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Deletion of RBP-J in dendritic cells compromises TLR-mediated DC activation accompanied by abnormal cytoskeleton reorganization.

Byline: Yun-Ru Chen (1), Fan Feng (2), Li Wang (2), Shuo-Yao Qu (2), Zhen-Qiang Zhang (2), Li Liu (1), Hong-Yan Qin (2), Ying-Min Liang (1), Hua Han (1,2) Keywords: Notch; RBP-J; Dendritic cells; Toll-like receptors; Cytoskeleton Abstract: Dendritic cells (DCs) are professional antigen presenting ce... Full description

Journal Title: Molecular biology reports February 2013, Vol.40(2), pp.1531-1539
Main Author: Chen, Yun-Ru
Other Authors: Feng, Fan , Wang, Li , Qu, Shuo-Yao , Zhang, Zhen-Qiang , Liu, Li , Qin, Hong-Yan , Liang, Ying-Min , Han, Hua
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1573-4978 ; DOI: 10.1007/s11033-012-2198-3
Link: http://search.proquest.com/docview/1273254388/?pq-origsite=primo
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title: Deletion of RBP-J in dendritic cells compromises TLR-mediated DC activation accompanied by abnormal cytoskeleton reorganization.
format: Article
creator:
  • Chen, Yun-Ru
  • Feng, Fan
  • Wang, Li
  • Qu, Shuo-Yao
  • Zhang, Zhen-Qiang
  • Liu, Li
  • Qin, Hong-Yan
  • Liang, Ying-Min
  • Han, Hua
subjects:
  • Animals–Metabolism
  • Calcium–Genetics
  • Calcium-Binding Proteins–Metabolism
  • Cell Communication–Metabolism
  • Cells, Cultured–Immunology
  • Cytoskeletal Proteins–Metabolism
  • Dendritic Cells–Ultrastructure
  • Gene Deletion–Deficiency
  • Immunoglobulin J Recombination Signal Sequence-Binding Protein–Genetics
  • Intercellular Signaling Peptides and Proteins–Genetics
  • Interleukin-10–Metabolism
  • Interleukin-12–Metabolism
  • Intracellular Signaling Peptides and Proteins–Metabolism
  • Membrane Proteins–Genetics
  • Mice–Metabolism
  • Mice, Inbred C57bl–Genetics
  • Mice, Transgenic–Metabolism
  • Receptors, Notch–Metabolism
  • Serrate-Jagged Proteins–Physiology
  • Signal Transduction–Metabolism
  • T-Lymphocytes–Metabolism
  • Toll-Like Receptors–Metabolism
  • Up-Regulation–Metabolism
  • Calcium-Binding Proteins
  • Cytoskeletal Proteins
  • Dll4 Protein, Mouse
  • Dlk1 Protein, Mouse
  • Il10 Protein, Mouse
  • Immunoglobulin J Recombination Signal Sequence-Binding Protein
  • Intercellular Signaling Peptides and Proteins
  • Intracellular Signaling Peptides and Proteins
  • Membrane Proteins
  • Rbpj Protein, Mouse
  • Receptors, Notch
  • Serrate-Jagged Proteins
  • Toll-Like Receptors
  • Interleukin-10
  • Interleukin-12
  • Calcium
ispartof: Molecular biology reports, February 2013, Vol.40(2), pp.1531-1539
description: Byline: Yun-Ru Chen (1), Fan Feng (2), Li Wang (2), Shuo-Yao Qu (2), Zhen-Qiang Zhang (2), Li Liu (1), Hong-Yan Qin (2), Ying-Min Liang (1), Hua Han (1,2) Keywords: Notch; RBP-J; Dendritic cells; Toll-like receptors; Cytoskeleton Abstract: Dendritic cells (DCs) are professional antigen presenting cells that activate and modulate immune responses, but the mechanisms underlying DC activation have not been fully understood. In this study, we investigated the role of Notch signaling in DC activation by using murine bone marrow-derived DCs. Triggering of Toll-like receptors (TLRs) of DCs led to upregulated expression of Notch ligands. Disruption of Notch signaling by the deletion of RBP-J, the critical transcription factor mediating the canonical signaling from all Notch receptors, resulted in a reduced capacity of DCs in activating T cells. Moreover, RBP-J deficiency altered the polarization of T cell activation, as manifested by downregulated interferon-I3 and upregulated interleukin-4 and -10 expressions after LPS or Poly(I:C) stimulation. Furthermore, we found that RBP-J.sup.-/- DCs had reduced intracellular calcium after TLR-triggering. Immunofluorescent staining showed that RBP-J deficient DCs exhibited attenuated cytoskeleton reorganization when contacting T cells. In summary, our results suggested that the canonical Notch signaling promotes the cytoskeleton reorganization and the TLR-mediated DC activation. Author Affiliation: (1) Department of Hematology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China (2) State Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Fourth Military Medical University, Chang-Le Xi Street 17, Xian, 710032, China Article History: Registration Date: 09/10/2012 Received Date: 07/05/2012 Accepted Date: 09/10/2012 Online Date: 09/11/2012 Article note: Yun-Ru Chen, Fan Feng, and Li Wang contributed equally to this study. Electronic supplementary material The online version of this article (doi: 10.1007/s11033-012-2198-3) contains supplementary material, which is available to authorized users.
language: eng
source:
identifier: E-ISSN: 1573-4978 ; DOI: 10.1007/s11033-012-2198-3
fulltext: fulltext
issn:
  • 15734978
  • 1573-4978
url: Link


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titleDeletion of RBP-J in dendritic cells compromises TLR-mediated DC activation accompanied by abnormal cytoskeleton reorganization.
creatorChen, Yun-Ru ; Feng, Fan ; Wang, Li ; Qu, Shuo-Yao ; Zhang, Zhen-Qiang ; Liu, Li ; Qin, Hong-Yan ; Liang, Ying-Min ; Han, Hua
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ispartofMolecular biology reports, February 2013, Vol.40(2), pp.1531-1539
identifierE-ISSN: 1573-4978 ; DOI: 10.1007/s11033-012-2198-3
subjectAnimals–Metabolism ; Calcium–Genetics ; Calcium-Binding Proteins–Metabolism ; Cell Communication–Metabolism ; Cells, Cultured–Immunology ; Cytoskeletal Proteins–Metabolism ; Dendritic Cells–Ultrastructure ; Gene Deletion–Deficiency ; Immunoglobulin J Recombination Signal Sequence-Binding Protein–Genetics ; Intercellular Signaling Peptides and Proteins–Genetics ; Interleukin-10–Metabolism ; Interleukin-12–Metabolism ; Intracellular Signaling Peptides and Proteins–Metabolism ; Membrane Proteins–Genetics ; Mice–Metabolism ; Mice, Inbred C57bl–Genetics ; Mice, Transgenic–Metabolism ; Receptors, Notch–Metabolism ; Serrate-Jagged Proteins–Physiology ; Signal Transduction–Metabolism ; T-Lymphocytes–Metabolism ; Toll-Like Receptors–Metabolism ; Up-Regulation–Metabolism ; Calcium-Binding Proteins ; Cytoskeletal Proteins ; Dll4 Protein, Mouse ; Dlk1 Protein, Mouse ; Il10 Protein, Mouse ; Immunoglobulin J Recombination Signal Sequence-Binding Protein ; Intercellular Signaling Peptides and Proteins ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Rbpj Protein, Mouse ; Receptors, Notch ; Serrate-Jagged Proteins ; Toll-Like Receptors ; Interleukin-10 ; Interleukin-12 ; Calcium
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descriptionByline: Yun-Ru Chen (1), Fan Feng (2), Li Wang (2), Shuo-Yao Qu (2), Zhen-Qiang Zhang (2), Li Liu (1), Hong-Yan Qin (2), Ying-Min Liang (1), Hua Han (1,2) Keywords: Notch; RBP-J; Dendritic cells; Toll-like receptors; Cytoskeleton Abstract: Dendritic cells (DCs) are professional antigen presenting cells that activate and modulate immune responses, but the mechanisms underlying DC activation have not been fully understood. In this study, we investigated the role of Notch signaling in DC activation by using murine bone marrow-derived DCs. Triggering of Toll-like receptors (TLRs) of DCs led to upregulated expression of Notch ligands. Disruption of Notch signaling by the deletion of RBP-J, the critical transcription factor mediating the canonical signaling from all Notch receptors, resulted in a reduced capacity of DCs in activating T cells. Moreover, RBP-J deficiency altered the polarization of T cell activation, as manifested by downregulated interferon-I3 and upregulated interleukin-4 and -10 expressions after LPS or Poly(I:C) stimulation. Furthermore, we found that RBP-J.sup.-/- DCs had reduced intracellular calcium after TLR-triggering. Immunofluorescent staining showed that RBP-J deficient DCs exhibited attenuated cytoskeleton reorganization when contacting T cells. In summary, our results suggested that the canonical Notch signaling promotes the cytoskeleton reorganization and the TLR-mediated DC activation. Author Affiliation: (1) Department of Hematology, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China (2) State Key Laboratory of Cancer Biology, Department of Medical Genetics and Developmental Biology, Fourth Military Medical University, Chang-Le Xi Street 17, Xian, 710032, China Article History: Registration Date: 09/10/2012 Received Date: 07/05/2012 Accepted Date: 09/10/2012 Online Date: 09/11/2012 Article note: Yun-Ru Chen, Fan Feng, and Li Wang contributed equally to this study. Electronic supplementary material The online version of this article (doi: 10.1007/s11033-012-2198-3) contains supplementary material, which is available to authorized users.
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titleDeletion of RBP-J in dendritic cells compromises TLR-mediated DC activation accompanied by abnormal cytoskeleton reorganization.
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11Interleukin-12–Metabolism
12Intracellular Signaling Peptides and Proteins–Metabolism
13Membrane Proteins–Genetics
14Mice–Metabolism
15Mice, Inbred C57bl–Genetics
16Mice, Transgenic–Metabolism
17Receptors, Notch–Metabolism
18Serrate-Jagged Proteins–Physiology
19Signal Transduction–Metabolism
20T-Lymphocytes–Metabolism
21Toll-Like Receptors–Metabolism
22Up-Regulation–Metabolism
23Calcium-Binding Proteins
24Cytoskeletal Proteins
25Dll4 Protein, Mouse
26Dlk1 Protein, Mouse
27Il10 Protein, Mouse
28Immunoglobulin J Recombination Signal Sequence-Binding Protein
29Intercellular Signaling Peptides and Proteins
30Intracellular Signaling Peptides and Proteins
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titleDeletion of RBP-J in dendritic cells compromises TLR-mediated DC activation accompanied by abnormal cytoskeleton reorganization.
authorChen, Yun-Ru ; Feng, Fan ; Wang, Li ; Qu, Shuo-Yao ; Zhang, Zhen-Qiang ; Liu, Li ; Qin, Hong-Yan ; Liang, Ying-Min ; Han, Hua
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27Il10 Protein, Mouse
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