Original Literature | Model OverView |
---|---|
Publication
Title
The Lps locus: genetic regulation of host responses to bacteriallipopolysaccharide.
Affiliation
Department of Medicine, McGill University, Montreal, Quebec, Canada.mc76@musica.mcgill.ca
Abstract
Lipopolysaccharide (LPS), an abundant glycolipid of the outer membrane ofgram-negative bacteria, is able to provoke a generalized proinflammatoryresponse in the infected host. Genetic regulation of this trait has beenlocalized to the Lps locus on mouse chromosome 4. Several inbred mouse strains,including C3H/HeJ, C57BL/10ScNCr and C57BL/10ScCr, bear mutations at the Lpslocus (Lps(d)) that confer hyporesponsiveness to the immunostimulatoryproperties of LPS and susceptibility to overwhelming gram-negative bacterialinfection. The phenotypic expression of Lps(d) is pleiotropic, affecting severalcell types crucial to host defense, including the macrophage. By positionalcloning, Toll-like receptor 4 (Tlr4), a transmembrane protein with a cytoplasmicdomain that bears homology to the Interleukin-1 receptor, has been identified asthe gene encoded by Lps. Tlr4 is a member of a novel gene family thatparticipates in host defense against microbial infection in plants,invertebrates and mammals. Discovery of the molecular basis of the Lps mutationrepresents a significant advance in defining the fundamental mechanisms ofcellular activation by LPS.
PMID
10669111
|
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PMID: 10669111 In this scheme, LBP complexes with monomeric LPS derived from circulating micelles and catalytically transfers it to CD14, either on the plasma membrane of host cells or in the serum
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PMID: 10669111 TLR4 is involved in LPS signaling leading to LPS-mediated NF-kB activation and transcription of immune response genes. Activation of these two transmembrane receptors by their respective ligands, Sp?tzle and IL-1, trigger parallel signaling pathways that culminate in nuclear translocation of the Drosophila protein dorsal and its mammalian homolog NF-kB, both of which stimulate gene transcription.
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PMID: 10669111 TLR4 is involved in LPS signaling leading to LPS-mediated NF-kB activation and transcription of immune response genes.
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PMID: 10669111 Activation of these two transmembrane receptors (TOLL and IL-1R) by their respective ligands, Sp?tzle and IL-1, trigger parallel signaling pathways that culminate in nuclear translocation of the Drosophila protein dorsal and its mammalian homolog NF-kB, both of which stimulate gene transcription.
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PMID: 10669111 Activation of these two transmembrane receptors (TOLL and IL-1R) by their respective ligands, Sp?tzle and IL-1, trigger parallel signaling pathways that culminate in nuclear translocation of the Drosophila protein dorsal and its mammalian homolog NF-kB, both of which stimulate gene transcription.
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PMID: 10669111 Activation of these two transmembrane receptors (TOLL and IL-1R)by their respective ligands, Sp?tzle and IL-1, trigger parallel signaling pathways that culminate in nuclear translocation of the Drosophila protein dorsal and its mammalian homolog NF-kB, both of which stimulate gene transcription.
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PMID: 10669111 Activation of these two transmembrane receptors (TOLL and IL-1R)by their respective ligands, Sp?tzle and IL-1, trigger parallel signaling pathways that culminate in nuclear translocation of the Drosophila protein dorsal and its mammalian homolog NF-kB, both of which stimulate gene transcription.
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PMID: 10669111 Activation of these two transmembrane receptors (TOLL and IL-1R)by their respective ligands, Sp?tzle and IL-1, trigger parallel signaling pathways that culminate in nuclear translocation of the Drosophila protein dorsal and its mammalian homolog NF-kB, both of which stimulate gene transcription.
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PMID: 10669111 Stable transfection and expression of a constitutively- active form of hToll (TLR4) activated NF-kB and stimulated transcriptional activation of several inflammatory cytokines including IL-1, IL-6 and IL-8 as well as the costimulatory molecule B7.1 which is necessary for differentiation of naive T cells.
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PMID: 10669111 Stable transfection and expression of a constitutively- active form of hToll (TLR4) activated NF-kB and stimulated transcriptional activation of several inflammatory cytokines including IL-1, IL-6 and IL-8 as well as the costimulatory molecule B7.1 which is necessary for differentiation of naive T cells.
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PMID: 10669111 Stable transfection and expression of a constitutively- active form of hToll (TLR4) activated NF-kB and stimulated transcriptional activation of several inflammatory cytokines including IL-1, IL-6 and IL-8 as well as the costimulatory molecule B7.1 which is necessary for differentiation of naive T cells.
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PMID: 10669111 In this scheme, LBP complexes with monomeric LPS derived from circulating micelles and catalytically transfers it to CD14, either on the plasma membrane of host cells or in the serum
--
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PMID: 10669111 Stable transfection and expression of a constitutively- active form of hToll (TLR4) activated NF-kB and stimulated transcriptional activation of several inflammatory cytokines including IL-1, IL-6 and IL-8 as well as the costimulatory molecule B7.1 which is necessary for differentiation of naive T cells.
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PMID: 10669111 In this scheme, LBP complexes with monomeric LPS derived from circulating micelles and catalytically transfers it to CD14, either on the plasma membrane of host cells or in the serum
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PMID: 10669111 TLR4 is involved in LPS signaling leading to LPS-mediated NF-kB activation and transcription of immune response genes.
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PMID: 10669111 TLR4 is involved in LPS signaling leading to LPS-mediated NF-kB activation and transcription of immune response genes.
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PMID: 10669111 TLR4 is involved in LPS signaling leading to LPS-mediated NF-kB activation and transcription of immune response genes.
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PMID: 10669111 TLR4 is involved in LPS signaling leading to LPS-mediated NF-kB activation and transcription of immune response genes.
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PMID: 10669111 TLR4 is involved in LPS signaling leading to LPS-mediated NF-kB activation and transcription of immune response genes.
--
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PMID: 10669111 TLR4 is involved in LPS signaling leading to LPS-mediated NF-kB activation and transcription of immune response genes.
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1,
--
cso30:c:InputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--
cso30:c:OutputProcess
threshold
--
0
1,
--