mcd14 Search Results


cd14  (InvivoGen)
92
InvivoGen cd14
Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with <t>CD14</t> and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).
Cd14, supplied by InvivoGen, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mcd14  (InvivoGen)
90
InvivoGen mcd14
Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with <t>CD14</t> and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).
Mcd14, supplied by InvivoGen, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mcd14/product/InvivoGen
Average 90 stars, based on 1 article reviews
mcd14 - by Bioz Stars, 2026-03
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mcd14–tlr4 complex  (Federation of European Neuroscience Societies)
90
Federation of European Neuroscience Societies mcd14–tlr4 complex
Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with <t>CD14</t> and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).
Mcd14–Tlr4 Complex, supplied by Federation of European Neuroscience Societies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mcd14–tlr4 complex/product/Federation of European Neuroscience Societies
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anti-mcd14-fitc  (Becton Dickinson)
90
Becton Dickinson anti-mcd14-fitc
Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with <t>CD14</t> and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).
Anti Mcd14 Fitc, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti-mcd14-fitc/product/Becton Dickinson
Average 90 stars, based on 1 article reviews
anti-mcd14-fitc - by Bioz Stars, 2026-03
90/100 stars
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mcd14  (Immunotec inc)
90
Immunotec inc mcd14
Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with <t>CD14</t> and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).
Mcd14, supplied by Immunotec inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mcd14/product/Immunotec inc
Average 90 stars, based on 1 article reviews
mcd14 - by Bioz Stars, 2026-03
90/100 stars
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mcd14  (Heumann Pharma)
90
Heumann Pharma mcd14
Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with <t>CD14</t> and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).
Mcd14, supplied by Heumann Pharma, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mcd14/product/Heumann Pharma
Average 90 stars, based on 1 article reviews
mcd14 - by Bioz Stars, 2026-03
90/100 stars
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mcd14–tlr complex  (Hartz Mountain Corporation)
90
Hartz Mountain Corporation mcd14–tlr complex
Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with <t>CD14</t> and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).
Mcd14–Tlr Complex, supplied by Hartz Mountain Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mcd14–tlr complex/product/Hartz Mountain Corporation
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90/100 stars
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small interfering rnas targeting mcd14 mcd14-sirna-180  (Shanghai GenePharma)
90
Shanghai GenePharma small interfering rnas targeting mcd14 mcd14-sirna-180
Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with <t>CD14</t> and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).
Small Interfering Rnas Targeting Mcd14 Mcd14 Sirna 180, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
small interfering rnas targeting mcd14 mcd14-sirna-180 - by Bioz Stars, 2026-03
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Image Search Results


Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with CD14 and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).

Journal: Molecular oral microbiology

Article Title: Mechanism and implications of CXCR4-mediated integrin activation by Porphyromonas gingivalis.

doi: 10.1111/omi.12021

Figure Lengend Snippet: Figure 6 Exploitation of CXCR4 by Porphyromonas gingivalis. In macrophages, P. gingivalis interacts with CD14 and the Toll-like receptor 2 (TLR2)/TLR1 signaling complex resulting in inside-out signaling for activating and binding CR3, which leads to a relatively ‘safe’ uptake of these organisms by macrophages (Hajishengallis et al., 2006, 2007; Wang et al., 2007). The signaling pathway that activates the high-affinity state of CR3 is mediated by Rac1, PI3K and cytohesin 1 (Cyt1) (Harokopakis & Hajishengallis, 2005; Harokopakis et al., 2006; Hajishengallis et al., 2009). The P. gingivalis-activated TLR2/TLR1 also induces a MyD88-dependent pathway that can potentially promote the killing of this bacterium (Hajishengallis et al., 2008, 2009). However, by means of its fimbriae, P. gingivalis instigates a crosstalk between CXCR4 and TLR2 which interferes with this antimicrobial mechanism (Hajishengallis et al., 2008). In this study, P. gingivalis was shown to also use CXCR4 to induce phosphatidylinositol-3 kinase (PI3K) -dependent activation of CR3, independently of TLR2, which further contributes to its capacity to evade killing. CXCR4 exploitation requires fully functional fimbriae, i.e. containing both the FimA and FimCDE components, which can directly bind CXCR4 (Pierce et al., 2009).

Article Snippet: Briefly, CHO-CR3 cells were transfected with human TLR2 and CD14, using a single plasmid (pDUO-hCD14/TLR2; Invivogen), with or without co-transfection with human CXCR4 (pORF-hCXCR4; Invivogen).

Techniques: Binding Assay, Activation Assay, Functional Assay