cell death Search Results


cidea  (ProSci Incorporated)
94
ProSci Incorporated cidea
Cidea, supplied by ProSci Incorporated, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ripk1  (Proteintech)
96
Proteintech ripk1
Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of <t>RIPK1,</t> RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.
Ripk1, supplied by Proteintech, 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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bim  (ProSci Incorporated)
90
ProSci Incorporated bim
Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of <t>RIPK1,</t> RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.
Bim, supplied by ProSci Incorporated, 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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rabbit anti alpha synuclein antibody mjfr1 abcam 138501 recombinant proteins respiratory syncytial virus fusion  (Bio X Cell)
92
Bio X Cell rabbit anti alpha synuclein antibody mjfr1 abcam 138501 recombinant proteins respiratory syncytial virus fusion
Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of <t>RIPK1,</t> RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.
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alg2 pdcd6  (Proteintech)
94
Proteintech alg2 pdcd6
Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of <t>RIPK1,</t> RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.
Alg2 Pdcd6, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p re ss  (Proteintech)
93
Proteintech p re ss
Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of <t>RIPK1,</t> RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.
P Re Ss, 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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cell death protein 1 pd 1  (Revvity)
91
Revvity cell death protein 1 pd 1
Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of <t>RIPK1,</t> RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.
Cell Death Protein 1 Pd 1, supplied by Revvity, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pd l1 detection kit  (Elabscience Biotechnology)
94
Elabscience Biotechnology pd l1 detection kit
Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of <t>RIPK1,</t> RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.
Pd L1 Detection Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pd 1 mutant  (Rockland Immunochemicals)
92
Rockland Immunochemicals pd 1 mutant
Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of <t>RIPK1,</t> RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.
Pd 1 Mutant, supplied by Rockland Immunochemicals, 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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ripk1  (Rockland Immunochemicals)
93
Rockland Immunochemicals ripk1
Figure 5 Wogonin fails to further reduce cisplatin-induced cell injury and inflammatory response in HK2 cells where <t>RIPK1</t> is blocked. (a) Western blot analysis and quantitative data of RIPK1/RIPK3/MLKL signaling in Nec-1-treated HK2 cells. (b) Western blot analysis and quantitative data of KIM-1. Results indicated that when RIPK1 was blocked, wogonin failed to further suppress the protein levels of KIM-1. (c) Real-time PCR showed that when RIPK1 was blocked, wogonin failed to further decrease IL-6 in mRNA level. Independent experiments were performed throughout the in vitro studies in triplicate or quadruplicate. *Po0.05, **Po0.01, ***Po0.001 compared with the control. ##Po0.01, ###Po0.001 compared with cisplatin-treated group. $$Po0.01, $$
Ripk1, supplied by Rockland Immunochemicals, 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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recombinant human flt3l fc  (Bio X Cell)
93
Bio X Cell recombinant human flt3l fc
Figure 5 Wogonin fails to further reduce cisplatin-induced cell injury and inflammatory response in HK2 cells where <t>RIPK1</t> is blocked. (a) Western blot analysis and quantitative data of RIPK1/RIPK3/MLKL signaling in Nec-1-treated HK2 cells. (b) Western blot analysis and quantitative data of KIM-1. Results indicated that when RIPK1 was blocked, wogonin failed to further suppress the protein levels of KIM-1. (c) Real-time PCR showed that when RIPK1 was blocked, wogonin failed to further decrease IL-6 in mRNA level. Independent experiments were performed throughout the in vitro studies in triplicate or quadruplicate. *Po0.05, **Po0.01, ***Po0.001 compared with the control. ##Po0.01, ###Po0.001 compared with cisplatin-treated group. $$Po0.01, $$
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anti mouse pd1 inhibitor antibody pd1i  (Bio X Cell)
94
Bio X Cell anti mouse pd1 inhibitor antibody pd1i
Fig. 3 The effect of different treatments on B16F10 tumor growth in mice. Significant tumor growth retardations (34–49%) were observed in the mice treated with effector cells armed with the nine-antibody cocktail and <t>PD1i,</t> as compared to PBS control group. Two-way ANOVA analysis of the data shows significantly differ- ent curves by treatment and time. *Significantly different (P ≤ 0.05) in comparison to PBS and PD1i alone groups as determined by Tukey’s multiple comparisons test. The values represent the mean ± SEM of six mice in each group. EC effector cells, EC armed with Ab Cocktail Effector cells armed with a cocktail of all the nine rabbit antibodies against selected mutated peptides, TCT tumor cell transplantation, T1– T5 EC treatment days, DPI days post-implantation
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Image Search Results


Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of RIPK1, RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: International Journal of Biological Sciences

Article Title: Curcumol Induces Necroptosis of Hepatic Stellate Cells by Targeting KAT8 to Suppress HK2 Lactylation and Promote HUWE1-Dependent Ubiquitination

doi: 10.7150/ijbs.125009

Figure Lengend Snippet: Curcumol induces HSC necroptosis. A. LX2 cells were treated with different concentrations of Curcumol (0-80 μM) for 24 h, and cell viability was assessed to determine the optimal intervention concentration (n = 5). B-C. Cell viability was measured in LX2 cells, human normal liver cells Thle-2, and mouse normal liver cells AML12 after treatment with Curcumol (0-45 μM) for 24 h (CCK-8 assay, n = 5). D. LX2 cells were treated with or without Curcumol (30 μM) and the necrotic necroptosis inhibitor Nec-1 (50 μM) for 24 h, and the ultrastructure of the cells was observed using a transmission electron microscope; the right image is an enlarged view of the area framed in the left image (scale bar: 5 μm). E. Under the same treatment conditions, the proportion of necroptotic cells was detected by flow cytometry, and the results were quantitatively analyzed (n = 3). F-G. Detection of LDH release levels in LX2 cells treated with different concentrations of Curcumol (0-45 μM) for 24 h (n = 5); simultaneous comparison of the effects of Nec-1 (50 μM) treatment on Curcumol (30 μM)-induced LDH release, with quantitative analysis (n = 3-5). H. Western blot was used to detect the expression levels of RIPK1, RIPK3, MLKL, and their phosphorylated proteins (p-RIPK1, p-RIPK3, p-MLKL) in LX2 cells after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). I. Co-IP assay to detect the interaction between RIPK1 and RIPK3 in LX2 cells after treatment with Curcumol (30 μM) for 24 h. J. Immunofluorescence assay to detect the expression of Collagen I and α-SMA in LX2 cells after treatment with Curcumol (30 μM) for 24 h (n = 3; scale bar: 10 μm). K-L. Western blotting was used to detect the protein levels of Collagen I and α-SMA in LX2 cells and mouse primary HSCs after 24 h of treatment with different concentrations of Curcumol (0-45 μM), and quantitative analysis was performed using grayscale analysis (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: The antibodies employed in this study include: RIPK1 (17519-1-AP), RIPK3 (17563-1-AP), P-RIPK1 (66854-1-Ig), MLKL (21066-1-AP), P-MLKL (82090-2-RR), HK2 (22029-1-AP), PKM2 (15822-1-AP), LDHA (19987-1-AP), PFKM (55028-1-AP), HUWE1 (19430-1-AP), Ubiquitin (10201-2-AP), HA (51064-2-AP), His (66005-1-Ig), EP300 (20695-1-AP) and P62 (18420-1-AP) from proteintech; KAT8 (sc-271691) from Santa Cruz Biotechnology; KAT6A from Bioswamp; Collagen I (ab26003), β-actin (ab8226), Tubulin (Ab721), anti-mouse IgG (ab190475), anti-rabbit IgG (ab288151) and LC3B (ab192890) from Abcam; Pan-Kla (AB_2868521) from PTM-Bio laboratory; KAT6B(A17116), P-RIPK3(AP1260), AARS(A15017), and AARS2 (A7826) from Abclonal.

Techniques: Concentration Assay, CCK-8 Assay, Transmission Assay, Microscopy, Flow Cytometry, Comparison, Western Blot, Expressing, Co-Immunoprecipitation Assay, Immunofluorescence

Curcumol induces HSCs necroptosis by suppressing HK2-mediated ubiquitination of RIPK1. A. Transmission electron microscopy images of LX2 cells treated with Curcumol (30 μM) for 24 h in the presence or absence of 2-DG (5 mM) (right: magnified region; scale bar: 5 μm). B, E. Western blot analysis of RIPK1, RIPK3, p-RIPK1, and p-RIPK3 expression in LX2 cells treated with Curcumol (30 μM) and 2-DG (5 mM) for 24 h, with densitometric quantification (n = 3). C, F. Western blot analysis of RIPK1, RIPK3, p-RIPK1, and p-RIPK3 expression in LX2 cells transfected with HK2 overexpression plasmid and treated with Curcumol (30 μM) for 24 h, with densitometric quantification (n = 3). D. Co-immunoprecipitation (Co-IP) analysis of RIPK1-RIPK3 interaction in LX2 cells transfected with HK2 overexpression plasmid and treated with Curcumol (30 μM) plus 2-DG (5 mM) for 24 h. G. Western blot analysis of RIPK1 expression in HK2 siRNA-transfected HK2-overexpressing LX2 cells, with densitometric quantification (n = 3). H. Immunofluorescence staining showing colocalization of HK2 and RIPK1 in LX2 cells treated with Curcumol (30 μM) for 24 h (n = 3; scale bar: 2.5 μm). I. RT-qPCR analysis of RIPK1 mRNA expression in LX2 cells treated with increasing concentrations of Curcumol (0-45 μM) for 24 h (n = 5). J. Immunoprecipitation analysis of RIPK1 ubiquitination in LX2 cells transfected with HK2 overexpression plasmid and treated with Curcumol (30 μM) for 24 h (n = 3). K. Western blot analysis of RIPK1 protein stability in LX2 cells treated with Curcumol (30 μM), cycloheximide (CHX, 20 μg/mL) for 24 h in the presence or absence of protein synthesis inhibitor, with quantification of half-life (n = 3). L. Western blot analysis of RIPK1 protein expression in LX2 cells treated with Curcumol (30 μM), cycloheximide (CHX, 20 μg/mL), proteasome inhibitor MG132 (10 μM), alone or in combination, with quantification (n = 3). M,N. Western blot analysis of RIPK1 protein levels in LX2 cells co-transfected with HK2 siRNA and HK2 overexpression plasmid, followed by Curcumol (30 μM) treatment for 24 h, with quantification (n = 3). O. Western blot analysis of RIPK1 expression in LX2 cells transfected with HK2 overexpression plasmid and treated with autophagy inhibitor chloroquine (CQ, 20 μg/mL), MG132 (10 μM), alone or in combination, for 24 h, with quantification (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: International Journal of Biological Sciences

Article Title: Curcumol Induces Necroptosis of Hepatic Stellate Cells by Targeting KAT8 to Suppress HK2 Lactylation and Promote HUWE1-Dependent Ubiquitination

doi: 10.7150/ijbs.125009

Figure Lengend Snippet: Curcumol induces HSCs necroptosis by suppressing HK2-mediated ubiquitination of RIPK1. A. Transmission electron microscopy images of LX2 cells treated with Curcumol (30 μM) for 24 h in the presence or absence of 2-DG (5 mM) (right: magnified region; scale bar: 5 μm). B, E. Western blot analysis of RIPK1, RIPK3, p-RIPK1, and p-RIPK3 expression in LX2 cells treated with Curcumol (30 μM) and 2-DG (5 mM) for 24 h, with densitometric quantification (n = 3). C, F. Western blot analysis of RIPK1, RIPK3, p-RIPK1, and p-RIPK3 expression in LX2 cells transfected with HK2 overexpression plasmid and treated with Curcumol (30 μM) for 24 h, with densitometric quantification (n = 3). D. Co-immunoprecipitation (Co-IP) analysis of RIPK1-RIPK3 interaction in LX2 cells transfected with HK2 overexpression plasmid and treated with Curcumol (30 μM) plus 2-DG (5 mM) for 24 h. G. Western blot analysis of RIPK1 expression in HK2 siRNA-transfected HK2-overexpressing LX2 cells, with densitometric quantification (n = 3). H. Immunofluorescence staining showing colocalization of HK2 and RIPK1 in LX2 cells treated with Curcumol (30 μM) for 24 h (n = 3; scale bar: 2.5 μm). I. RT-qPCR analysis of RIPK1 mRNA expression in LX2 cells treated with increasing concentrations of Curcumol (0-45 μM) for 24 h (n = 5). J. Immunoprecipitation analysis of RIPK1 ubiquitination in LX2 cells transfected with HK2 overexpression plasmid and treated with Curcumol (30 μM) for 24 h (n = 3). K. Western blot analysis of RIPK1 protein stability in LX2 cells treated with Curcumol (30 μM), cycloheximide (CHX, 20 μg/mL) for 24 h in the presence or absence of protein synthesis inhibitor, with quantification of half-life (n = 3). L. Western blot analysis of RIPK1 protein expression in LX2 cells treated with Curcumol (30 μM), cycloheximide (CHX, 20 μg/mL), proteasome inhibitor MG132 (10 μM), alone or in combination, with quantification (n = 3). M,N. Western blot analysis of RIPK1 protein levels in LX2 cells co-transfected with HK2 siRNA and HK2 overexpression plasmid, followed by Curcumol (30 μM) treatment for 24 h, with quantification (n = 3). O. Western blot analysis of RIPK1 expression in LX2 cells transfected with HK2 overexpression plasmid and treated with autophagy inhibitor chloroquine (CQ, 20 μg/mL), MG132 (10 μM), alone or in combination, for 24 h, with quantification (n = 3). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: The antibodies employed in this study include: RIPK1 (17519-1-AP), RIPK3 (17563-1-AP), P-RIPK1 (66854-1-Ig), MLKL (21066-1-AP), P-MLKL (82090-2-RR), HK2 (22029-1-AP), PKM2 (15822-1-AP), LDHA (19987-1-AP), PFKM (55028-1-AP), HUWE1 (19430-1-AP), Ubiquitin (10201-2-AP), HA (51064-2-AP), His (66005-1-Ig), EP300 (20695-1-AP) and P62 (18420-1-AP) from proteintech; KAT8 (sc-271691) from Santa Cruz Biotechnology; KAT6A from Bioswamp; Collagen I (ab26003), β-actin (ab8226), Tubulin (Ab721), anti-mouse IgG (ab190475), anti-rabbit IgG (ab288151) and LC3B (ab192890) from Abcam; Pan-Kla (AB_2868521) from PTM-Bio laboratory; KAT6B(A17116), P-RIPK3(AP1260), AARS(A15017), and AARS2 (A7826) from Abclonal.

Techniques: Ubiquitin Proteomics, Transmission Assay, Electron Microscopy, Western Blot, Expressing, Transfection, Over Expression, Plasmid Preparation, Immunoprecipitation, Co-Immunoprecipitation Assay, Immunofluorescence, Staining, Quantitative RT-PCR

Curcumol targets KAT8 to suppress glycolysis and induce necroptosis in hepatic stellate cells (HSCs) in vivo . A. Representative images of liver sections from vehicle, different doses of Curcumol, and CCl₄-induced fibrotic mice (n = 5), stained with hematoxylin-eosin (H&E), Masson, and Sirius Red, and analyzed by immunohistochemistry (IHC) for α-SMA, Collagen I, and KAT8. Scale bar = 200 μm. B. Liver-to-body weight ratios of mice in the CCl₄ model group, Curcumol treatment group (n = 5). C-E. Serum levels of aspartate aminotransferase (AST), laminin (LN), and hyaluronic acid (HA) in CCl₄-induced fibrotic mice treated with vehicle, measured by biochemical assays (n = 5). F, G. Immunofluorescence analysis of colocalization between α-SMA (green) and HK2 (red), or α-SMA (green) and RIPK1 (red), in liver tissues from normal and CCl₄-induced fibrotic mice (n = 3). Scale bar = 20 μm. H,J. Serum levels of ALT and collagen IV (Col IV) in CCl₄-induced fibrotic mice treated with vehicle, Curcumol, measured by ELISA (n = 5). I. Western blot analysis of KAT8 and HK2 protein expression in liver tissues from vehicle-, Curcumol-, and CCl₄-treated mice, with densitometric quantification (n = 5). K-L. Western blot analysis of α-SMA, Collagen I, PFK1, PKM2, HK2, LDHA, RIPK1, RIPK3, phosphorylated RIPK1 (p-RIPK1), and phosphorylated RIPK3 (p-RIPK3) in liver tissues from vehicle-, Curcumol-, and KAT8 OE + Curcumol-treated CCl₄-induced fibrotic mice (n=3), with densitometric quantification. M. Western blot analysis of α-SMA, Collagen I, PFK1, PKM2, HK2, LDHA, RIPK1, RIPK3, phosphorylated RIPK1 (p-RIPK1), and phosphorylated RIPK3 (p-RIPK3) in liver tissues from vehicle-, Curcumol-, and KAT8 OE + Curcumol-treated TGF-β induced primary HSCs (n=3), with densitometric quantification. N. Serum lactate levels in CCl₄-induced fibrotic mice treated with different doses of Curcumol, measured by lactate assay kits (n = 5). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: International Journal of Biological Sciences

Article Title: Curcumol Induces Necroptosis of Hepatic Stellate Cells by Targeting KAT8 to Suppress HK2 Lactylation and Promote HUWE1-Dependent Ubiquitination

doi: 10.7150/ijbs.125009

Figure Lengend Snippet: Curcumol targets KAT8 to suppress glycolysis and induce necroptosis in hepatic stellate cells (HSCs) in vivo . A. Representative images of liver sections from vehicle, different doses of Curcumol, and CCl₄-induced fibrotic mice (n = 5), stained with hematoxylin-eosin (H&E), Masson, and Sirius Red, and analyzed by immunohistochemistry (IHC) for α-SMA, Collagen I, and KAT8. Scale bar = 200 μm. B. Liver-to-body weight ratios of mice in the CCl₄ model group, Curcumol treatment group (n = 5). C-E. Serum levels of aspartate aminotransferase (AST), laminin (LN), and hyaluronic acid (HA) in CCl₄-induced fibrotic mice treated with vehicle, measured by biochemical assays (n = 5). F, G. Immunofluorescence analysis of colocalization between α-SMA (green) and HK2 (red), or α-SMA (green) and RIPK1 (red), in liver tissues from normal and CCl₄-induced fibrotic mice (n = 3). Scale bar = 20 μm. H,J. Serum levels of ALT and collagen IV (Col IV) in CCl₄-induced fibrotic mice treated with vehicle, Curcumol, measured by ELISA (n = 5). I. Western blot analysis of KAT8 and HK2 protein expression in liver tissues from vehicle-, Curcumol-, and CCl₄-treated mice, with densitometric quantification (n = 5). K-L. Western blot analysis of α-SMA, Collagen I, PFK1, PKM2, HK2, LDHA, RIPK1, RIPK3, phosphorylated RIPK1 (p-RIPK1), and phosphorylated RIPK3 (p-RIPK3) in liver tissues from vehicle-, Curcumol-, and KAT8 OE + Curcumol-treated CCl₄-induced fibrotic mice (n=3), with densitometric quantification. M. Western blot analysis of α-SMA, Collagen I, PFK1, PKM2, HK2, LDHA, RIPK1, RIPK3, phosphorylated RIPK1 (p-RIPK1), and phosphorylated RIPK3 (p-RIPK3) in liver tissues from vehicle-, Curcumol-, and KAT8 OE + Curcumol-treated TGF-β induced primary HSCs (n=3), with densitometric quantification. N. Serum lactate levels in CCl₄-induced fibrotic mice treated with different doses of Curcumol, measured by lactate assay kits (n = 5). Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: The antibodies employed in this study include: RIPK1 (17519-1-AP), RIPK3 (17563-1-AP), P-RIPK1 (66854-1-Ig), MLKL (21066-1-AP), P-MLKL (82090-2-RR), HK2 (22029-1-AP), PKM2 (15822-1-AP), LDHA (19987-1-AP), PFKM (55028-1-AP), HUWE1 (19430-1-AP), Ubiquitin (10201-2-AP), HA (51064-2-AP), His (66005-1-Ig), EP300 (20695-1-AP) and P62 (18420-1-AP) from proteintech; KAT8 (sc-271691) from Santa Cruz Biotechnology; KAT6A from Bioswamp; Collagen I (ab26003), β-actin (ab8226), Tubulin (Ab721), anti-mouse IgG (ab190475), anti-rabbit IgG (ab288151) and LC3B (ab192890) from Abcam; Pan-Kla (AB_2868521) from PTM-Bio laboratory; KAT6B(A17116), P-RIPK3(AP1260), AARS(A15017), and AARS2 (A7826) from Abclonal.

Techniques: In Vivo, Staining, Immunohistochemistry, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Lactate Assay

KAT8 promotes hepatic fibrosis in vivo via HK2-mediated regulation of RIPK1-dependent necroptosis. A. Liver fibrosis staging was performed using the Ishak score. For histopathological analysis, H&E, Masson, and IHC were used to stain a-SMA, HK2 and KAT8 in 15 human liver samples (F0/1, 3; F2, 3; F3, 4; F4, 5). Representative images are shown. Scale bar: 200µm, n=6/group. B. Quantification of positive KAT8 and HK2 IHC staining (n= 6 / group). C-E. Liver tissues from CCl4-induced fibrotic mice (n=5) treated with vehicle, Curcumol, or KAT8 overexpression combined with Curcumol (KAT8 OE + Curcumol 30mg/kg) were subjected to hematoxylin and eosin (H&E) staining, Masson's trichrome staining, Sirius Red staining, and immunohistochemical (IHC) analysis for α-smooth muscle actin (α-SMA), collagen I, and KAT8. Scale bar = 200 μm. F. Protein expression of KAT8 and hexokinase 2 (HK2) in heart, liver, lung, kidney, and spleen tissues from CCl4-induced fibrotic mice (vehicle and KAT8 OE groups, n=5) was quantified by immunoblotting (n=3). G. Western blot analysis was performed to determine protein levels of α-SMA, collagen I, pyruvate kinase M2 (PKM2), phosphofructokinase-1 (PFK1), HK2, and lactate dehydrogenase A (LDHA) in liver tissues from vehicle, Curcumol, KAT8 OE, and KAT8 OE + Curcumol (30mg/kg) groups (n=5). H. Primary mouse hepatic stellate cells (HSCs) were subjected to KAT8 knockdown or overexpression, and immunoblotting was performed to assess collagen I and α-SMA expression after 24 h of Curcumol (30mg/kg) treatment (n=3; scale bar: 10 μm). I. Serum biochemical parameters, including aspartate aminotransferase (AST), alanine aminotransferase (ALT)and alkaline phosphatase (ALP) were evaluated in vehicle, Curcumol (30mg/kg), KAT8 OE, and KAT8 OE + Curcumol (30mg/kg) groups (n=5). J. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of hyaluronic acid (HA), laminin (LN), procollagen III (PCIII), and collagen IV (Col IV) in the same groups (n=5). K. Immunofluorescence analysis was performed to examine the co-localization of α-SMA (green) and HK2 (red) in liver tissues from CCl4-induced fibrotic mice (vehicle, KAT8 OE, and KAT8 OE + Curcumol (30mg/kg) groups, n=3). Scale bar = 20 μm. Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: International Journal of Biological Sciences

Article Title: Curcumol Induces Necroptosis of Hepatic Stellate Cells by Targeting KAT8 to Suppress HK2 Lactylation and Promote HUWE1-Dependent Ubiquitination

doi: 10.7150/ijbs.125009

Figure Lengend Snippet: KAT8 promotes hepatic fibrosis in vivo via HK2-mediated regulation of RIPK1-dependent necroptosis. A. Liver fibrosis staging was performed using the Ishak score. For histopathological analysis, H&E, Masson, and IHC were used to stain a-SMA, HK2 and KAT8 in 15 human liver samples (F0/1, 3; F2, 3; F3, 4; F4, 5). Representative images are shown. Scale bar: 200µm, n=6/group. B. Quantification of positive KAT8 and HK2 IHC staining (n= 6 / group). C-E. Liver tissues from CCl4-induced fibrotic mice (n=5) treated with vehicle, Curcumol, or KAT8 overexpression combined with Curcumol (KAT8 OE + Curcumol 30mg/kg) were subjected to hematoxylin and eosin (H&E) staining, Masson's trichrome staining, Sirius Red staining, and immunohistochemical (IHC) analysis for α-smooth muscle actin (α-SMA), collagen I, and KAT8. Scale bar = 200 μm. F. Protein expression of KAT8 and hexokinase 2 (HK2) in heart, liver, lung, kidney, and spleen tissues from CCl4-induced fibrotic mice (vehicle and KAT8 OE groups, n=5) was quantified by immunoblotting (n=3). G. Western blot analysis was performed to determine protein levels of α-SMA, collagen I, pyruvate kinase M2 (PKM2), phosphofructokinase-1 (PFK1), HK2, and lactate dehydrogenase A (LDHA) in liver tissues from vehicle, Curcumol, KAT8 OE, and KAT8 OE + Curcumol (30mg/kg) groups (n=5). H. Primary mouse hepatic stellate cells (HSCs) were subjected to KAT8 knockdown or overexpression, and immunoblotting was performed to assess collagen I and α-SMA expression after 24 h of Curcumol (30mg/kg) treatment (n=3; scale bar: 10 μm). I. Serum biochemical parameters, including aspartate aminotransferase (AST), alanine aminotransferase (ALT)and alkaline phosphatase (ALP) were evaluated in vehicle, Curcumol (30mg/kg), KAT8 OE, and KAT8 OE + Curcumol (30mg/kg) groups (n=5). J. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of hyaluronic acid (HA), laminin (LN), procollagen III (PCIII), and collagen IV (Col IV) in the same groups (n=5). K. Immunofluorescence analysis was performed to examine the co-localization of α-SMA (green) and HK2 (red) in liver tissues from CCl4-induced fibrotic mice (vehicle, KAT8 OE, and KAT8 OE + Curcumol (30mg/kg) groups, n=3). Scale bar = 20 μm. Data are shown as mean ± SD, and statistical differences were analyzed by one-way ANOVA. ns indicates no significance; *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: The antibodies employed in this study include: RIPK1 (17519-1-AP), RIPK3 (17563-1-AP), P-RIPK1 (66854-1-Ig), MLKL (21066-1-AP), P-MLKL (82090-2-RR), HK2 (22029-1-AP), PKM2 (15822-1-AP), LDHA (19987-1-AP), PFKM (55028-1-AP), HUWE1 (19430-1-AP), Ubiquitin (10201-2-AP), HA (51064-2-AP), His (66005-1-Ig), EP300 (20695-1-AP) and P62 (18420-1-AP) from proteintech; KAT8 (sc-271691) from Santa Cruz Biotechnology; KAT6A from Bioswamp; Collagen I (ab26003), β-actin (ab8226), Tubulin (Ab721), anti-mouse IgG (ab190475), anti-rabbit IgG (ab288151) and LC3B (ab192890) from Abcam; Pan-Kla (AB_2868521) from PTM-Bio laboratory; KAT6B(A17116), P-RIPK3(AP1260), AARS(A15017), and AARS2 (A7826) from Abclonal.

Techniques: In Vivo, Staining, Immunohistochemistry, Over Expression, Immunohistochemical staining, Expressing, Western Blot, Knockdown, Enzyme-linked Immunosorbent Assay, Immunofluorescence

Figure 5 Wogonin fails to further reduce cisplatin-induced cell injury and inflammatory response in HK2 cells where RIPK1 is blocked. (a) Western blot analysis and quantitative data of RIPK1/RIPK3/MLKL signaling in Nec-1-treated HK2 cells. (b) Western blot analysis and quantitative data of KIM-1. Results indicated that when RIPK1 was blocked, wogonin failed to further suppress the protein levels of KIM-1. (c) Real-time PCR showed that when RIPK1 was blocked, wogonin failed to further decrease IL-6 in mRNA level. Independent experiments were performed throughout the in vitro studies in triplicate or quadruplicate. *Po0.05, **Po0.01, ***Po0.001 compared with the control. ##Po0.01, ###Po0.001 compared with cisplatin-treated group. $$Po0.01, $$

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Wogonin protects against cisplatin-induced acute kidney injury by targeting RIPK1-mediated necroptosis.

doi: 10.1038/labinvest.2017.115

Figure Lengend Snippet: Figure 5 Wogonin fails to further reduce cisplatin-induced cell injury and inflammatory response in HK2 cells where RIPK1 is blocked. (a) Western blot analysis and quantitative data of RIPK1/RIPK3/MLKL signaling in Nec-1-treated HK2 cells. (b) Western blot analysis and quantitative data of KIM-1. Results indicated that when RIPK1 was blocked, wogonin failed to further suppress the protein levels of KIM-1. (c) Real-time PCR showed that when RIPK1 was blocked, wogonin failed to further decrease IL-6 in mRNA level. Independent experiments were performed throughout the in vitro studies in triplicate or quadruplicate. *Po0.05, **Po0.01, ***Po0.001 compared with the control. ##Po0.01, ###Po0.001 compared with cisplatin-treated group. $$Po0.01, $$

Article Snippet: Then, western blot analysis was performed as described previously.16,17 After blocking nonspecific binding with 5% BSA (room temperature, 1 h), membranes were consequently incubated with the primary antibody against KIM-1, RIPK1, RIPK3, p-MLKL, cleaved-caspase-3, cleaved-caspase-8 and β-actin overnight at 4 °C, followed by treated with IRDye 800-conjugated secondary antibody (Rockland immunochemicals, Gilbertsville, PA, USA).

Techniques: Western Blot, Real-time Polymerase Chain Reaction, In Vitro, Control

Figure 6 Wogonin fails to further reduce cisplatin-induced cell injury and inflammatory response in HK2 cells where RIPK3 is disrupted. (a) Western blot analysis and quantitative data of RIPK3 in HK2 cells. Results showed that RIPK3 was downregulated by transfection of RIPK3 shRNA plasmid. (b) Western blot analysis and quantitative data of RIPK1/RIPK3/MLKL signaling in RIPK3 knockdown HK2 cells. (c) Western blot analysis and quantitative data of KIM-1. Results indicated that when RIPK3 was knockdown, wogonin failed to further decrease the protein levels of KIM-1. (d) Real-time PCR identified that when RIPK3 was disrupted, wogonin failed to further decrease mRNA levels of TNF-α and IL-6. Independent experiments were performed throughout the in vitro studies in triplicate or quadruplicate. **Po0.01,***Po0.001 compared with the control. #Po0.05, ##Po0.01, ###Po0.001 compared with cisplatin-treated group. $$Po0.01,$$$Po0.001 compared with RIPK3 EV group. Cis, cisplatin; Wog, wogonin; EV, empty vector; KD, knockdown.

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Wogonin protects against cisplatin-induced acute kidney injury by targeting RIPK1-mediated necroptosis.

doi: 10.1038/labinvest.2017.115

Figure Lengend Snippet: Figure 6 Wogonin fails to further reduce cisplatin-induced cell injury and inflammatory response in HK2 cells where RIPK3 is disrupted. (a) Western blot analysis and quantitative data of RIPK3 in HK2 cells. Results showed that RIPK3 was downregulated by transfection of RIPK3 shRNA plasmid. (b) Western blot analysis and quantitative data of RIPK1/RIPK3/MLKL signaling in RIPK3 knockdown HK2 cells. (c) Western blot analysis and quantitative data of KIM-1. Results indicated that when RIPK3 was knockdown, wogonin failed to further decrease the protein levels of KIM-1. (d) Real-time PCR identified that when RIPK3 was disrupted, wogonin failed to further decrease mRNA levels of TNF-α and IL-6. Independent experiments were performed throughout the in vitro studies in triplicate or quadruplicate. **Po0.01,***Po0.001 compared with the control. #Po0.05, ##Po0.01, ###Po0.001 compared with cisplatin-treated group. $$Po0.01,$$$Po0.001 compared with RIPK3 EV group. Cis, cisplatin; Wog, wogonin; EV, empty vector; KD, knockdown.

Article Snippet: Then, western blot analysis was performed as described previously.16,17 After blocking nonspecific binding with 5% BSA (room temperature, 1 h), membranes were consequently incubated with the primary antibody against KIM-1, RIPK1, RIPK3, p-MLKL, cleaved-caspase-3, cleaved-caspase-8 and β-actin overnight at 4 °C, followed by treated with IRDye 800-conjugated secondary antibody (Rockland immunochemicals, Gilbertsville, PA, USA).

Techniques: Western Blot, Transfection, shRNA, Plasmid Preparation, Knockdown, Real-time Polymerase Chain Reaction, In Vitro, Control

Figure 9 Wogonin prevents RIPK1-mediated necroptosis in cisplatin nephropathy. (a) Electron microscope. Results clearly demonstrated that wogonin largely reduced nuclear structure damage and abnormal cell organelle content in injured kidney. (b) Western blot analysis of RIPK1/RIPK3/MLKL signaling. Results showed that treatment of wogonin significantly suppressed the activation of RIPK1/RIPK3/MLKL axis in cisplatin-injured kidney. Data represent the mean ± s.e.m. for 6–8 mice. ***Po0.001 compared with control. ##Po0.01, ###Po0.001 compared with model. Cis, cisplatin; Wog, wogonin.

Journal: Laboratory investigation; a journal of technical methods and pathology

Article Title: Wogonin protects against cisplatin-induced acute kidney injury by targeting RIPK1-mediated necroptosis.

doi: 10.1038/labinvest.2017.115

Figure Lengend Snippet: Figure 9 Wogonin prevents RIPK1-mediated necroptosis in cisplatin nephropathy. (a) Electron microscope. Results clearly demonstrated that wogonin largely reduced nuclear structure damage and abnormal cell organelle content in injured kidney. (b) Western blot analysis of RIPK1/RIPK3/MLKL signaling. Results showed that treatment of wogonin significantly suppressed the activation of RIPK1/RIPK3/MLKL axis in cisplatin-injured kidney. Data represent the mean ± s.e.m. for 6–8 mice. ***Po0.001 compared with control. ##Po0.01, ###Po0.001 compared with model. Cis, cisplatin; Wog, wogonin.

Article Snippet: Then, western blot analysis was performed as described previously.16,17 After blocking nonspecific binding with 5% BSA (room temperature, 1 h), membranes were consequently incubated with the primary antibody against KIM-1, RIPK1, RIPK3, p-MLKL, cleaved-caspase-3, cleaved-caspase-8 and β-actin overnight at 4 °C, followed by treated with IRDye 800-conjugated secondary antibody (Rockland immunochemicals, Gilbertsville, PA, USA).

Techniques: Microscopy, Western Blot, Activation Assay, Control

Fig. 3 The effect of different treatments on B16F10 tumor growth in mice. Significant tumor growth retardations (34–49%) were observed in the mice treated with effector cells armed with the nine-antibody cocktail and PD1i, as compared to PBS control group. Two-way ANOVA analysis of the data shows significantly differ- ent curves by treatment and time. *Significantly different (P ≤ 0.05) in comparison to PBS and PD1i alone groups as determined by Tukey’s multiple comparisons test. The values represent the mean ± SEM of six mice in each group. EC effector cells, EC armed with Ab Cocktail Effector cells armed with a cocktail of all the nine rabbit antibodies against selected mutated peptides, TCT tumor cell transplantation, T1– T5 EC treatment days, DPI days post-implantation

Journal: Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico

Article Title: Multiple antibodies targeting tumor-specific mutations redirect immune cells to inhibit tumor growth and increase survival in experimental animal models.

doi: 10.1007/s12094-019-02235-3

Figure Lengend Snippet: Fig. 3 The effect of different treatments on B16F10 tumor growth in mice. Significant tumor growth retardations (34–49%) were observed in the mice treated with effector cells armed with the nine-antibody cocktail and PD1i, as compared to PBS control group. Two-way ANOVA analysis of the data shows significantly differ- ent curves by treatment and time. *Significantly different (P ≤ 0.05) in comparison to PBS and PD1i alone groups as determined by Tukey’s multiple comparisons test. The values represent the mean ± SEM of six mice in each group. EC effector cells, EC armed with Ab Cocktail Effector cells armed with a cocktail of all the nine rabbit antibodies against selected mutated peptides, TCT tumor cell transplantation, T1– T5 EC treatment days, DPI days post-implantation

Article Snippet: Anti-mouse PD1 inhibitor antibody (PD1i) was supplied by Bio X cell (West Lebanon, NH).

Techniques: Control, Comparison, Transplantation Assay

Fig. 4 The effect of different treatments on survival of mice implanted with B16F10 mela- noma cells. The combined treat- ment with effector cells armed with nine-antibody cocktail and PD1i increased the survival of mice. EC effector cells, EC armed with Ab Cocktail effector cells armed with a cocktail of all the nine antibodies against selected mutated peptides, TCT tumor cell transplanta- tion, T1–T5 EC treatment days, DPI days post-implantation

Journal: Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico

Article Title: Multiple antibodies targeting tumor-specific mutations redirect immune cells to inhibit tumor growth and increase survival in experimental animal models.

doi: 10.1007/s12094-019-02235-3

Figure Lengend Snippet: Fig. 4 The effect of different treatments on survival of mice implanted with B16F10 mela- noma cells. The combined treat- ment with effector cells armed with nine-antibody cocktail and PD1i increased the survival of mice. EC effector cells, EC armed with Ab Cocktail effector cells armed with a cocktail of all the nine antibodies against selected mutated peptides, TCT tumor cell transplanta- tion, T1–T5 EC treatment days, DPI days post-implantation

Article Snippet: Anti-mouse PD1 inhibitor antibody (PD1i) was supplied by Bio X cell (West Lebanon, NH).

Techniques: