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  1. AU="Nathan P. Manes"
  2. AU="Forcillo, Jessica"
  3. AU="Santos, Daniel Wagner de Castro Lima"
  4. AU="Dong, Yujie"
  5. AU="Cnockaert, Margo"
  6. AU="Hong, Fan"
  7. AU="Zhao, Shiteng"
  8. AU="Zimmermann, Lisa"
  9. AU="Malone, Daniel C"
  10. AU="Kuo, Sheree"
  11. AU="Leonard, Warren J"
  12. AU=Hawthorne Dawn M
  13. AU=Zein Ahmad Fariz Malvi Zamzam
  14. AU="Delgado, Fernanda"
  15. AU="André Scherag"
  16. AU="Simring, Steven"
  17. AU="Gowdy, John M."
  18. AU="Yeldandi, Anjana"
  19. AU="Mierdel, Katrin"
  20. AU="Karaaslan, Ayse"
  21. AU="Fuchs, Ch"
  22. AU="Toro, Diana"
  23. AU="Lindner, Robert"
  24. AU="Meshkat, Shakila"
  25. AU="Geist, Felix"
  26. AU="Xiong, Yinyi"
  27. AU="Larciprete, R"
  28. AU="Camila Mugnai Vieira"
  29. AU="Michael Sjöström"
  30. AU="Bouchau, Robin"
  31. AU="Shahabi Rabori, Venus"
  32. AU="Jeronimo, Matthew"
  33. AU="Misra, Maitreyi"
  34. AU="Liu, Xuping"
  35. AU="Corinna Lüneburg"
  36. AU="Clement, Lionel C"
  37. AU="Parkhill, Julian"
  38. AU="Wiita, Arun P"
  39. AU=Lubrano Riccardo
  40. AU=Biggs Andrew
  41. AU="Lian, Kejian"
  42. AU="Almutairi, Abdulrahman"
  43. AU="Cosculluela-Pueyo, Rafaél"
  44. AU="Gehrs, Teresa"
  45. AU="Munir, Atif"
  46. AU="Ou, Ya-Nan"
  47. AU=Brown James E AU=Brown James E
  48. AU="Wang, Zhongmin"
  49. AU="Lemieux, Audrée"
  50. AU="Abdelhameed, Mohamed F"
  51. AU="Schaible, Lonnie M"
  52. AU="Yazie, Taklo Simeneh Yazie"
  53. AU="Jude Orumuah Agbugui"
  54. AU="Kruse, Robert L"
  55. AU="Shyama Nandakumar"
  56. AU="Gelb, M"
  57. AU="Gasparini, L"
  58. AU="Ulvila, J"
  59. AU="Länsimies, Helena"

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  1. Artikel ; Online: Myristoylated, alanine-rich C-kinase substrate (MARCKS) regulates toll-like receptor 4 signaling in macrophages

    Jiraphorn Issara-Amphorn / Virginie H. Sjoelund / Margery Smelkinson / Sebastian Montalvo / Sung Hwan Yoon / Nathan P. Manes / Aleksandra Nita-Lazar

    Scientific Reports, Vol 13, Iss 1, Pp 1-

    2023  Band 15

    Abstract: Abstract MARCKS (myristoylated alanine-rich C-kinase substrate) is a membrane-associated protein expressed in many cell types, including macrophages. MARCKS is functionally implicated in cell adhesion, phagocytosis, and inflammation. LPS ( ... ...

    Abstract Abstract MARCKS (myristoylated alanine-rich C-kinase substrate) is a membrane-associated protein expressed in many cell types, including macrophages. MARCKS is functionally implicated in cell adhesion, phagocytosis, and inflammation. LPS (lipopolysaccharide) triggers inflammation via TLR4 (toll-like receptor 4).The presence of MARCKS and the formation of phospho-MARCKS in various cell types have been described, but the role(s) of MARCKS in regulating macrophage functions remain unclear. We investigated the role of MARCKS in inflammation. Confocal microscopy revealed that MARCKS and phospho-MARCKS increased localization to endosomes and the Golgi apparatus upon LPS stimulation.CRISPR-CAS9 mediated knockout of MARCKS in macrophages downregulated the production of TNF and IL6, suggesting a role for MARCKS in inflammatory responses. Our comprehensive proteomics analysis together with real-time metabolic assays comparing LPS-stimulation of WT and MARCKS knock-out macrophages provided insights into the involvement of MARCKS in specific biological processes including innate immune response, inflammatory response, cytokine production, and molecular functions such as extracellularly ATP-gated cation channel activity, electron transfer activity and oxidoreductase activity, uncovering specific proteins involved in regulating MARCKS activity upon LPS stimulation. MARCKS appears to be a key regulator of inflammation whose inhibition might be beneficial for therapeutic intervention in inflammatory diseases.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2023-11-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: The minichromosome maintenance complex drives esophageal basal zone hyperplasia

    Mark Rochman / Yrina Rochman / Julie M. Caldwell / Lydia E. Mack / John A. Besse / Nathan P. Manes / Sung Hwan Yoon / Tetsuo Shoda / Aleksandra Nita-Lazar / Marc E. Rothenberg

    JCI Insight, Vol 8, Iss

    2023  Band 17

    Abstract: Eosinophilic esophagitis (EoE) is a chronic gastrointestinal disorder characterized by food antigen–driven eosinophilic inflammation and hyperproliferation of esophageal mucosa. By utilizing a large-scale, proteomic screen of esophageal biopsies, we ... ...

    Abstract Eosinophilic esophagitis (EoE) is a chronic gastrointestinal disorder characterized by food antigen–driven eosinophilic inflammation and hyperproliferation of esophageal mucosa. By utilizing a large-scale, proteomic screen of esophageal biopsies, we aimed to uncover molecular drivers of the disease. Proteomic analysis by liquid chromatography–tandem mass spectrometry identified 402 differentially expressed proteins (DEPs) that correlated with the EoE transcriptome. Immune cell–related proteins were among the most highly upregulated DEPs in EoE compared with controls, whereas proteins linked to epithelial differentiation were primarily downregulated. Notably, in the inflamed esophageal tissue, all 6 subunits of the minichromosome maintenance (MCM) complex, a DNA helicase essential for genomic DNA replication, were significantly upregulated at the gene and protein levels. Furthermore, treating esophageal epithelial cells with a known inhibitor of the MCM complex (ciprofloxacin) blocked esophageal epithelial proliferation. In a murine model of EoE driven by overexpression of IL-13, ciprofloxacin treatment decreased basal zone thickness and reduced dilated intercellular spaces by blocking the transition of epithelial cells through the S-phase of the cell cycle. Collectively, a broad-spectrum proteomic screen has identified the involvement of the MCM complex in EoE and has highlighted MCM inhibitors as potential therapeutic agents for the disease.
    Schlagwörter Gastroenterology ; Immunology ; Medicine ; R
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-09-01T00:00:00Z
    Verlag American Society for Clinical investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Absolute protein quantitation of the mouse macrophage Toll-like receptor and chemotaxis pathways

    Nathan P. Manes / Jessica M. Calzola / Pauline R. Kaplan / Iain D. C. Fraser / Ronald N. Germain / Martin Meier-Schellersheim / Aleksandra Nita-Lazar

    Scientific Data, Vol 9, Iss 1, Pp 1-

    2022  Band 13

    Abstract: Measurement(s) molecules per cell Technology Type(s) nanoflow high-performance liquid chromatography-electrospray ionisation tandem mass spectrometry Sample Characteristic - Organism Mus ... ...

    Abstract Measurement(s) molecules per cell Technology Type(s) nanoflow high-performance liquid chromatography-electrospray ionisation tandem mass spectrometry Sample Characteristic - Organism Mus musculus
    Schlagwörter Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2022-08-01T00:00:00Z
    Verlag Nature Portfolio
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: Multi-omics Comparative Analysis Reveals Multiple Layers of Host Signaling Pathway Regulation by the Gut Microbiota

    Nathan P. Manes / Natalia Shulzhenko / Arthur G. Nuccio / Sara Azeem / Andrey Morgun / Aleksandra Nita-Lazar

    mSystems, Vol 2, Iss

    2017  Band 5

    Abstract: ABSTRACT The bodies of mammals are hosts to vast microbial communities composed of trillions of bacteria from thousands of species, whose effects on health and development have begun to be appreciated only recently. In this investigation, an integrated ... ...

    Abstract ABSTRACT The bodies of mammals are hosts to vast microbial communities composed of trillions of bacteria from thousands of species, whose effects on health and development have begun to be appreciated only recently. In this investigation, an integrated analysis combining proteomics and transcriptomics was used to quantitatively compare the terminal ilia from conventional and germfree mice. Female and male mice responded similarly to the microbiota, but C57BL/10A mice responded more strongly than BALB/c mice at both the transcriptome and proteome levels. The microbiota primarily caused upregulation of immunological pathways and downregulation of metabolic pathways in the conventional mice. Many of the affected pathways were altered only at either the transcriptome or proteome level. Of the pathways that were affected at both levels, most were affected concordantly. The discordant pathways were not principally involved in the immune system but instead were related to metabolism, oxidative phosphorylation, protein translation, transport, and turnover. To broaden the discovery of affected host pathways, a meta-analysis was performed using intestinal transcriptomics data from previously published studies of germfree versus conventional mice with diverse microbiota populations. Similar transcript-level responses to the microbiota were found, and many additional affected host pathways were discovered. IMPORTANCE Multiple host pathways were affected by its adaptation to the microbiota. We have found significant transcriptome-proteome discordance caused by the microbiota. This discovery leads to the definite conclusion that transcript-level analysis is not sufficient to predict protein levels and their influence on the function of many specific cellular pathways, so only analysis of combinations of the quantitative data determined at different levels will lead to a complete understanding of the complex relationships between the host and the microbiota. Therefore, our results demonstrate the importance of using an ...
    Schlagwörter cell signaling ; host-microbiome interaction ; microbiota ; multi-omics ; proteomics ; systems biology ; Microbiology ; QR1-502
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2017-10-01T00:00:00Z
    Verlag American Society for Microbiology
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Bacillus anthracis interacts with plasmin(ogen) to evade C3b-dependent innate immunity.

    Myung-Chul Chung / Jessica H Tonry / Aarthi Narayanan / Nathan P Manes / Ryan S Mackie / Bradford Gutting / Dhritiman V Mukherjee / Taissia G Popova / Fatah Kashanchi / Charles L Bailey / Serguei G Popov

    PLoS ONE, Vol 6, Iss 3, p e

    2011  Band 18119

    Abstract: The causative agent of anthrax, Bacillus anthracis, is capable of circumventing the humoral and innate immune defense of the host and modulating the blood chemistry in circulation to initiate a productive infection. It has been shown that the pathogen ... ...

    Abstract The causative agent of anthrax, Bacillus anthracis, is capable of circumventing the humoral and innate immune defense of the host and modulating the blood chemistry in circulation to initiate a productive infection. It has been shown that the pathogen employs a number of strategies against immune cells using secreted pathogenic factors such as toxins. However, interference of B. anthracis with the innate immune system through specific interaction of the spore surface with host proteins such as the complement system has heretofore attracted little attention. In order to assess the mechanisms by which B. anthracis evades the defense system, we employed a proteomic analysis to identify human serum proteins interacting with B. anthracis spores, and found that plasminogen (PLG) is a major surface-bound protein. PLG efficiently bound to spores in a lysine- and exosporium-dependent manner. We identified α-enolase and elongation factor tu as PLG receptors. PLG-bound spores were capable of exhibiting anti-opsonic properties by cleaving C3b molecules in vitro and in rabbit bronchoalveolar lavage fluid, resulting in a decrease in macrophage phagocytosis. Our findings represent a step forward in understanding the mechanisms involved in the evasion of innate immunity by B. anthracis through recruitment of PLG resulting in the enhancement of anti-complement and anti-opsonization properties of the pathogen.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2011-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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