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MedChemExpress recombinant tweak
Arg1 + MMP12 + macrophage-derived <t>TWEAK</t> licenses PDGFB production in fibroTECs via Fn14 signaling. (A) Ligand-receptor communication analysis between different cell types in IRI kidneys. (B) The major incoming signaling of different cell types. (C) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between myeloid cell subsets and TEC subsets. (D) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between TEC subsets and myeloid cell subsets. (E, F) WT/AMPKα1 −/− BMDMs were treated with IL-4 and IL-13, and the expression levels of Arg 1 , Mmp12 , and Tnfsf12 were analyzed by qPCR (n = 5). (G, H) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs. The expression of Pdgfb , Cxcl1 , and Egfr in TCMK-1 cells was analyzed by qPCR (n = 5). (I, J) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs or together with <t>recombinant</t> TWEAK <t>(rTWEAK).</t> The expression of Pdgfb in TCMK-1 cells was analyzed by qPCR (n = 5). (K, L) TCMK-1 cells were treated with rTWEAK or rTWEAK and an Fn14 inhibitor. The expression of Pdgfb in TCMK-1 cells was detected by qPCR (n = 5). (M) Immunoblots and quantification of IKK-β and nuclear NF-κB p65 in TCMK-1 cells treated with PBS or rTWEAK (n = 3). The results represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
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Arg1 + MMP12 + macrophage-derived <t>TWEAK</t> licenses PDGFB production in fibroTECs via Fn14 signaling. (A) Ligand-receptor communication analysis between different cell types in IRI kidneys. (B) The major incoming signaling of different cell types. (C) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between myeloid cell subsets and TEC subsets. (D) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between TEC subsets and myeloid cell subsets. (E, F) WT/AMPKα1 −/− BMDMs were treated with IL-4 and IL-13, and the expression levels of Arg 1 , Mmp12 , and Tnfsf12 were analyzed by qPCR (n = 5). (G, H) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs. The expression of Pdgfb , Cxcl1 , and Egfr in TCMK-1 cells was analyzed by qPCR (n = 5). (I, J) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs or together with <t>recombinant</t> TWEAK <t>(rTWEAK).</t> The expression of Pdgfb in TCMK-1 cells was analyzed by qPCR (n = 5). (K, L) TCMK-1 cells were treated with rTWEAK or rTWEAK and an Fn14 inhibitor. The expression of Pdgfb in TCMK-1 cells was detected by qPCR (n = 5). (M) Immunoblots and quantification of IKK-β and nuclear NF-κB p65 in TCMK-1 cells treated with PBS or rTWEAK (n = 3). The results represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
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Arg1 + MMP12 + macrophage-derived <t>TWEAK</t> licenses PDGFB production in fibroTECs via Fn14 signaling. (A) Ligand-receptor communication analysis between different cell types in IRI kidneys. (B) The major incoming signaling of different cell types. (C) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between myeloid cell subsets and TEC subsets. (D) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between TEC subsets and myeloid cell subsets. (E, F) WT/AMPKα1 −/− BMDMs were treated with IL-4 and IL-13, and the expression levels of Arg 1 , Mmp12 , and Tnfsf12 were analyzed by qPCR (n = 5). (G, H) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs. The expression of Pdgfb , Cxcl1 , and Egfr in TCMK-1 cells was analyzed by qPCR (n = 5). (I, J) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs or together with <t>recombinant</t> TWEAK <t>(rTWEAK).</t> The expression of Pdgfb in TCMK-1 cells was analyzed by qPCR (n = 5). (K, L) TCMK-1 cells were treated with rTWEAK or rTWEAK and an Fn14 inhibitor. The expression of Pdgfb in TCMK-1 cells was detected by qPCR (n = 5). (M) Immunoblots and quantification of IKK-β and nuclear NF-κB p65 in TCMK-1 cells treated with PBS or rTWEAK (n = 3). The results represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
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R&D Systems recombinant murine tweak
Arg1 + MMP12 + macrophage-derived <t>TWEAK</t> licenses PDGFB production in fibroTECs via Fn14 signaling. (A) Ligand-receptor communication analysis between different cell types in IRI kidneys. (B) The major incoming signaling of different cell types. (C) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between myeloid cell subsets and TEC subsets. (D) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between TEC subsets and myeloid cell subsets. (E, F) WT/AMPKα1 −/− BMDMs were treated with IL-4 and IL-13, and the expression levels of Arg 1 , Mmp12 , and Tnfsf12 were analyzed by qPCR (n = 5). (G, H) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs. The expression of Pdgfb , Cxcl1 , and Egfr in TCMK-1 cells was analyzed by qPCR (n = 5). (I, J) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs or together with <t>recombinant</t> TWEAK <t>(rTWEAK).</t> The expression of Pdgfb in TCMK-1 cells was analyzed by qPCR (n = 5). (K, L) TCMK-1 cells were treated with rTWEAK or rTWEAK and an Fn14 inhibitor. The expression of Pdgfb in TCMK-1 cells was detected by qPCR (n = 5). (M) Immunoblots and quantification of IKK-β and nuclear NF-κB p65 in TCMK-1 cells treated with PBS or rTWEAK (n = 3). The results represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
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Arg1 + MMP12 + macrophage-derived <t>TWEAK</t> licenses PDGFB production in fibroTECs via Fn14 signaling. (A) Ligand-receptor communication analysis between different cell types in IRI kidneys. (B) The major incoming signaling of different cell types. (C) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between myeloid cell subsets and TEC subsets. (D) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between TEC subsets and myeloid cell subsets. (E, F) WT/AMPKα1 −/− BMDMs were treated with IL-4 and IL-13, and the expression levels of Arg 1 , Mmp12 , and Tnfsf12 were analyzed by qPCR (n = 5). (G, H) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs. The expression of Pdgfb , Cxcl1 , and Egfr in TCMK-1 cells was analyzed by qPCR (n = 5). (I, J) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs or together with <t>recombinant</t> TWEAK <t>(rTWEAK).</t> The expression of Pdgfb in TCMK-1 cells was analyzed by qPCR (n = 5). (K, L) TCMK-1 cells were treated with rTWEAK or rTWEAK and an Fn14 inhibitor. The expression of Pdgfb in TCMK-1 cells was detected by qPCR (n = 5). (M) Immunoblots and quantification of IKK-β and nuclear NF-κB p65 in TCMK-1 cells treated with PBS or rTWEAK (n = 3). The results represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.
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Independent protein-level validation of candidate biomarkers in CTD-ILD and IPF. A Plasma levels of <t>TWEAK,</t> ( B ) MMP-10, and ( C ) ADA were quantified by <t>ELISA</t> in an independent validation cohort (CTD-ILD, n = 38; IPF, n = 22). Statistical significance was assessed using the Mann–Whitney U test (*** p < 0.001)
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Cell Signaling Technology Inc anti tweak
Independent protein-level validation of candidate biomarkers in CTD-ILD and IPF. A Plasma levels of <t>TWEAK,</t> ( B ) MMP-10, and ( C ) ADA were quantified by <t>ELISA</t> in an independent validation cohort (CTD-ILD, n = 38; IPF, n = 22). Statistical significance was assessed using the Mann–Whitney U test (*** p < 0.001)
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Independent protein-level validation of candidate biomarkers in CTD-ILD and IPF. A Plasma levels of <t>TWEAK,</t> ( B ) MMP-10, and ( C ) ADA were quantified by <t>ELISA</t> in an independent validation cohort (CTD-ILD, n = 38; IPF, n = 22). Statistical significance was assessed using the Mann–Whitney U test (*** p < 0.001)
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Image Search Results


Arg1 + MMP12 + macrophage-derived TWEAK licenses PDGFB production in fibroTECs via Fn14 signaling. (A) Ligand-receptor communication analysis between different cell types in IRI kidneys. (B) The major incoming signaling of different cell types. (C) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between myeloid cell subsets and TEC subsets. (D) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between TEC subsets and myeloid cell subsets. (E, F) WT/AMPKα1 −/− BMDMs were treated with IL-4 and IL-13, and the expression levels of Arg 1 , Mmp12 , and Tnfsf12 were analyzed by qPCR (n = 5). (G, H) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs. The expression of Pdgfb , Cxcl1 , and Egfr in TCMK-1 cells was analyzed by qPCR (n = 5). (I, J) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs or together with recombinant TWEAK (rTWEAK). The expression of Pdgfb in TCMK-1 cells was analyzed by qPCR (n = 5). (K, L) TCMK-1 cells were treated with rTWEAK or rTWEAK and an Fn14 inhibitor. The expression of Pdgfb in TCMK-1 cells was detected by qPCR (n = 5). (M) Immunoblots and quantification of IKK-β and nuclear NF-κB p65 in TCMK-1 cells treated with PBS or rTWEAK (n = 3). The results represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Redox Biology

Article Title: Macrophage AMPK activated by oxidative stress drives profibrotic crosstalk with tubular cells to accelerate renal fibrosis after ischemic and reperfusion injury

doi: 10.1016/j.redox.2025.104002

Figure Lengend Snippet: Arg1 + MMP12 + macrophage-derived TWEAK licenses PDGFB production in fibroTECs via Fn14 signaling. (A) Ligand-receptor communication analysis between different cell types in IRI kidneys. (B) The major incoming signaling of different cell types. (C) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between myeloid cell subsets and TEC subsets. (D) Bubble plots showing the expression of specific ligand-receptor pairs in the interaction between TEC subsets and myeloid cell subsets. (E, F) WT/AMPKα1 −/− BMDMs were treated with IL-4 and IL-13, and the expression levels of Arg 1 , Mmp12 , and Tnfsf12 were analyzed by qPCR (n = 5). (G, H) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs. The expression of Pdgfb , Cxcl1 , and Egfr in TCMK-1 cells was analyzed by qPCR (n = 5). (I, J) TCMK-1 cells were treated with CM from IL-4 and IL-13-stimulated WT/AMPKα1 −/− BMDMs or together with recombinant TWEAK (rTWEAK). The expression of Pdgfb in TCMK-1 cells was analyzed by qPCR (n = 5). (K, L) TCMK-1 cells were treated with rTWEAK or rTWEAK and an Fn14 inhibitor. The expression of Pdgfb in TCMK-1 cells was detected by qPCR (n = 5). (M) Immunoblots and quantification of IKK-β and nuclear NF-κB p65 in TCMK-1 cells treated with PBS or rTWEAK (n = 3). The results represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: To examine the role of the TWEAK-Fn14 axis, cells were treated with recombinant TWEAK (MCE, HY-P7309, 100 ng/ml) and the Fn14 inhibitor, L524-0366 (Sigma, 509374, 10 μM).

Techniques: Derivative Assay, Expressing, Recombinant, Western Blot

Independent protein-level validation of candidate biomarkers in CTD-ILD and IPF. A Plasma levels of TWEAK, ( B ) MMP-10, and ( C ) ADA were quantified by ELISA in an independent validation cohort (CTD-ILD, n = 38; IPF, n = 22). Statistical significance was assessed using the Mann–Whitney U test (*** p < 0.001)

Journal: Respiratory Research

Article Title: Plasma proteomic and machine learning models for differentiating idiopathic pulmonary fibrosis and connective tissue disease–associated interstitial lung disease: findings from a prospective cohort

doi: 10.1186/s12931-026-03596-4

Figure Lengend Snippet: Independent protein-level validation of candidate biomarkers in CTD-ILD and IPF. A Plasma levels of TWEAK, ( B ) MMP-10, and ( C ) ADA were quantified by ELISA in an independent validation cohort (CTD-ILD, n = 38; IPF, n = 22). Statistical significance was assessed using the Mann–Whitney U test (*** p < 0.001)

Article Snippet: FGF-19 concentrations were determined using the Human FGF-19 ELISA kit (DY969, R&D Systems), and TWEAK levels were quantified using the Human TWEAK ELISA kit (DY1090, R&D Systems).

Techniques: Biomarker Discovery, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY