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faz 3532  (MedChemExpress)


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    MedChemExpress faz 3532
    Faz 3532, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/faz 3532/product/MedChemExpress
    Average 94 stars, based on 4 article reviews
    faz 3532 - by Bioz Stars, 2026-02
    94/100 stars

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    (A) Quantification of the SG marker EIF4G by HCM in U2OS wildtype (WT), UBAP2L knockout (ΔUBAP2L), and G3BP1&2 double knockout (ΔΔG3BP1/2) cells treated with 4 mM LLOMe for 1 h. White masks, algorithm-defined cell boundaries; green masks, computer-identified EIF4G puncta. (B) Quantification of the stress granule (SG) marker EIF4G by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2), or treated with SG inhibitors (20 µM <t>FAZ3532/FAZ3780).</t> Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (C) Quantification of the PB marker DCP1A by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2) or treated with SG inhibitors. Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (D-G) Quantification of data shown in (B) and (C). Quantification of the SG marker EIF4G (H) and the PB marker DDX6 (I) by HCM in U2OS cells. Cells were treated with 4 mM LLOMe with or without 15 µM BAPTA-AM, or with 100 nM Bafilomycin A1(BafA1) for 1 h, followed by a 30 min recovery after washout. NT, untreated cells. Data, means ± SEM (n = 3); HCM: n ≥ 3 (each experiment: 500 valid cells per well, ≥5 wells/sample). † p ≥ 0.05 (not significant), **p < 0.01, ANOVA. See also .
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    (A) Quantification of the SG marker EIF4G by HCM in U2OS wildtype (WT), UBAP2L knockout (ΔUBAP2L), and G3BP1&2 double knockout (ΔΔG3BP1/2) cells treated with 4 mM LLOMe for 1 h. White masks, algorithm-defined cell boundaries; green masks, computer-identified EIF4G puncta. (B) Quantification of the stress granule (SG) marker EIF4G by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2), or treated with SG inhibitors (20 µM <t>FAZ3532/FAZ3780).</t> Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (C) Quantification of the PB marker DCP1A by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2) or treated with SG inhibitors. Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (D-G) Quantification of data shown in (B) and (C). Quantification of the SG marker EIF4G (H) and the PB marker DDX6 (I) by HCM in U2OS cells. Cells were treated with 4 mM LLOMe with or without 15 µM BAPTA-AM, or with 100 nM Bafilomycin A1(BafA1) for 1 h, followed by a 30 min recovery after washout. NT, untreated cells. Data, means ± SEM (n = 3); HCM: n ≥ 3 (each experiment: 500 valid cells per well, ≥5 wells/sample). † p ≥ 0.05 (not significant), **p < 0.01, ANOVA. See also .
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    (A) Quantification of the SG marker EIF4G by HCM in U2OS wildtype (WT), UBAP2L knockout (ΔUBAP2L), and G3BP1&2 double knockout (ΔΔG3BP1/2) cells treated with 4 mM LLOMe for 1 h. White masks, algorithm-defined cell boundaries; green masks, computer-identified EIF4G puncta. (B) Quantification of the stress granule (SG) marker EIF4G by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2), or treated with SG inhibitors (20 µM <t>FAZ3532/FAZ3780).</t> Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (C) Quantification of the PB marker DCP1A by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2) or treated with SG inhibitors. Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (D-G) Quantification of data shown in (B) and (C). Quantification of the SG marker EIF4G (H) and the PB marker DDX6 (I) by HCM in U2OS cells. Cells were treated with 4 mM LLOMe with or without 15 µM BAPTA-AM, or with 100 nM Bafilomycin A1(BafA1) for 1 h, followed by a 30 min recovery after washout. NT, untreated cells. Data, means ± SEM (n = 3); HCM: n ≥ 3 (each experiment: 500 valid cells per well, ≥5 wells/sample). † p ≥ 0.05 (not significant), **p < 0.01, ANOVA. See also .
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    (A) Quantification of the SG marker EIF4G by HCM in U2OS wildtype (WT), UBAP2L knockout (ΔUBAP2L), and G3BP1&2 double knockout (ΔΔG3BP1/2) cells treated with 4 mM LLOMe for 1 h. White masks, algorithm-defined cell boundaries; green masks, computer-identified EIF4G puncta. (B) Quantification of the stress granule (SG) marker EIF4G by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2), or treated with SG inhibitors (20 µM <t>FAZ3532/FAZ3780).</t> Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (C) Quantification of the PB marker DCP1A by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2) or treated with SG inhibitors. Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (D-G) Quantification of data shown in (B) and (C). Quantification of the SG marker EIF4G (H) and the PB marker DDX6 (I) by HCM in U2OS cells. Cells were treated with 4 mM LLOMe with or without 15 µM BAPTA-AM, or with 100 nM Bafilomycin A1(BafA1) for 1 h, followed by a 30 min recovery after washout. NT, untreated cells. Data, means ± SEM (n = 3); HCM: n ≥ 3 (each experiment: 500 valid cells per well, ≥5 wells/sample). † p ≥ 0.05 (not significant), **p < 0.01, ANOVA. See also .
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    (A) Quantification of the SG marker EIF4G by HCM in U2OS wildtype (WT), UBAP2L knockout (ΔUBAP2L), and G3BP1&2 double knockout (ΔΔG3BP1/2) cells treated with 4 mM LLOMe for 1 h. White masks, algorithm-defined cell boundaries; green masks, computer-identified EIF4G puncta. (B) Quantification of the stress granule (SG) marker EIF4G by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2), or treated with SG inhibitors (20 µM FAZ3532/FAZ3780). Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (C) Quantification of the PB marker DCP1A by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2) or treated with SG inhibitors. Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (D-G) Quantification of data shown in (B) and (C). Quantification of the SG marker EIF4G (H) and the PB marker DDX6 (I) by HCM in U2OS cells. Cells were treated with 4 mM LLOMe with or without 15 µM BAPTA-AM, or with 100 nM Bafilomycin A1(BafA1) for 1 h, followed by a 30 min recovery after washout. NT, untreated cells. Data, means ± SEM (n = 3); HCM: n ≥ 3 (each experiment: 500 valid cells per well, ≥5 wells/sample). † p ≥ 0.05 (not significant), **p < 0.01, ANOVA. See also .

    Journal: bioRxiv

    Article Title: Processing bodies promote lysosomal quality control and cell survival during recovery from lysosomal damage

    doi: 10.1101/2025.08.27.672666

    Figure Lengend Snippet: (A) Quantification of the SG marker EIF4G by HCM in U2OS wildtype (WT), UBAP2L knockout (ΔUBAP2L), and G3BP1&2 double knockout (ΔΔG3BP1/2) cells treated with 4 mM LLOMe for 1 h. White masks, algorithm-defined cell boundaries; green masks, computer-identified EIF4G puncta. (B) Quantification of the stress granule (SG) marker EIF4G by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2), or treated with SG inhibitors (20 µM FAZ3532/FAZ3780). Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (C) Quantification of the PB marker DCP1A by HCM in Huh7 cells transfected with either scrambled siRNA as control (CTR) or siRNA targeting G3BP1 and G3BP2 for knockdown (siG3BP1/2) or treated with SG inhibitors. Cells were treated with 4 mM LLOMe for 1 h to induce damage, or for 30 min followed by a 30 min recovery after washout. (D-G) Quantification of data shown in (B) and (C). Quantification of the SG marker EIF4G (H) and the PB marker DDX6 (I) by HCM in U2OS cells. Cells were treated with 4 mM LLOMe with or without 15 µM BAPTA-AM, or with 100 nM Bafilomycin A1(BafA1) for 1 h, followed by a 30 min recovery after washout. NT, untreated cells. Data, means ± SEM (n = 3); HCM: n ≥ 3 (each experiment: 500 valid cells per well, ≥5 wells/sample). † p ≥ 0.05 (not significant), **p < 0.01, ANOVA. See also .

    Article Snippet: Other reagents used in this study were from the following sources: Protease Inhibitor from Roche (11697498001); FAZ3532 and FAZ3780 from MedChemExpress (HY-162288 and HY-162289); BAPTA-AM from ThermoFisher (B1205); Anti-HA Magnetic Beads from ThermoFisher (88836); Bafilomycin A1 from InvivoGen.

    Techniques: Marker, Knock-Out, Double Knockout, Transfection, Control, Knockdown