, Jose C -- Van Treuren, William -- Walters, William A -- Knight, Rob -- Newgard, Christopher B -- Heath, Andrew C -- Gordon, Jeffrey I -- DK078669/DK/NIDDK NIH HHS/ -- DK58398/DK/NIDDK NIH HHS/ -- DK70977/DK/NIDDK NIH HHS/ -- F32 DK091044/DK/NIDDK NIH HHS/ -- K01 DK095774/DK/NIDDK NIH HHS/ -- K05 AA017688/AA/NIAAA NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P30 AG028716/AG/NIA NIH HHS/ -- P30 DK020579/DK/NIDDK NIH HHS/ -- P30 DK056341/DK/NIDDK NIH HHS/ -- P30-AG028716/AG/NIA NIH HHS/ -- R01 DK070977/DK/NIDDK NIH HHS/ -- R01 DK076729/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Sep 6;341(6150):1241214. doi: 10.1126/science.1241214.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009397" target="_blank"〉PubMed〈/a〉
    Keywords: *Adiposity ; Adult ; Animals ; Bacteroidetes/genetics/*physiology ; Cecum/metabolism/microbiology ; Diet, Fat-Restricted ; Feces/microbiology ; Female ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Humans ; Metabolome ; Metagenome/genetics/*physiology ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Obesity/genetics/*metabolism ; Thinness/microbiology ; Twins ; Weight Gain ; Young Adult
    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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  • 5
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    The translational landscape of mTOR signalling steers cancer initiation and metastasis (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-03-01
    Description: The mammalian target of rapamycin (mTOR) kinase is a master regulator of protein synthesis that couples nutrient sensing to cell growth and cancer. However, the downstream translationally regulated nodes of gene expression that may direct cancer development are poorly characterized. Using ribosome profiling, we uncover specialized translation of the prostate cancer genome by oncogenic mTOR signalling, revealing a remarkably specific repertoire of genes involved in cell proliferation, metabolism and invasion. We extend these findings by functionally characterizing a class of translationally controlled pro-invasion messenger RNAs that we show direct prostate cancer invasion and metastasis downstream of oncogenic mTOR signalling. Furthermore, we develop a clinically relevant ATP site inhibitor of mTOR, INK128, which reprograms this gene expression signature with therapeutic benefit for prostate cancer metastasis, for which there is presently no cure. Together, these findings extend our understanding of how the 'cancerous' translation machinery steers specific cancer cell behaviours, including metastasis, and may be therapeutically targeted.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3663483/" 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/PMC3663483/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsieh, Andrew C -- Liu, Yi -- Edlind, Merritt P -- Ingolia, Nicholas T -- Janes, Matthew R -- Sher, Annie -- Shi, Evan Y -- Stumpf, Craig R -- Christensen, Carly -- Bonham, Michael J -- Wang, Shunyou -- Ren, Pingda -- Martin, Michael -- Jessen, Katti -- Feldman, Morris E -- Weissman, Jonathan S -- Shokat, Kevan M -- Rommel, Christian -- Ruggero, Davide -- R01 CA140456/CA/NCI NIH HHS/ -- R01 CA154916/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Feb 22;485(7396):55-61. doi: 10.1038/nature10912.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Medicine and Department of Urology, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22367541" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Benzoxazoles/pharmacology ; Cell Line, Tumor ; Cell Movement/drug effects/genetics ; Eukaryotic Initiation Factor-4E/metabolism ; Eukaryotic Initiation Factors/metabolism ; Gene Expression Regulation, Neoplastic/drug effects/genetics ; Genome/genetics ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Neoplasm Invasiveness/genetics ; *Neoplasm Metastasis/drug therapy/genetics ; Phosphoproteins/metabolism ; Prostatic Neoplasms/drug therapy/genetics/*pathology ; *Protein Biosynthesis ; Pyrimidines/pharmacology ; RNA, Messenger/genetics/metabolism ; Repressor Proteins/metabolism ; *Signal Transduction ; TOR Serine-Threonine Kinases/antagonists & inhibitors/*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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    An ultraviolet-radiation-independent pathway to melanoma carcinogenesis in the red hair/fair skin background (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-11-06
    Description: People with pale skin, red hair, freckles and an inability to tan--the 'red hair/fair skin' phenotype--are at highest risk of developing melanoma, compared to all other pigmentation types. Genetically, this phenotype is frequently the product of inactivating polymorphisms in the melanocortin 1 receptor (MC1R) gene. MC1R encodes a cyclic AMP-stimulating G-protein-coupled receptor that controls pigment production. Minimal receptor activity, as in red hair/fair skin polymorphisms, produces the red/yellow pheomelanin pigment, whereas increasing MC1R activity stimulates the production of black/brown eumelanin. Pheomelanin has weak shielding capacity against ultraviolet radiation relative to eumelanin, and has been shown to amplify ultraviolet-A-induced reactive oxygen species. Several observations, however, complicate the assumption that melanoma risk is completely ultraviolet-radiation-dependent. For example, unlike non-melanoma skin cancers, melanoma is not restricted to sun-exposed skin and ultraviolet radiation signature mutations are infrequently oncogenic drivers. Although linkage of melanoma risk to ultraviolet radiation exposure is beyond doubt, ultraviolet-radiation-independent events are likely to have a significant role. Here we introduce a conditional, melanocyte-targeted allele of the most common melanoma oncoprotein, BRAF(V600E), into mice carrying an inactivating mutation in the Mc1r gene (these mice have a phenotype analogous to red hair/fair skin humans). We observed a high incidence of invasive melanomas without providing additional gene aberrations or ultraviolet radiation exposure. To investigate the mechanism of ultraviolet-radiation-independent carcinogenesis, we introduced an albino allele, which ablates all pigment production on the Mc1r(e/e) background. Selective absence of pheomelanin synthesis was protective against melanoma development. In addition, normal Mc1r(e/e) mouse skin was found to have significantly greater oxidative DNA and lipid damage than albino-Mc1r(e/e) mouse skin. These data suggest that the pheomelanin pigment pathway produces ultraviolet-radiation-independent carcinogenic contributions to melanomagenesis by a mechanism of oxidative damage. Although protection from ultraviolet radiation remains important, additional strategies may be required for optimal melanoma prevention.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3521494/" 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/PMC3521494/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mitra, Devarati -- Luo, Xi -- Morgan, Ann -- Wang, Jin -- Hoang, Mai P -- Lo, Jennifer -- Guerrero, Candace R -- Lennerz, Jochen K -- Mihm, Martin C -- Wargo, Jennifer A -- Robinson, Kathleen C -- Devi, Suprabha P -- Vanover, Jillian C -- D'Orazio, John A -- McMahon, Martin -- Bosenberg, Marcus W -- Haigis, Kevin M -- Haber, Daniel A -- Wang, Yinsheng -- Fisher, David E -- 5R01 AR043369-16/AR/NIAMS NIH HHS/ -- F30 ES020663-01/ES/NIEHS NIH HHS/ -- R01 AR043369/AR/NIAMS NIH HHS/ -- R01 CA101864/CA/NCI NIH HHS/ -- R01 CA129933/CA/NCI NIH HHS/ -- R01 CA131075/CA/NCI NIH HHS/ -- R01 CA176839/CA/NCI NIH HHS/ -- R01-CA101864/CA/NCI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- England -- Nature. 2012 Nov 15;491(7424):449-53. doi: 10.1038/nature11624. Epub 2012 Oct 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cutaneous Biology Research Center, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23123854" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Gene Expression Regulation/drug effects ; Hair Color/*genetics ; Indoles/pharmacology ; Melanins/metabolism ; Melanoma/*genetics ; Mice ; Mice, Inbred C57BL ; Monophenol Monooxygenase/genetics ; Peroxidases/metabolism ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf/genetics ; Receptor, Melanocortin, Type 1/genetics ; Skin Pigmentation/*genetics ; Sulfonamides/pharmacology ; Survival Analysis ; Tumor Cells, Cultured ; *Ultraviolet Rays
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Motor control by sensory cortex (2010)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2010-11-27
    Description: Classical studies of mammalian movement control define a prominent role for the primary motor cortex. Investigating the mouse whisker system, we found an additional and equally direct pathway for cortical motor control driven by the primary somatosensory cortex. Whereas activity in primary motor cortex directly evokes exploratory whisker protraction, primary somatosensory cortex directly drives whisker retraction, providing a rapid negative feedback signal for sensorimotor integration. Motor control by sensory cortex suggests the need to reevaluate the functional organization of cortical maps.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matyas, Ferenc -- Sreenivasan, Varun -- Marbach, Fred -- Wacongne, Catherine -- Barsy, Boglarka -- Mateo, Celine -- Aronoff, Rachel -- Petersen, Carl C H -- New York, N.Y. -- Science. 2010 Nov 26;330(6008):1240-3. doi: 10.1126/science.1195797.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Sensory Processing, Brain Mind Institute, Faculty of Life Sciences, Ecole Polytechnique Federale de Lausanne (EPFL), CH-1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21109671" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Electric Stimulation ; Feedback, Sensory ; Mice ; Mice, Inbred C57BL ; *Motor Activity ; Motor Cortex/physiology ; Neural Pathways/physiology ; Signal Transduction ; Somatosensory Cortex/*physiology ; Vibrissae/*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)
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  • 8
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    Self-organizing and stochastic behaviors during the regeneration of hair stem cells (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-04-30
    Description: Stem cells cycle through active and quiescent states. Large populations of stem cells in an organ may cycle randomly or in a coordinated manner. Although stem cell cycling within single hair follicles has been studied, less is known about regenerative behavior in a hair follicle population. By combining predictive mathematical modeling with in vivo studies in mice and rabbits, we show that a follicle progresses through cycling stages by continuous integration of inputs from intrinsic follicular and extrinsic environmental signals based on universal patterning principles. Signaling from the WNT/bone morphogenetic protein activator/inhibitor pair is coopted to mediate interactions among follicles in the population. This regenerative strategy is robust and versatile because relative activator/inhibitor strengths can be modulated easily, adapting the organism to different physiological and evolutionary needs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321266/" 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/PMC3321266/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plikus, Maksim V -- Baker, Ruth E -- Chen, Chih-Chiang -- Fare, Clyde -- de la Cruz, Damon -- Andl, Thomas -- Maini, Philip K -- Millar, Sarah E -- Widelitz, Randall -- Chuong, Cheng-Ming -- AR47364/AR/NIAMS NIH HHS/ -- AR60306/AR/NIAMS NIH HHS/ -- R01 AR042177/AR/NIAMS NIH HHS/ -- R01 AR042177-17/AR/NIAMS NIH HHS/ -- R01 AR042177-18/AR/NIAMS NIH HHS/ -- R01 AR060306/AR/NIAMS NIH HHS/ -- R01 AR060306-02/AR/NIAMS NIH HHS/ -- R01 AR060306-03/AR/NIAMS NIH HHS/ -- R01-AR42177/AR/NIAMS NIH HHS/ -- R01-AR47709/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 29;332(6029):586-9. doi: 10.1126/science.1201647.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of Southern California (USC), Los Angeles, CA 90033, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21527712" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Morphogenetic Proteins/*metabolism ; Computer Simulation ; Hair Follicle/*cytology/*growth & development/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Biological ; Rabbits ; *Regeneration ; *Signal Transduction ; Stem Cells/*physiology ; Stochastic Processes ; Wnt Proteins/*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)
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    Cocaine disinhibits dopamine neurons by potentiation of GABA transmission in the ventral tegmental area (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-09-28
    Description: Drug-evoked synaptic plasticity in the mesolimbic system reshapes circuit function and drives drug-adaptive behavior. Much research has focused on excitatory transmission in the ventral tegmental area (VTA) and the nucleus accumbens (NAc). How drug-evoked synaptic plasticity of inhibitory transmission affects circuit adaptations remains unknown. We found that medium spiny neurons expressing dopamine (DA) receptor type 1 (D1R-MSNs) of the NAc project to the VTA, strongly preferring the GABA neurons of the VTA. Repeated in vivo exposure to cocaine evoked synaptic potentiation at this synapse, occluding homosynaptic inhibitory long-term potentiation. The activity of the VTA GABA neurons was thus reduced and DA neurons were disinhibited. Cocaine-evoked potentiation of GABA release from D1R-MSNs affected drug-adaptive behavior, which identifies these neurons as a promising target for novel addiction treatments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bocklisch, Christina -- Pascoli, Vincent -- Wong, Jovi C Y -- House, David R C -- Yvon, Cedric -- de Roo, Mathias -- Tan, Kelly R -- Luscher, Christian -- New York, N.Y. -- Science. 2013 Sep 27;341(6153):1521-5. doi: 10.1126/science.1237059.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Basic Neurosciences, Medical Faculty, University of Geneva, CH-1211 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072923" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/*pharmacology ; Cocaine-Related Disorders/physiopathology ; Dopaminergic Neurons/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neuronal Plasticity/drug effects ; Synaptic Transmission/drug effects/physiology ; Ventral Tegmental Area/*metabolism ; gamma-Aminobutyric Acid/*drug effects/metabolism
    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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    mTOR- and HIF-1alpha-mediated aerobic glycolysis as metabolic basis for trained immunity (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-09-27
    Description: Epigenetic reprogramming of myeloid cells, also known as trained immunity, confers nonspecific protection from secondary infections. Using histone modification profiles of human monocytes trained with the Candida albicans cell wall constituent beta-glucan, together with a genome-wide transcriptome, we identified the induced expression of genes involved in glucose metabolism. Trained monocytes display high glucose consumption, high lactate production, and a high ratio of nicotinamide adenine dinucleotide (NAD(+)) to its reduced form (NADH), reflecting a shift in metabolism with an increase in glycolysis dependent on the activation of mammalian target of rapamycin (mTOR) through a dectin-1-Akt-HIF-1alpha (hypoxia-inducible factor-1alpha) pathway. Inhibition of Akt, mTOR, or HIF-1alpha blocked monocyte induction of trained immunity, whereas the adenosine monophosphate-activated protein kinase activator metformin inhibited the innate immune response to fungal infection. Mice with a myeloid cell-specific defect in HIF-1alpha were unable to mount trained immunity against bacterial sepsis. Our results indicate that induction of aerobic glycolysis through an Akt-mTOR-HIF-1alpha pathway represents the metabolic basis of trained immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4226238/" 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/PMC4226238/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cheng, Shih-Chin -- Quintin, Jessica -- Cramer, Robert A -- Shepardson, Kelly M -- Saeed, Sadia -- Kumar, Vinod -- Giamarellos-Bourboulis, Evangelos J -- Martens, Joost H A -- Rao, Nagesha Appukudige -- Aghajanirefah, Ali -- Manjeri, Ganesh R -- Li, Yang -- Ifrim, Daniela C -- Arts, Rob J W -- van der Veer, Brian M J W -- Deen, Peter M T -- Logie, Colin -- O'Neill, Luke A -- Willems, Peter -- van de Veerdonk, Frank L -- van der Meer, Jos W M -- Ng, Aylwin -- Joosten, Leo A B -- Wijmenga, Cisca -- Stunnenberg, Hendrik G -- Xavier, Ramnik J -- Netea, Mihai G -- 1P30GM106394-01/GM/NIGMS NIH HHS/ -- 5P30GM103415-03/GM/NIGMS NIH HHS/ -- DK097485/DK/NIDDK NIH HHS/ -- DK43351/DK/NIDDK NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30 GM103415/GM/NIGMS NIH HHS/ -- P30 GM106394/GM/NIGMS NIH HHS/ -- R01 AI081838/AI/NIAID NIH HHS/ -- R01 DK097485/DK/NIDDK NIH HHS/ -- R01AI81838/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 26;345(6204):1250684. doi: 10.1126/science.1250684.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. ; Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA. ; Department of Molecular Biology, Faculties of Science and Medicine, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. ; Department of Genetics, University of Groningen, University Medical Center Groningen, Groningen, Netherlands. ; 4th Department of Internal Medicine, University of Athens Medical School, 12462 Athens, Greece. ; Department of Biochemistry, Faculties of Science and Medicine, Nijmegen Centre for Molecular Life Sciences, Radboud University, 6500 HB Nijmegen, Netherlands. ; Department of Physiology, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. ; School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland. ; Center for Computational and Integrative Biology and Gastrointestinal Unit, Massachusetts General Hospital, Harvard School of Medicine, Boston, MA 02114, USA. Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. ; Department of Internal Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands. mihai.netea@radboudumc.nl.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25258083" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis/immunology ; Animals ; Candida albicans/immunology ; Candidiasis/immunology/metabolism ; Disease Models, Animal ; *Epigenesis, Genetic ; Female ; Glucose/metabolism ; Glycolysis/*immunology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism ; Immunity, Innate/*genetics ; Immunologic Memory/*genetics ; Male ; Mice ; Mice, Inbred C57BL ; Monocytes/*immunology/metabolism ; Sepsis/genetics/immunology/metabolism ; Staphylococcal Infections/immunology/metabolism ; Staphylococcus aureus ; TOR Serine-Threonine Kinases/genetics/*metabolism ; Transcriptome ; beta-Glucans/immunology
    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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