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  • 1
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    Novel habitat use supports population maintenance in a reconfigured landscape (2016)
    Wiley
    In: Ecosphere
    Details
    Publication Date: 2016-03-09
    Description: Given the limited scope of unaltered, protected areas in most regions, understanding the contributions to imperiled species conservation by landscapes in which habitat elements have been reconfigured is critical. Commercial forestry has been a driver of altered structure and composition of forests and of distribution and character of aquatic systems. In eastern North America, extensive historical wetland drainage reconfigured hydrologic environments from low-gradient wet flats and isolated wetlands to connected networks of linear ditches. Landscapes where both uplands and aquatic environments differ from historic conditions may affect most ecological aspects of semi-aquatic species, including reptiles. Our objective was to determine if habitat selection and use decisions by spotted turtles ( Clemmys guttata ), a rare semi-aquatic species, supported population maintenance in a reconfigured forest landscape in eastern North Carolina, USA. We captured 280 individuals and radiomarked 31 adults to examine habitat selection at multiple spatial scales with paired logistic regression, movements and home ranges with location data and utilization distributions (UDs), survival with a known-fate model, and abundance with N-mixture modeling. Across local and landscape scales, turtles selected features associated with ditches despite abundant, more natural aquatic depressions across the study area. Habitat metrics describing understory closure and substrate characteristics were important at local scales, and closed canopy forest and habitat heterogeneity was positively associated with activity areas at landscape-scale spatial grains. Both movements and home ranges were centered on ditches, and turtles exploited ditches to access mates, nest sites, or uplands for estivation. In this highly reconfigured landscape, this species appeared to have sufficient behavioral plasticity to acquire key resources contributing to high survival and an abundant population. Isolation from road traffic and collection, both which negatively affect turtles elsewhere, was facilitated by limited public access. Our results suggest that conservation and management of rare species should not rely solely on habitat information gained from studies in more pristine areas because such results may not demonstrate the range in variation in behavior that might allow persistence in novel environments, absent key threats.
    Electronic ISSN: 2150-8925
    Topics: Energy, Environment Protection, Nuclear Power Engineering
    Published by Wiley on behalf of The Ecological Society of America (ESA).
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  • 2
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    Impaired T(H)17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-03-14
    Description: The autosomal dominant hyper-IgE syndrome (HIES, 'Job's syndrome') is characterized by recurrent and often severe pulmonary infections, pneumatoceles, eczema, staphylococcal abscesses, mucocutaneous candidiasis, and abnormalities of bone and connective tissue. Mutations presumed to underlie HIES have recently been identified in stat3, the gene encoding STAT3 (signal transducer and activator of transcription 3) (refs 3, 4). Although impaired production of interferon-gamma and tumour-necrosis factor by T cells, diminished memory T-cell populations, decreased delayed-type-hypersensitivity responses and decreased in vitro lymphoproliferation in response to specific antigens have variably been described, specific immunological abnormalities that can explain the unique susceptibility to particular infections seen in HIES have not yet been defined. Here we show that interleukin (IL)-17 production by T cells is absent in HIES individuals. We observed that ex vivo T cells from subjects with HIES failed to produce IL-17, but not IL-2, tumour-necrosis factor or interferon-gamma, on mitogenic stimulation with staphylococcal enterotoxin B or on antigenic stimulation with Candida albicans or streptokinase. Purified naive T cells were unable to differentiate into IL-17-producing (T(H)17) T helper cells in vitro and had lower expression of retinoid-related orphan receptor (ROR)-gammat, which is consistent with a crucial role for STAT3 signalling in the generation of T(H)17 cells. T(H)17 cells have emerged as an important subset of helper T cells that are believed to be critical in the clearance of fungal and extracellular bacterial infections. Thus, our data suggest that the inability to produce T(H)17 cells is a mechanism underlying the susceptibility to the recurrent infections commonly seen in HIES.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864108/" 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/PMC2864108/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Milner, Joshua D -- Brenchley, Jason M -- Laurence, Arian -- Freeman, Alexandra F -- Hill, Brenna J -- Elias, Kevin M -- Kanno, Yuka -- Spalding, Christine -- Elloumi, Houda Z -- Paulson, Michelle L -- Davis, Joie -- Hsu, Amy -- Asher, Ava I -- O'Shea, John -- Holland, Steven M -- Paul, William E -- Douek, Daniel C -- Z99 AI999999/Intramural NIH HHS/ -- England -- Nature. 2008 Apr 10;452(7188):773-6. doi: 10.1038/nature06764. Epub 2008 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunology, 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/18337720" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Candida albicans/immunology ; *Cell Differentiation ; Child ; Child, Preschool ; Enterotoxins/immunology ; Female ; *Genes, Dominant ; Humans ; Interferon-gamma/biosynthesis/immunology ; Interleukin-17/*biosynthesis ; Interleukin-2/biosynthesis/immunology ; Job Syndrome/genetics/*immunology/metabolism/*pathology ; Male ; Middle Aged ; Streptokinase/metabolism ; T-Lymphocytes, Helper-Inducer/immunology/*metabolism/*pathology ; Tumor Necrosis Factor-alpha/biosynthesis/immunology
    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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    Super-enhancers delineate disease-associated regulatory nodes in T cells (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-02-18
    Description: Enhancers regulate spatiotemporal gene expression and impart cell-specific transcriptional outputs that drive cell identity. Super-enhancers (SEs), also known as stretch-enhancers, are a subset of enhancers especially important for genes associated with cell identity and genetic risk of disease. CD4(+) T cells are critical for host defence and autoimmunity. Here we analysed maps of mouse T-cell SEs as a non-biased means of identifying key regulatory nodes involved in cell specification. We found that cytokines and cytokine receptors were the dominant class of genes exhibiting SE architecture in T cells. Nonetheless, the locus encoding Bach2, a key negative regulator of effector differentiation, emerged as the most prominent T-cell SE, revealing a network in which SE-associated genes critical for T-cell biology are repressed by BACH2. Disease-associated single-nucleotide polymorphisms for immune-mediated disorders, including rheumatoid arthritis, were highly enriched for T-cell SEs versus typical enhancers or SEs in other cell lineages. Intriguingly, treatment of T cells with the Janus kinase (JAK) inhibitor tofacitinib disproportionately altered the expression of rheumatoid arthritis risk genes with SE structures. Together, these results indicate that genes with SE architecture in T cells encompass a variety of cytokines and cytokine receptors but are controlled by a 'guardian' transcription factor, itself endowed with an SE. Thus, enumeration of SEs allows the unbiased determination of key regulatory nodes in T cells, which are preferentially modulated by pharmacological intervention.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4409450/" 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/PMC4409450/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vahedi, Golnaz -- Kanno, Yuka -- Furumoto, Yasuko -- Jiang, Kan -- Parker, Stephen C J -- Erdos, Michael R -- Davis, Sean R -- Roychoudhuri, Rahul -- Restifo, Nicholas P -- Gadina, Massimo -- Tang, Zhonghui -- Ruan, Yijun -- Collins, Francis S -- Sartorelli, Vittorio -- O'Shea, John J -- 105663/Z/14/Z/Wellcome Trust/United Kingdom -- R01 CA186714/CA/NCI NIH HHS/ -- ZIA AR041159-07/Intramural NIH HHS/ -- England -- Nature. 2015 Apr 23;520(7548):558-62. doi: 10.1038/nature14154. Epub 2015 Feb 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Cell Biology Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA. ; Translational Immunology Section, NIAMS, NIH, Bethesda, Maryland 20892, USA. ; Medical Genomics and Metabolic Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland 20892, USA. ; Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA. ; The Jackson Laboratory for Genomic Medicine and Department of Genetic and Development Biology, University of Connecticut, Farmington, Connecticut 06030, USA. ; Laboratory of Muscle Stem Cells and Gene Regulation, NIAMS, NIH, Bethesda, Maryland 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25686607" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis, Rheumatoid/*genetics/immunology/pathology ; Basic-Leucine Zipper Transcription Factors/metabolism ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Enhancer Elements, Genetic/*genetics ; Gene Expression Regulation/genetics ; Genetic Predisposition to Disease/genetics ; Janus Kinase 3/antagonists & inhibitors ; Mice ; Mice, Inbred C57BL ; Piperidines/pharmacology ; Pyrimidines/pharmacology ; Pyrroles/pharmacology ; RNA, Untranslated/genetics ; T-Lymphocytes, Helper-Inducer/immunology/*metabolism/*pathology ; Transcription, Genetic/genetics ; p300-CBP Transcription Factors/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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  • 4
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    Gibberellin acts positively then negatively to control onset of flower formation in Arabidopsis (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-05-09
    Description: The switch to reproductive development is biphasic in many plants, a feature important for optimal pollination and yield. We show that dual opposite roles of the phytohormone gibberellin underpin this phenomenon in Arabidopsis. Although gibberellin promotes termination of vegetative development, it inhibits flower formation. To overcome this effect, the transcription factor LEAFY induces expression of a gibberellin catabolism gene; consequently, increased LEAFY activity causes reduced gibberellin levels. This allows accumulation of gibberellin-sensitive DELLA proteins. The DELLA proteins are recruited by SQUAMOSA PROMOTER BINDING PROTEIN-LIKE transcription factors to regulatory regions of the floral commitment gene APETALA1 and promote APETALA1 up-regulation and floral fate synergistically with LEAFY. The two opposing functions of gibberellin may facilitate evolutionary and environmental modulation of plant inflorescence architecture.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, Nobutoshi -- Winter, Cara M -- Wu, Miin-Feng -- Kanno, Yuri -- Yamaguchi, Ayako -- Seo, Mitsunori -- Wagner, Doris -- T32-HD007516/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2014 May 9;344(6184):638-41. doi: 10.1126/science.1250498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Pennsylvania, 415 South University Avenue, Philadelphia, PA 19104-6018, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24812402" target="_blank"〉PubMed〈/a〉
    Keywords: Arabidopsis/genetics/*growth & development/metabolism ; Arabidopsis Proteins/metabolism ; Flowers/genetics/*growth & development/metabolism ; Gibberellins/metabolism/pharmacology/*physiology ; MADS Domain Proteins/metabolism ; Transcription Factors/genetics/metabolism ; Up-Regulation
    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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  • 5
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    Cell signaling. Stat acetylation--a key facet of cytokine signaling? (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉O'Shea, John J -- Kanno, Yuka -- Chen, Xiaomin -- Levy, David E -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):217-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653493" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetyltransferases/metabolism ; Active Transport, Cell Nucleus ; Cell Nucleus/metabolism ; Cells, Cultured ; Cytokines/*physiology ; Cytoplasm/metabolism ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Dimerization ; Histone Acetyltransferases ; Histone Deacetylases/metabolism ; Lysine/*metabolism ; Mutation ; NF-kappa B/metabolism ; Nuclear Proteins/metabolism ; Phosphorylation ; Protein Processing, Post-Translational ; STAT3 Transcription Factor ; *Signal Transduction ; Trans-Activators/chemistry/genetics/*metabolism ; Transcriptional Activation ; src Homology Domains
    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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  • 6
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    Author Correction: Self-organization of a human organizer by combined Wnt and Nodal signalling (2018)
    Springer Nature
    In: Nature
    Details
    Publication Date: 2018
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Springer Nature
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  • 7
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    Generation of pathogenic T(H)17 cells in the absence of TGF-beta signalling (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-10-22
    Description: CD4(+) T-helper cells that selectively produce interleukin (IL)-17 (T(H)17), are critical for host defence and autoimmunity. Although crucial for T(H)17 cells in vivo, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-beta1 have been proposed to be the factors responsible for initiating specification. Here we show that T(H)17 differentiation can occur in the absence of TGF-beta signalling. Neither IL-6 nor IL-23 alone efficiently generated T(H)17 cells; however, these cytokines in combination with IL-1beta effectively induced IL-17 production in naive precursors, independently of TGF-beta. Epigenetic modification of the Il17a, Il17f and Rorc promoters proceeded without TGF-beta1, allowing the generation of cells that co-expressed RORgammat (encoded by Rorc) and T-bet. T-bet(+)RORgammat(+) T(H)17 cells are generated in vivo during experimental allergic encephalomyelitis, and adoptively transferred T(H)17 cells generated with IL-23 without TGF-beta1 were pathogenic in this disease model. These data indicate an alternative mode for T(H)17 differentiation. Consistent with genetic data linking IL23R with autoimmunity, our findings re-emphasize the importance of IL-23 and therefore may have therapeutic implications.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3108066/" 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/PMC3108066/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghoreschi, Kamran -- Laurence, Arian -- Yang, Xiang-Ping -- Tato, Cristina M -- McGeachy, Mandy J -- Konkel, Joanne E -- Ramos, Haydee L -- Wei, Lai -- Davidson, Todd S -- Bouladoux, Nicolas -- Grainger, John R -- Chen, Qian -- Kanno, Yuka -- Watford, Wendy T -- Sun, Hong-Wei -- Eberl, Gerard -- Shevach, Ethan M -- Belkaid, Yasmine -- Cua, Daniel J -- Chen, Wanjun -- O'Shea, John J -- Z99 AR999999/Intramural NIH HHS/ -- England -- Nature. 2010 Oct 21;467(7318):967-71. doi: 10.1038/nature09447.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ghoreschik@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20962846" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmune Diseases/immunology/pathology ; Autoimmunity/immunology ; Cell Differentiation/drug effects ; Central Nervous System/pathology ; Inflammation ; Interleukin-10 ; Interleukin-17/secretion ; Interleukin-1beta/immunology ; Interleukin-23/immunology/pharmacology ; Interleukin-6/immunology ; Interleukin-9 ; Interleukins/biosynthesis ; Mice ; Mice, Inbred C57BL ; Mucous Membrane/cytology/immunology ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Receptors, Interleukin/metabolism ; *Signal Transduction ; Th17 Cells/drug effects/metabolism/*pathology ; *Transforming Growth Factor beta
    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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  • 8
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    BACH2 represses effector programs to stabilize T(reg)-mediated immune homeostasis (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-06-04
    Description: Through their functional diversification, distinct lineages of CD4(+) T cells can act to either drive or constrain immune-mediated pathology. Transcription factors are critical in the generation of cellular diversity, and negative regulators antagonistic to alternate fates often act in conjunction with positive regulators to stabilize lineage commitment. Genetic polymorphisms within a single locus encoding the transcription factor BACH2 are associated with numerous autoimmune and allergic diseases including asthma, Crohn's disease, coeliac disease, vitiligo, multiple sclerosis and type 1 diabetes. Although these associations point to a shared mechanism underlying susceptibility to diverse immune-mediated diseases, a function for BACH2 in the maintenance of immune homeostasis has not been established. Here, by studying mice in which the Bach2 gene is disrupted, we define BACH2 as a broad regulator of immune activation that stabilizes immunoregulatory capacity while repressing the differentiation programs of multiple effector lineages in CD4(+) T cells. BACH2 was required for efficient formation of regulatory (Treg) cells and consequently for suppression of lethal inflammation in a manner that was Treg-cell-dependent. Assessment of the genome-wide function of BACH2, however, revealed that it represses genes associated with effector cell differentiation. Consequently, its absence during Treg polarization resulted in inappropriate diversion to effector lineages. In addition, BACH2 constrained full effector differentiation within TH1, TH2 and TH17 cell lineages. These findings identify BACH2 as a key regulator of CD4(+) T-cell differentiation that prevents inflammatory disease by controlling the balance between tolerance and immunity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710737/" 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/PMC3710737/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roychoudhuri, Rahul -- Hirahara, Kiyoshi -- Mousavi, Kambiz -- Clever, David -- Klebanoff, Christopher A -- Bonelli, Michael -- Sciume, Giuseppe -- Zare, Hossein -- Vahedi, Golnaz -- Dema, Barbara -- Yu, Zhiya -- Liu, Hui -- Takahashi, Hayato -- Rao, Mahadev -- Muranski, Pawel -- Crompton, Joseph G -- Punkosdy, George -- Bedognetti, Davide -- Wang, Ena -- Hoffmann, Victoria -- Rivera, Juan -- Marincola, Francesco M -- Nakamura, Atsushi -- Sartorelli, Vittorio -- Kanno, Yuka -- Gattinoni, Luca -- Muto, Akihiko -- Igarashi, Kazuhiko -- O'Shea, John J -- Restifo, Nicholas P -- Z01 BC011037-01/Intramural NIH HHS/ -- Z99 CA999999/Intramural NIH HHS/ -- ZIA BC011037-02/Intramural NIH HHS/ -- England -- Nature. 2013 Jun 27;498(7455):506-10. doi: 10.1038/nature12199. Epub 2013 Jun 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cancer Research, National Cancer Institute, National Institutes of Health (NIH), Bethesda, Maryland 20892, USA. roychoudhuri@mail.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23728300" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoimmunity/immunology ; Basic-Leucine Zipper Transcription Factors/deficiency/genetics/*metabolism ; CD4-Positive T-Lymphocytes/cytology/immunology/metabolism ; Cell Differentiation/genetics/immunology ; Female ; Forkhead Transcription Factors/genetics/metabolism ; Homeostasis/genetics/*immunology ; Humans ; Immune Tolerance/genetics/immunology ; Inflammation/genetics/immunology/mortality/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; T-Lymphocytes, Regulatory/cytology/drug effects/*immunology/metabolism ; Transforming Growth Factor beta/pharmacology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    Metabolic rates of epipelagic marine copepods as a function of body mass and temperature (2001)
    Springer
    Details
    Publication Date: 2001-11-01
    Print ISSN: 0025-3162
    Electronic ISSN: 1432-1793
    Topics: Biology
    Published by Springer
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  • 10
    Electronic Resource
    Electronic Resource
    Survival of BSC-1 cells through the maintenance of cell volume brought about by epidermal growth factor depends on attachment to the substratum (1990)
    Springer
    Cellular and molecular life sciences 46 (1990), S. 492-495 
    Details
    ISSN: 1420-9071
    Keywords: BSC-1 cells ; cell survival ; cell volume ; cell adhesion ; epidermal growth factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Addition of epidermal growth factor to culture medium without calf serum suppressed the increase in cell volume and then enhanced the survival of BSC-1 cells attached to culture dishes. However, these effects of epidermal growth factor were not observed in the case of cells on dishes coated with heat-denatured bovine serum albumin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01954243
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