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human asc protein  (MedChemExpress)


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    MedChemExpress human asc protein
    Human Asc Protein, 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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    Average 93 stars, based on 1 article reviews
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    93/100 stars

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    Figure 3. Monocytes from CMML KRASmut patients present a constitutive inflammasome activation (A) Percentage of <t>ASC-specking</t> monocytes in healthy controls (white bars), CMML patients without KRAS mutation (KRASwt, blue bars), and CMML patients with a KRAS mutation (KRASmut, orange bars) at baseline or treated as indicated for NLRP3 (LPS+ATP) or pyrin (LPS+TcdB) inflammasome activation. (B and C) Release of IL-1b from peripheral blood mononuclear cells (PBMCs) (B) and the formation of ASC specks in monocytes (C) in CMML KRASmut patients at baseline or after the indicated stimulation or treatment (LPS+ATP and LPS+TcdB for NLRP3 or pyrin inflammasome, respectively), in the absence/presence of MCC950. (B) Fold increase was calculated to control non-stimulated conditions, where the average of the higher value used to calculate fold increase is 1,066.58 pg/mL. (D) Percentage of extracellular LDH from untreated PBMCs from healthy donors (white bar), KRASwt patients (blue bar), and KRASmut patients (orange bar). Data are normalized to the percentage of monocytes. (E) Plasma concentration of HMGB1 <t>and</t> <t>P2X7</t> receptor from healthy donors (white bar), KRASwt patients (blue bar), and KRASmut patients (orange bar). For (A)–(E), data are represented as mean ± SEM; each dot represents an individual patient; ordinary one-way ANOVA test (two-tailed) was used for (A) (* compares CMML KRASmut vs. healthy controls; y compares CMML KRASmut vs. CMML KRASwt), and two-tailed t test in (B)–(E). Note that * or yp < 0.05; **p < 0.01; ***p < 0.001; **** or yyyyp < 0.0001; ns, no significant difference (p > 0.05).
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    Figure 3. Monocytes from CMML KRASmut patients present a constitutive inflammasome activation (A) Percentage of <t>ASC-specking</t> monocytes in healthy controls (white bars), CMML patients without KRAS mutation (KRASwt, blue bars), and CMML patients with a KRAS mutation (KRASmut, orange bars) at baseline or treated as indicated for NLRP3 (LPS+ATP) or pyrin (LPS+TcdB) inflammasome activation. (B and C) Release of IL-1b from peripheral blood mononuclear cells (PBMCs) (B) and the formation of ASC specks in monocytes (C) in CMML KRASmut patients at baseline or after the indicated stimulation or treatment (LPS+ATP and LPS+TcdB for NLRP3 or pyrin inflammasome, respectively), in the absence/presence of MCC950. (B) Fold increase was calculated to control non-stimulated conditions, where the average of the higher value used to calculate fold increase is 1,066.58 pg/mL. (D) Percentage of extracellular LDH from untreated PBMCs from healthy donors (white bar), KRASwt patients (blue bar), and KRASmut patients (orange bar). Data are normalized to the percentage of monocytes. (E) Plasma concentration of HMGB1 <t>and</t> <t>P2X7</t> receptor from healthy donors (white bar), KRASwt patients (blue bar), and KRASmut patients (orange bar). For (A)–(E), data are represented as mean ± SEM; each dot represents an individual patient; ordinary one-way ANOVA test (two-tailed) was used for (A) (* compares CMML KRASmut vs. healthy controls; y compares CMML KRASmut vs. CMML KRASwt), and two-tailed t test in (B)–(E). Note that * or yp < 0.05; **p < 0.01; ***p < 0.001; **** or yyyyp < 0.0001; ns, no significant difference (p > 0.05).
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    Figure 3. Monocytes from CMML KRASmut patients present a constitutive inflammasome activation (A) Percentage of ASC-specking monocytes in healthy controls (white bars), CMML patients without KRAS mutation (KRASwt, blue bars), and CMML patients with a KRAS mutation (KRASmut, orange bars) at baseline or treated as indicated for NLRP3 (LPS+ATP) or pyrin (LPS+TcdB) inflammasome activation. (B and C) Release of IL-1b from peripheral blood mononuclear cells (PBMCs) (B) and the formation of ASC specks in monocytes (C) in CMML KRASmut patients at baseline or after the indicated stimulation or treatment (LPS+ATP and LPS+TcdB for NLRP3 or pyrin inflammasome, respectively), in the absence/presence of MCC950. (B) Fold increase was calculated to control non-stimulated conditions, where the average of the higher value used to calculate fold increase is 1,066.58 pg/mL. (D) Percentage of extracellular LDH from untreated PBMCs from healthy donors (white bar), KRASwt patients (blue bar), and KRASmut patients (orange bar). Data are normalized to the percentage of monocytes. (E) Plasma concentration of HMGB1 and P2X7 receptor from healthy donors (white bar), KRASwt patients (blue bar), and KRASmut patients (orange bar). For (A)–(E), data are represented as mean ± SEM; each dot represents an individual patient; ordinary one-way ANOVA test (two-tailed) was used for (A) (* compares CMML KRASmut vs. healthy controls; y compares CMML KRASmut vs. CMML KRASwt), and two-tailed t test in (B)–(E). Note that * or yp < 0.05; **p < 0.01; ***p < 0.001; **** or yyyyp < 0.0001; ns, no significant difference (p > 0.05).

    Journal: Cell reports. Medicine

    Article Title: NLRP3 inflammasome activation and symptom burden in KRAS-mutated CMML patients is reverted by IL-1 blocking therapy.

    doi: 10.1016/j.xcrm.2023.101329

    Figure Lengend Snippet: Figure 3. Monocytes from CMML KRASmut patients present a constitutive inflammasome activation (A) Percentage of ASC-specking monocytes in healthy controls (white bars), CMML patients without KRAS mutation (KRASwt, blue bars), and CMML patients with a KRAS mutation (KRASmut, orange bars) at baseline or treated as indicated for NLRP3 (LPS+ATP) or pyrin (LPS+TcdB) inflammasome activation. (B and C) Release of IL-1b from peripheral blood mononuclear cells (PBMCs) (B) and the formation of ASC specks in monocytes (C) in CMML KRASmut patients at baseline or after the indicated stimulation or treatment (LPS+ATP and LPS+TcdB for NLRP3 or pyrin inflammasome, respectively), in the absence/presence of MCC950. (B) Fold increase was calculated to control non-stimulated conditions, where the average of the higher value used to calculate fold increase is 1,066.58 pg/mL. (D) Percentage of extracellular LDH from untreated PBMCs from healthy donors (white bar), KRASwt patients (blue bar), and KRASmut patients (orange bar). Data are normalized to the percentage of monocytes. (E) Plasma concentration of HMGB1 and P2X7 receptor from healthy donors (white bar), KRASwt patients (blue bar), and KRASmut patients (orange bar). For (A)–(E), data are represented as mean ± SEM; each dot represents an individual patient; ordinary one-way ANOVA test (two-tailed) was used for (A) (* compares CMML KRASmut vs. healthy controls; y compares CMML KRASmut vs. CMML KRASwt), and two-tailed t test in (B)–(E). Note that * or yp < 0.05; **p < 0.01; ***p < 0.001; **** or yyyyp < 0.0001; ns, no significant difference (p > 0.05).

    Article Snippet: Plasma or cell-free supernatants from fresh EDTA-anticoagulated PB samples from CMML patients and controls were used to quantify the concentration of human IL-1b (#BMS224INST, Invitrogen), human IL-18 (#7620, MBL), human IL-18BP (#EHIL18BP, Invitrogen), human TNF-a (#DTA00D, R&D Systems), human IL-6 (#D6050, R&D Systems), human ASC (#CSB-EL019114HU, Cusabio), human soluble P2X7 receptor (#CSB-EL017325HU, Cusabio), and human HMGB1 (#ARG81185, Arigo Biolaboratories) by ELISA following the manufacturer’s instructions.

    Techniques: Activation Assay, Mutagenesis, Control, Clinical Proteomics, Concentration Assay, Two Tailed Test