nod Search Results


nod in 1  (MedChemExpress)
93
MedChemExpress nod in 1
MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and <t>NOD‐IN‐1</t> (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).
Nod In 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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compound 4  (TargetMol)
93
TargetMol compound 4
MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and <t>NOD‐IN‐1</t> (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).
Compound 4, supplied by TargetMol, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nod scid mice  (Envigo)
95
Envigo nod scid mice
MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and <t>NOD‐IN‐1</t> (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).
Nod Scid Mice, supplied by Envigo, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nod scid mice  (Taconic Biosciences)
96
Taconic Biosciences nod scid mice
MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and <t>NOD‐IN‐1</t> (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).
Nod Scid Mice, supplied by Taconic Biosciences, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nod inhibitor mdk19922  (Selleck Chemicals)
93
Selleck Chemicals nod inhibitor mdk19922
MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and <t>NOD‐IN‐1</t> (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).
Nod Inhibitor Mdk19922, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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2 3 2 plasmid constructs pcdna3 1 archt bfp2 tserex  (Addgene inc)
92
Addgene inc 2 3 2 plasmid constructs pcdna3 1 archt bfp2 tserex
MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and <t>NOD‐IN‐1</t> (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).
2 3 2 Plasmid Constructs Pcdna3 1 Archt Bfp2 Tserex, supplied by Addgene inc, 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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male diabetic taconic nod mice  (Taconic Biosciences)
93
Taconic Biosciences male diabetic taconic nod mice
MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and <t>NOD‐IN‐1</t> (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).
Male Diabetic Taconic Nod Mice, supplied by Taconic Biosciences, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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old ciea nog mice  (Taconic Biosciences)
95
Taconic Biosciences old ciea nog mice
MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and <t>NOD‐IN‐1</t> (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).
Old Ciea Nog Mice, supplied by Taconic Biosciences, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human t cell tumor cell admixed xenograft model nod scid mice  (Envigo)
96
Envigo human t cell tumor cell admixed xenograft model nod scid mice
Activity of MEDI6383 using primary <t>human</t> <t>T</t> cells. Figure 3 shows the activity of MEDI6383 immobilized to tissue culture plastic or clustered by CD32A-expressing cells with OX40-expressing activated primary human T cells. (A) Schematic illustration of the bioactivity assay using plate immobilized MEDI6383. (B) IFNγ and (C) TNFα release into cell culture supernatants and (D) proliferation of cells plated under the conditions described next to each graph. Solution phase MEDI6383 indicates drug added to medium instead of captured on the plate surface, and no anti-CD3 indicates omission of anti-CD3 mAb clone OKT3 stimulation in the wells. (E) Bioactivity of MEDI6383 with OX40-expressing activated primary human CD4 T cells co-cultured with CD32A-expressing HEK293 cells and a sub-optimal amount of anti-CD3 mAb clone OKT3. No drug, no anti-CD3, and no HEK CD32A indicate bioassay conditions containing all components except MEDI6383, anti-CD3 mAb clone OKT3, or CD32A-expressing HEK293 cells, respectively. T cells only indicate the presence of CFSE-labeled CD4 T cells alone in the absence of drug, anti-CD3 mAb clone OKT3, and CD32A expressing HEK293 cells. Results for plate-immobilized or HEK CD32 clustered MEDI6383 are each representative of 3 independent experiments, with data points and error bars representing the mean and SEM of triplicate measurements, respectively. M, molarity.
Human T Cell Tumor Cell Admixed Xenograft Model Nod Scid Mice, supplied by Envigo, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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gsdmd  (Proteintech)
93
Proteintech gsdmd
Fig. <t>2.</t> <t>ETV5</t> expression was lower in ALI mouse lung tissue, whereas pyroptosis was more prevalent. (A) ETV5 mRNA levels in lung tissues. (B) ETV5 protein levels in different groups of lung tissues. (C) Relative expression of ETV5 protein in the lung of mice was detected by western blot analysis and quantified by ImageJ software. (D) ETV5 immunofluorescence staining in lung tissues. (E) NLRP3 mRNA levels in lung tissues. (F) <t>GSDMD</t> mRNA levels in lung tissues. (G) Caspase-1 mRNA levels in lung tissues. (H) Protein levels of caspase-1, NLRP3, total GSDMD, and membrane-bound GSDMD in different groups of lung tissues. Relative expression of (I) membrane-bound GSDMD, (J) NLRP3, (K) total GSDMD, and (L) Caspase-1 in the lung of mice was detected by western blot analysis and quantified by ImageJ software. m. GSDMD Immunofluorescence staining of lung tissues. n = 4 per group. Data are presented as mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ALI, acute lung injury; ATP1A1, sodium/potassium-transporting ATPase subunit alpha-1; ETV5, E-twenty-six variant gene 5; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; GSDMD, gasdermin D; LPS, lipopolysaccharide; NLRP3, NOD-, LRR- and pyrin domain protein 3; SEM, standard error of means.
Gsdmd, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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us spleen cells mhc nod mrktac h2g7 nod taconic biosciences  (Taconic Biosciences)
93
Taconic Biosciences us spleen cells mhc nod mrktac h2g7 nod taconic biosciences
Fig. <t>2.</t> <t>ETV5</t> expression was lower in ALI mouse lung tissue, whereas pyroptosis was more prevalent. (A) ETV5 mRNA levels in lung tissues. (B) ETV5 protein levels in different groups of lung tissues. (C) Relative expression of ETV5 protein in the lung of mice was detected by western blot analysis and quantified by ImageJ software. (D) ETV5 immunofluorescence staining in lung tissues. (E) NLRP3 mRNA levels in lung tissues. (F) <t>GSDMD</t> mRNA levels in lung tissues. (G) Caspase-1 mRNA levels in lung tissues. (H) Protein levels of caspase-1, NLRP3, total GSDMD, and membrane-bound GSDMD in different groups of lung tissues. Relative expression of (I) membrane-bound GSDMD, (J) NLRP3, (K) total GSDMD, and (L) Caspase-1 in the lung of mice was detected by western blot analysis and quantified by ImageJ software. m. GSDMD Immunofluorescence staining of lung tissues. n = 4 per group. Data are presented as mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ALI, acute lung injury; ATP1A1, sodium/potassium-transporting ATPase subunit alpha-1; ETV5, E-twenty-six variant gene 5; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; GSDMD, gasdermin D; LPS, lipopolysaccharide; NLRP3, NOD-, LRR- and pyrin domain protein 3; SEM, standard error of means.
Us Spleen Cells Mhc Nod Mrktac H2g7 Nod Taconic Biosciences, supplied by Taconic Biosciences, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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nlrp3 genlisa elisa  (Krishgen Biosystems)
93
Krishgen Biosystems nlrp3 genlisa elisa
Effect of BET and VCO on molecular markers. (A) <t>NLRP3</t> (B) IL-1β Data are expressed as mean ± SEM, **p < 0.01, *p < 0.05when compared with normal control, ****p < 0.0001 ***p < 0.001**p < 0.01,*p < 0.05 when compared to treatment group.
Nlrp3 Genlisa Elisa, supplied by Krishgen Biosystems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).

Journal: Advanced Science

Article Title: The NLRP11 Protein Bridges the Histone Lysine Acetyltransferase KAT7 to Acetylate Vimentin in the Early Stage of Lung Adenocarcinoma

doi: 10.1002/advs.202300971

Figure Lengend Snippet: MCC950 constricts the malignant behavior of LUAD cells with high expression of vimentin. A) The binding sites of MCC950 and NLRP11 protein were simulated using AutoDock Vina v.1.2.2 molecular docking analysis, whose low binding energy is −8.109 kcal mol −1 . B,C) The effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the expression of vimentin and vimentin‐K104Ac were detected using western blot in A549 and H1299 cells. D) Ubiquitin‐IP was used to measure the effects of DMSO, Nodinitib‐1 (5 µ m ), MCC950 (10 µ m ), CY‐09 (10 µ m ), and NOD‐IN‐1 (10 µ m ) on the ubiquitination of vimentin. E) Confocal microscopy was performed to test the impacts of MCC950 on the colocalization of KAT7 and vimentin in A549 cells overexpressing NLRP11. F) Co‐IP was performed to explain the influence of MCC950 on the combination of KAT7 and vimentin in A549 cells overexpressing NLRP11. G) Co‐IP was performed to detect the influence of MCC950 on the combination of NLRP11 and KAT7 or vimentin in A549 cells overexpressing NLRP11. H) Tumor sphere formation assays were used to estimate the sphere‐forming capability of A549 and H1299 cells treated with MCC950. I,J) Xenograft tumor assays were used to estimate the proliferation of A549 (I) and H1299 (J) cells treated with MCC950, and IHC was used to detect the expression of NLRP11 and vimentin in vivo (* P < 0.05, ** P < 0.01, *** P < 0.001).

Article Snippet: The NOD‐like inhibitors, CY‐09, MCC950, Nodinitib‐1, and NOD‐IN‐1 (MedChemExpress, NJ, USA) were used to treat the cells.

Techniques: Expressing, Binding Assay, Western Blot, Confocal Microscopy, Co-Immunoprecipitation Assay, In Vivo

Activity of MEDI6383 using primary human T cells. Figure 3 shows the activity of MEDI6383 immobilized to tissue culture plastic or clustered by CD32A-expressing cells with OX40-expressing activated primary human T cells. (A) Schematic illustration of the bioactivity assay using plate immobilized MEDI6383. (B) IFNγ and (C) TNFα release into cell culture supernatants and (D) proliferation of cells plated under the conditions described next to each graph. Solution phase MEDI6383 indicates drug added to medium instead of captured on the plate surface, and no anti-CD3 indicates omission of anti-CD3 mAb clone OKT3 stimulation in the wells. (E) Bioactivity of MEDI6383 with OX40-expressing activated primary human CD4 T cells co-cultured with CD32A-expressing HEK293 cells and a sub-optimal amount of anti-CD3 mAb clone OKT3. No drug, no anti-CD3, and no HEK CD32A indicate bioassay conditions containing all components except MEDI6383, anti-CD3 mAb clone OKT3, or CD32A-expressing HEK293 cells, respectively. T cells only indicate the presence of CFSE-labeled CD4 T cells alone in the absence of drug, anti-CD3 mAb clone OKT3, and CD32A expressing HEK293 cells. Results for plate-immobilized or HEK CD32 clustered MEDI6383 are each representative of 3 independent experiments, with data points and error bars representing the mean and SEM of triplicate measurements, respectively. M, molarity.

Journal: Molecular cancer therapeutics

Article Title: Potent Immune Modulation by MEDI6383, an Engineered Human OX40 Ligand IgG4P Fc Fusion Protein

doi: 10.1158/1535-7163.MCT-17-0200

Figure Lengend Snippet: Activity of MEDI6383 using primary human T cells. Figure 3 shows the activity of MEDI6383 immobilized to tissue culture plastic or clustered by CD32A-expressing cells with OX40-expressing activated primary human T cells. (A) Schematic illustration of the bioactivity assay using plate immobilized MEDI6383. (B) IFNγ and (C) TNFα release into cell culture supernatants and (D) proliferation of cells plated under the conditions described next to each graph. Solution phase MEDI6383 indicates drug added to medium instead of captured on the plate surface, and no anti-CD3 indicates omission of anti-CD3 mAb clone OKT3 stimulation in the wells. (E) Bioactivity of MEDI6383 with OX40-expressing activated primary human CD4 T cells co-cultured with CD32A-expressing HEK293 cells and a sub-optimal amount of anti-CD3 mAb clone OKT3. No drug, no anti-CD3, and no HEK CD32A indicate bioassay conditions containing all components except MEDI6383, anti-CD3 mAb clone OKT3, or CD32A-expressing HEK293 cells, respectively. T cells only indicate the presence of CFSE-labeled CD4 T cells alone in the absence of drug, anti-CD3 mAb clone OKT3, and CD32A expressing HEK293 cells. Results for plate-immobilized or HEK CD32 clustered MEDI6383 are each representative of 3 independent experiments, with data points and error bars representing the mean and SEM of triplicate measurements, respectively. M, molarity.

Article Snippet: Human T cell/tumor cell admixed xenograft model NOD/SCID mice of 5-9 weeks of age were purchased from Envigo Harlan Laboratories, Inc. (Indianapolis, IN).

Techniques: Activity Assay, Expressing, Cell Culture, Labeling

Anti-tumor activity of MEDI6383. Figure 5 demonstrates the T cell dependent activity of MEDI6383 in a human T cell/tumor cell admixed model in NOD/SCID mice. (A) Statistically significant tumor growth inhibition by MEDI6383 administered over a range of dose levels in mice engrafted with human A375 melanoma tumor cells admixed with allogeneic A375-reactive human CD4 and CD8 T cells. (B) Lack of MEDI6383 activity in mice engrafted with A375 tumor cells but in the absence of human T cells. (C) Activity of MEDI6383 when allogeneic A375-reactive human T cells were engrafted with A375 tumor cells. *, p<0.05 by Mann-Whitney rank sum test of mean tumor size at day 28 for MEDI6383 treated groups compared to isotype control group. Arrows indicate times after tumor injection when MEDI6383 was administered to mice. Statistically significant differences in mean tumor size between MEDI6383 and isotype control group was demonstrated in three independent experiments, with representative data shown.

Journal: Molecular cancer therapeutics

Article Title: Potent Immune Modulation by MEDI6383, an Engineered Human OX40 Ligand IgG4P Fc Fusion Protein

doi: 10.1158/1535-7163.MCT-17-0200

Figure Lengend Snippet: Anti-tumor activity of MEDI6383. Figure 5 demonstrates the T cell dependent activity of MEDI6383 in a human T cell/tumor cell admixed model in NOD/SCID mice. (A) Statistically significant tumor growth inhibition by MEDI6383 administered over a range of dose levels in mice engrafted with human A375 melanoma tumor cells admixed with allogeneic A375-reactive human CD4 and CD8 T cells. (B) Lack of MEDI6383 activity in mice engrafted with A375 tumor cells but in the absence of human T cells. (C) Activity of MEDI6383 when allogeneic A375-reactive human T cells were engrafted with A375 tumor cells. *, p<0.05 by Mann-Whitney rank sum test of mean tumor size at day 28 for MEDI6383 treated groups compared to isotype control group. Arrows indicate times after tumor injection when MEDI6383 was administered to mice. Statistically significant differences in mean tumor size between MEDI6383 and isotype control group was demonstrated in three independent experiments, with representative data shown.

Article Snippet: Human T cell/tumor cell admixed xenograft model NOD/SCID mice of 5-9 weeks of age were purchased from Envigo Harlan Laboratories, Inc. (Indianapolis, IN).

Techniques: Activity Assay, Inhibition, MANN-WHITNEY, Injection

Fig. 2. ETV5 expression was lower in ALI mouse lung tissue, whereas pyroptosis was more prevalent. (A) ETV5 mRNA levels in lung tissues. (B) ETV5 protein levels in different groups of lung tissues. (C) Relative expression of ETV5 protein in the lung of mice was detected by western blot analysis and quantified by ImageJ software. (D) ETV5 immunofluorescence staining in lung tissues. (E) NLRP3 mRNA levels in lung tissues. (F) GSDMD mRNA levels in lung tissues. (G) Caspase-1 mRNA levels in lung tissues. (H) Protein levels of caspase-1, NLRP3, total GSDMD, and membrane-bound GSDMD in different groups of lung tissues. Relative expression of (I) membrane-bound GSDMD, (J) NLRP3, (K) total GSDMD, and (L) Caspase-1 in the lung of mice was detected by western blot analysis and quantified by ImageJ software. m. GSDMD Immunofluorescence staining of lung tissues. n = 4 per group. Data are presented as mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ALI, acute lung injury; ATP1A1, sodium/potassium-transporting ATPase subunit alpha-1; ETV5, E-twenty-six variant gene 5; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; GSDMD, gasdermin D; LPS, lipopolysaccharide; NLRP3, NOD-, LRR- and pyrin domain protein 3; SEM, standard error of means.

Journal: Respiratory physiology & neurobiology

Article Title: Pyroptosis inhibition alleviates acute lung injury via E-twenty-six variant gene 5-mediated downregulation of gasdermin D.

doi: 10.1016/j.resp.2024.104346

Figure Lengend Snippet: Fig. 2. ETV5 expression was lower in ALI mouse lung tissue, whereas pyroptosis was more prevalent. (A) ETV5 mRNA levels in lung tissues. (B) ETV5 protein levels in different groups of lung tissues. (C) Relative expression of ETV5 protein in the lung of mice was detected by western blot analysis and quantified by ImageJ software. (D) ETV5 immunofluorescence staining in lung tissues. (E) NLRP3 mRNA levels in lung tissues. (F) GSDMD mRNA levels in lung tissues. (G) Caspase-1 mRNA levels in lung tissues. (H) Protein levels of caspase-1, NLRP3, total GSDMD, and membrane-bound GSDMD in different groups of lung tissues. Relative expression of (I) membrane-bound GSDMD, (J) NLRP3, (K) total GSDMD, and (L) Caspase-1 in the lung of mice was detected by western blot analysis and quantified by ImageJ software. m. GSDMD Immunofluorescence staining of lung tissues. n = 4 per group. Data are presented as mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ALI, acute lung injury; ATP1A1, sodium/potassium-transporting ATPase subunit alpha-1; ETV5, E-twenty-six variant gene 5; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; GSDMD, gasdermin D; LPS, lipopolysaccharide; NLRP3, NOD-, LRR- and pyrin domain protein 3; SEM, standard error of means.

Article Snippet: Polyclonal primary antibodies used for the western blot included anti- ETV5 (13011–1-AP, 1:1000; Proteintech), GSDMD (20770–1-AP, 1:1000; Proteintech), NOD, LRR- and pyrin domain protein 3 ([NLRP3]; 27458–1-AP, 1:1000; Proteintech), caspase-1/p20/p10 (22915–1-AP, 1:1000; Proteintech), lamin B (HY-P80205, 1:1000; MedChemExpress, Shanghai, China), β-actin (8H10D10, 1:1000; Cell Signaling Technology, Shanghai, China), and sodium/potassium-transporting ATPase subunit alpha-1 ([ATP1A1]; PAB17289, 1:1000; Abnova, Taiwan, China) antibodies.

Techniques: Expressing, Western Blot, Software, Immunofluorescence, Staining, Membrane, Control, Variant Assay

Fig. 3. The GSDMD gene is a putative downstream target of ETV5 in lung bronchial epithelial cells. The ETV5 motif (A) and ETV5 binding site on the GSDMD promoter (B). (C) ETV5 binding to the GSDMD promoter prediction and test using the luciferase reporter gene. (D) Results of protein-protein docking of ETV5 and GSDMD. (E) ETV5 mRNA level in BEAS-2B cells. (F) GSDMD mRNA levels in BEAS-2B cells. (G) NLRP3 mRNA levels in BEAS-2B cells. (H) Caspase-1 mRNA levels in BEAS-2B cells. (I) Protein levels of ETV5, caspase-1, NLRP3, total GSDMD, and membrane-bound GSDMD in different groups of BEAS-2B cells. Relative expression of (J) membrane-bound GSDMD, (K) NLRP3, (L) ETV5, (M) total GSDMD, and (N) caspase-1 in BEAS-2B cells was detected by western blot analysis and quantified by ImageJ software. (O) IL-6 mRNA levels in BEAS-2B cells. (P) TNF-α mRNA levels in BEAS-2B cells. (Q) IL-1β mRNA levels in BEAS-2B cells. (R) IL-6 protein con centrations in BEAS-2B cell culture supernatants. (S) TNF-α concentrations in BEAS-2B cell culture supernatants. (T) IL-1β concentrations in BEAS-2B cell culture supernatants. n = 4 per group. Data are presented as mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ATP1A1, sodium/ potassium-transporting ATPase subunit alpha-1; ETV5, E-twenty-six variant gene 5; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; GSDMD, gasdermin D; IL, interleukin; NLRP3, NOD-, LRR- and pyrin domain protein 3; SEM, standard error of means; TNF-α, tumor necrosis factor – alpha.

Journal: Respiratory physiology & neurobiology

Article Title: Pyroptosis inhibition alleviates acute lung injury via E-twenty-six variant gene 5-mediated downregulation of gasdermin D.

doi: 10.1016/j.resp.2024.104346

Figure Lengend Snippet: Fig. 3. The GSDMD gene is a putative downstream target of ETV5 in lung bronchial epithelial cells. The ETV5 motif (A) and ETV5 binding site on the GSDMD promoter (B). (C) ETV5 binding to the GSDMD promoter prediction and test using the luciferase reporter gene. (D) Results of protein-protein docking of ETV5 and GSDMD. (E) ETV5 mRNA level in BEAS-2B cells. (F) GSDMD mRNA levels in BEAS-2B cells. (G) NLRP3 mRNA levels in BEAS-2B cells. (H) Caspase-1 mRNA levels in BEAS-2B cells. (I) Protein levels of ETV5, caspase-1, NLRP3, total GSDMD, and membrane-bound GSDMD in different groups of BEAS-2B cells. Relative expression of (J) membrane-bound GSDMD, (K) NLRP3, (L) ETV5, (M) total GSDMD, and (N) caspase-1 in BEAS-2B cells was detected by western blot analysis and quantified by ImageJ software. (O) IL-6 mRNA levels in BEAS-2B cells. (P) TNF-α mRNA levels in BEAS-2B cells. (Q) IL-1β mRNA levels in BEAS-2B cells. (R) IL-6 protein con centrations in BEAS-2B cell culture supernatants. (S) TNF-α concentrations in BEAS-2B cell culture supernatants. (T) IL-1β concentrations in BEAS-2B cell culture supernatants. n = 4 per group. Data are presented as mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ATP1A1, sodium/ potassium-transporting ATPase subunit alpha-1; ETV5, E-twenty-six variant gene 5; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; GSDMD, gasdermin D; IL, interleukin; NLRP3, NOD-, LRR- and pyrin domain protein 3; SEM, standard error of means; TNF-α, tumor necrosis factor – alpha.

Article Snippet: Polyclonal primary antibodies used for the western blot included anti- ETV5 (13011–1-AP, 1:1000; Proteintech), GSDMD (20770–1-AP, 1:1000; Proteintech), NOD, LRR- and pyrin domain protein 3 ([NLRP3]; 27458–1-AP, 1:1000; Proteintech), caspase-1/p20/p10 (22915–1-AP, 1:1000; Proteintech), lamin B (HY-P80205, 1:1000; MedChemExpress, Shanghai, China), β-actin (8H10D10, 1:1000; Cell Signaling Technology, Shanghai, China), and sodium/potassium-transporting ATPase subunit alpha-1 ([ATP1A1]; PAB17289, 1:1000; Abnova, Taiwan, China) antibodies.

Techniques: Binding Assay, Luciferase, Membrane, Expressing, Western Blot, Software, Cell Culture, Control, Variant Assay

Fig. 4. By inhibiting GSDMD expression, ETV5 reduces inflammation in bronchial epithelial cells. (A) ETV5 mRNA levels in BEAS-2B cells. (B) NLRP3 mRNA levels in BEAS-2B cells. (C) GSDMD mRNA levels in BEAS-2B cells. (D) Caspase-1 mRNA levels in BEAS-2B cells. (E) Protein levels of caspase-1, NLRP3, total GSDMD, and membrane-bound GSDMD in different groups of BEAS-2B cells. Relative expression of (F) membrane-bound GSDMD, (G) NLRP3, (H) total GSDMD, and (I) caspase-1 in BEAS-2B cells was detected by western blot analysis and quantified by ImageJ software. (J) IL-6 mRNA levels in BEAS-2B cells. (K) TNF-α mRNA levels in BEAS-2B cells. (L) IL-1β mRNA levels in BEAS-2B cells. (M) IL-6 levels in BEAS-2B cell culture supernatants (N) TNF-α concentrations in BEAS-2B cell culture su pernatants. (O) IL-1β levels in BEAS-2B cell culture supernatants. n = 4 per group. Data are presented as the mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ATP1A1, sodium/potassium-transporting ATPase subunit alpha-1; ETV5, E-twenty-six variant gene 5; GAPDH, glyceraldehyde 3- phosphate dehydrogenase; GSDMD, gasdermin D; IL, interleukin; LPS, lipopolysaccharide; NLRP3, NOD-, LRR- and pyrin domain protein 3; SEM, standard error of means; TNF-α, tumor necrosis factor – alpha.

Journal: Respiratory physiology & neurobiology

Article Title: Pyroptosis inhibition alleviates acute lung injury via E-twenty-six variant gene 5-mediated downregulation of gasdermin D.

doi: 10.1016/j.resp.2024.104346

Figure Lengend Snippet: Fig. 4. By inhibiting GSDMD expression, ETV5 reduces inflammation in bronchial epithelial cells. (A) ETV5 mRNA levels in BEAS-2B cells. (B) NLRP3 mRNA levels in BEAS-2B cells. (C) GSDMD mRNA levels in BEAS-2B cells. (D) Caspase-1 mRNA levels in BEAS-2B cells. (E) Protein levels of caspase-1, NLRP3, total GSDMD, and membrane-bound GSDMD in different groups of BEAS-2B cells. Relative expression of (F) membrane-bound GSDMD, (G) NLRP3, (H) total GSDMD, and (I) caspase-1 in BEAS-2B cells was detected by western blot analysis and quantified by ImageJ software. (J) IL-6 mRNA levels in BEAS-2B cells. (K) TNF-α mRNA levels in BEAS-2B cells. (L) IL-1β mRNA levels in BEAS-2B cells. (M) IL-6 levels in BEAS-2B cell culture supernatants (N) TNF-α concentrations in BEAS-2B cell culture su pernatants. (O) IL-1β levels in BEAS-2B cell culture supernatants. n = 4 per group. Data are presented as the mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ATP1A1, sodium/potassium-transporting ATPase subunit alpha-1; ETV5, E-twenty-six variant gene 5; GAPDH, glyceraldehyde 3- phosphate dehydrogenase; GSDMD, gasdermin D; IL, interleukin; LPS, lipopolysaccharide; NLRP3, NOD-, LRR- and pyrin domain protein 3; SEM, standard error of means; TNF-α, tumor necrosis factor – alpha.

Article Snippet: Polyclonal primary antibodies used for the western blot included anti- ETV5 (13011–1-AP, 1:1000; Proteintech), GSDMD (20770–1-AP, 1:1000; Proteintech), NOD, LRR- and pyrin domain protein 3 ([NLRP3]; 27458–1-AP, 1:1000; Proteintech), caspase-1/p20/p10 (22915–1-AP, 1:1000; Proteintech), lamin B (HY-P80205, 1:1000; MedChemExpress, Shanghai, China), β-actin (8H10D10, 1:1000; Cell Signaling Technology, Shanghai, China), and sodium/potassium-transporting ATPase subunit alpha-1 ([ATP1A1]; PAB17289, 1:1000; Abnova, Taiwan, China) antibodies.

Techniques: Expressing, Membrane, Western Blot, Software, Cell Culture, Control, Variant Assay

Fig. 5. Effects of GSDMD silencing on ETV5. (A) ETV5 mRNA levels in BEAS-2B cells. (B) GSDMD mRNA levels in BEAS-2B cells. (C-E) ETV5 and total GSDMD protein levels in BEAS-2B cells; the bar graph represents the quantification of gray value (D and E). (F) ETV5 mRNA levels in MBEC cells. (G) GSDMD mRNA levels in MBEC cells. (H) ETV5 and total GSDMD protein levels in MBEC cells; the bar graph represents the quantification of gray value (I and J). n = 4 per group. Data are presented as the mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ETV5, E-twenty-six variant gene 5; GSDMD, gasdermin D; SEM, standard error of means.

Journal: Respiratory physiology & neurobiology

Article Title: Pyroptosis inhibition alleviates acute lung injury via E-twenty-six variant gene 5-mediated downregulation of gasdermin D.

doi: 10.1016/j.resp.2024.104346

Figure Lengend Snippet: Fig. 5. Effects of GSDMD silencing on ETV5. (A) ETV5 mRNA levels in BEAS-2B cells. (B) GSDMD mRNA levels in BEAS-2B cells. (C-E) ETV5 and total GSDMD protein levels in BEAS-2B cells; the bar graph represents the quantification of gray value (D and E). (F) ETV5 mRNA levels in MBEC cells. (G) GSDMD mRNA levels in MBEC cells. (H) ETV5 and total GSDMD protein levels in MBEC cells; the bar graph represents the quantification of gray value (I and J). n = 4 per group. Data are presented as the mean and SEM values. **, P<0.01 and ***, P<0.001 vs. control; unpaired Student’s t-test. ETV5, E-twenty-six variant gene 5; GSDMD, gasdermin D; SEM, standard error of means.

Article Snippet: Polyclonal primary antibodies used for the western blot included anti- ETV5 (13011–1-AP, 1:1000; Proteintech), GSDMD (20770–1-AP, 1:1000; Proteintech), NOD, LRR- and pyrin domain protein 3 ([NLRP3]; 27458–1-AP, 1:1000; Proteintech), caspase-1/p20/p10 (22915–1-AP, 1:1000; Proteintech), lamin B (HY-P80205, 1:1000; MedChemExpress, Shanghai, China), β-actin (8H10D10, 1:1000; Cell Signaling Technology, Shanghai, China), and sodium/potassium-transporting ATPase subunit alpha-1 ([ATP1A1]; PAB17289, 1:1000; Abnova, Taiwan, China) antibodies.

Techniques: Control, Variant Assay

Effect of BET and VCO on molecular markers. (A) NLRP3 (B) IL-1β Data are expressed as mean ± SEM, **p < 0.01, *p < 0.05when compared with normal control, ****p < 0.0001 ***p < 0.001**p < 0.01,*p < 0.05 when compared to treatment group.

Journal: Journal of Traditional and Complementary Medicine

Article Title: Betanin combined with virgin coconut oil inhibits neuroinflammation in aluminum chloride-induced toxicity in rats by regulating NLRP3 inflammasome

doi: 10.1016/j.jtcme.2023.11.001

Figure Lengend Snippet: Effect of BET and VCO on molecular markers. (A) NLRP3 (B) IL-1β Data are expressed as mean ± SEM, **p < 0.01, *p < 0.05when compared with normal control, ****p < 0.0001 ***p < 0.001**p < 0.01,*p < 0.05 when compared to treatment group.

Article Snippet: To determine NLRP3, a commercially available Rat Nod-like Receptor Pyrin-3, NLRP3 GENLISA™ ELISA (Krishgen Biosystems, India), was used per the manufacturer's instructions.

Techniques: Control

BET combined with VCO prevents neuroinflammation by inhibiting NLRP3 inflammasome activation in microglia.

Journal: Journal of Traditional and Complementary Medicine

Article Title: Betanin combined with virgin coconut oil inhibits neuroinflammation in aluminum chloride-induced toxicity in rats by regulating NLRP3 inflammasome

doi: 10.1016/j.jtcme.2023.11.001

Figure Lengend Snippet: BET combined with VCO prevents neuroinflammation by inhibiting NLRP3 inflammasome activation in microglia.

Article Snippet: To determine NLRP3, a commercially available Rat Nod-like Receptor Pyrin-3, NLRP3 GENLISA™ ELISA (Krishgen Biosystems, India), was used per the manufacturer's instructions.

Techniques: Activation Assay