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  • 1
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    The growth factor progranulin binds to TNF receptors and is therapeutic against inflammatory arthritis in mice (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-03-12
    Description: The growth factor progranulin (PGRN) has been implicated in embryonic development, tissue repair, tumorigenesis, and inflammation, but its receptors remain unidentified. We report that PGRN bound directly to tumor necrosis factor receptors (TNFRs) and disturbed the TNFalpha-TNFR interaction. PGRN-deficient mice were susceptible to collagen-induced arthritis, and administration of PGRN reversed inflammatory arthritis. Atsttrin, an engineered protein composed of three PGRN fragments, exhibited selective TNFR binding. PGRN and Atsttrin prevented inflammation in multiple arthritis mouse models and inhibited TNFalpha-activated intracellular signaling. Collectively, these findings demonstrate that PGRN is a ligand of TNFR, an antagonist of TNFalpha signaling, and plays a critical role in the pathogenesis of inflammatory arthritis in mice. They also suggest new potential therapeutic interventions for various TNFalpha-mediated pathologies and conditions, including rheumatoid arthritis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3104397/" 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/PMC3104397/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Wei -- Lu, Yi -- Tian, Qing-Yun -- Zhang, Yan -- Guo, Feng-Jin -- Liu, Guang-Yi -- Syed, Nabeel Muzaffar -- Lai, Yongjie -- Lin, Edward Alan -- Kong, Li -- Su, Jeffrey -- Yin, Fangfang -- Ding, Ai-Hao -- Zanin-Zhorov, Alexandra -- Dustin, Michael L -- Tao, Jian -- Craft, Joseph -- Yin, Zhinan -- Feng, Jian Q -- Abramson, Steven B -- Yu, Xiu-Ping -- Liu, Chuan-ju -- AI43542/AI/NIAID NIH HHS/ -- AR040072/AR/NIAMS NIH HHS/ -- AR050620/AR/NIAMS NIH HHS/ -- AR053210/AR/NIAMS NIH HHS/ -- GM061710/GM/NIGMS NIH HHS/ -- R01 AI030165/AI/NIAID NIH HHS/ -- R01 AI030165-20/AI/NIAID NIH HHS/ -- R01 GM061710/GM/NIGMS NIH HHS/ -- R01 GM061710-08/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2011 Apr 22;332(6028):478-84. doi: 10.1126/science.1199214. Epub 2011 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Orthopaedic Surgery, New York University School of Medicine and NYU Hospital for Joint Diseases, New York, NY 10003, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21393509" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/metabolism/pharmacology/therapeutic use ; Arthritis, Experimental/*drug therapy/*immunology/pathology/physiopathology ; Cartilage, Articular/metabolism/pathology ; Female ; Humans ; Intercellular Signaling Peptides and ; Proteins/chemistry/genetics/*metabolism/therapeutic use ; Ligands ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Middle Aged ; Protein Interaction Domains and Motifs ; Receptors, Tumor Necrosis Factor, Type I/genetics/*metabolism ; Receptors, Tumor Necrosis Factor, Type II/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism/pharmacology/therapeutic use ; Recombinant Proteins/therapeutic use ; Signal Transduction ; T-Lymphocytes, Regulatory/immunology/physiology ; Tumor Necrosis Factor-alpha/*metabolism ; Young Adult
    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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  • 2
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    Cadmium toxicity induces ER stress and apoptosis via impairing energy homeostasis in cardiomyocytes (2015)
    Portland Press
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    Publication Date: 2015-04-11
    Description: Cadmium (Cd), a highly toxic environmental pollutant, is reported to induce toxicity and apoptosis in multiple organs and cells, all possibly contributing to apoptosis in certain pathophysiologic situations. Previous studies have described that cadmium toxicity induces biochemical and physiological changes in the heart, and finally leads to cardiac dysfunctions, such as decreasing contractile tension, rate of tension development, heart rate, coronary flow rate, and atrioventricular node conductivity. Although many progresses have been made, the mechanism responsible for cadmium-induced cellular alternations and cardiac toxicity is still not fully understood. Here, we demonstrated that cadmium toxicity induced dramatic ER stress and impaired energy homeostasis in cultured cardiomyocytes. Moreover, cadmium toxicity may inhibit AKT/mTOR pathway to reduce energy productions, by either disrupting the glucose metabolism or inhibiting mitochondrial respiratory gene expressions. Our work will help to reveal a novel mechanism to clarify the role of cadmium toxicity to cardiomyocytes, and providenew possibilities for the treatment of cardiovascular diseases related to cadmium toxicity.
    Print ISSN: 0144-8463
    Electronic ISSN: 1573-4935
    Topics: Biology , Chemistry and Pharmacology
    Published by Portland Press
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  • 3
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    SerRS-tRNASec complex structures reveal mechanism of the first step in selenocysteine biosynthesis (2015)
    Oxford University Press
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    Publication Date: 2015-12-02
    Description: Selenocysteine (Sec) is found in the catalytic centers of many selenoproteins and plays important roles in living organisms. Malfunctions of selenoproteins lead to various human disorders including cancer. Known as the 21st amino acid, the biosynthesis of Sec involves unusual pathways consisting of several stages. While the later stages of the pathways are well elucidated, the molecular basis of the first stage—the serylation of Sec-specific tRNA (tRNA Sec ) catalyzed by seryl-tRNA synthetase (SerRS)—is unclear. Here we present two cocrystal structures of human SerRS bound with tRNA Sec in different stoichiometry and confirm the formation of both complexes in solution by various characterization techniques. We discovered that the enzyme mainly recognizes the backbone of the long variable arm of tRNA Sec with few base-specific contacts. The N-terminal coiled-coil region works like a long-range lever to precisely direct tRNA 3' end to the other protein subunit for aminoacylation in a conformation-dependent manner. Restraints of the flexibility of the coiled-coil greatly reduce serylation efficiencies. Lastly, modeling studies suggest that the local differences present in the D- and T-regions as well as the characteristic U20:G19:C56 base triple in tRNA Sec may allow SerRS to distinguish tRNA Sec from closely related tRNA Ser substrate.
    Print ISSN: 0305-1048
    Electronic ISSN: 1362-4962
    Topics: Biology
    Published by Oxford University Press
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  • 4
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    Disruption of metal ion homeostasis in soils is associated with nitrogen deposition-induced species loss in an Inner Mongolia steppe (2015)
    Copernicus
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    Publication Date: 2015-01-27
    Description: Enhanced deposition of atmospheric nitrogen (N) resulting from anthropogenic activities has negative impacts on plant diversity in grassland ecosystems globally. Several mechanisms have been proposed to explain the species loss. Ion toxicity due to N deposition-induced soil acidification has been suggested to be responsible for species loss in acidic grasslands, while few studies have evaluated the role of soil-mediated homeostasis of ions in species loss under elevated N deposition in alkaline grasslands. To determine whether soil-mediated processes are involved in changes in species composition by N deposition, the effects of 9 yr N addition on soil properties, aboveground biomass (AGB) and species composition were investigated in an Inner Mongolia steppe. Low to moderate N addition rate (2, 4, 8 g N m−2 yr−1) significantly enhanced AGB of grasses, while high N addition rate (〉 16 g N m−2 yr−1) reduced AGB of forbs, leading to an overall increase in AGB of the community under low to moderate N addition rates. Forb richness was significantly reduced by N addition at rates greater than 8 g N m−2 yr−1, while no effect of N addition on grass richness was observed, resulting in decline in total species richness. N addition depleted base cations (Ca2+, Mg2+ and K+) in soils, reduced soil pH and mobilized Mn2+, Fe3+ and Cu2+ ions in soils. Soil inorganic-N concentration was negatively correlated with forb richness, explaining 27.2% variation of forb richness. The concentrations of base cations (Ca2+ and Mg2+) and metal ions (Mn2+ and Cu2+) showed positively and negatively linear correlation with forb richness, accounting for 25.9 and 41.4% variation of forb richness, respectively. These results reveal that disruption of metal ion homeostasis in soils by N addition, particularly enhanced release of soil Mn2+ and Cu2+ may be associated with reduction in forb richness in temperate steppe of Inner Mongolia.
    Print ISSN: 1810-6277
    Electronic ISSN: 1810-6285
    Topics: Biology , Geosciences
    Published by Copernicus on behalf of European Geosciences Union.
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  • 5
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    Corrigendum to "Disruption of metal ion homeostasis in soils is associated with nitrogen deposition-induced species loss in an Inner Mongolia steppe" published in Biogeosciences, 12, 3499–3512, 2015 (2015)
    Copernicus
    Details
    Publication Date: 2015-06-11
    Print ISSN: 1726-4170
    Electronic ISSN: 1726-4189
    Topics: Biology , Geosciences
    Published by Copernicus on behalf of European Geosciences Union.
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  • 6
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    Disruption of metal ion homeostasis in soils is associated with nitrogen deposition-induced species loss in an Inner Mongolia steppe (2015)
    Copernicus
    Details
    Publication Date: 2015-06-09
    Description: Enhanced deposition of atmospheric nitrogen (N) resulting from anthropogenic activities has negative impacts on plant diversity in ecosystems. Several mechanisms have been proposed to explain the species loss. Ion toxicity due to N deposition-induced soil acidification has been suggested to be responsible for species loss in acidic grasslands, while few studies have evaluated the role of soil-mediated homeostasis of ions in species loss under elevated N deposition in grasslands with neutral or alkaline soils. To determine whether soil-mediated processes are involved in changes in biodiversity induced by N deposition, the effects of 9-year N addition on soil properties, aboveground biomass (AGB) and species richness were investigated in an Inner Mongolia steppe. Low to moderate N addition rate (2, 4, 8 g N m−2 yr−1) significantly enhanced AGB of graminoids, while high N addition rate (≥ 16 g N m−2 yr−1) reduced AGB of forbs, leading to an overall increase in AGB of the community under low to moderate N addition rates. Forb richness was significantly reduced by N addition at rates greater than 8 g N m−2 yr−1, while no effect of N addition on graminoid richness was observed, resulting in decline in total species richness. N addition reduced soil pH, depleted base cations (Ca2+, Mg2+ and K+) and mobilized Mn2+, Fe3+, Cu2+ and Al3+ ions in soils. Soil inorganic-N concentration was negatively correlated with forb richness and biomass, explaining 23.59% variation of forb biomass. The concentrations of base cations (Ca2+ and Mg2+) and metal ions (Mn2+, Cu2+ and, Fe3+) showed positively and negatively linear correlation with forb richness, respectively. Changes in the metal ion concentrations accounted for 42.77% variation of forb richness, while reduction of base cations was not associated with the reduction in forb richness. These results reveal that patterns of plant biodiversity in the temperate steppe of Inner Mongolia are primarily driven by increases in metal ion availability, particularly enhanced release of soil Mn2+.
    Print ISSN: 1726-4170
    Electronic ISSN: 1726-4189
    Topics: Biology , Geosciences
    Published by Copernicus on behalf of European Geosciences Union.
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