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94
OriGene casp8
Long-term exposure to 5.0% ethanol triggers apoptosis, which undermines cell growth. A . An equal number of HEEC cells was seeded in 6-well plates and incubated with the complete medium containing DMSO (control), the medium containing 5.0% ethanol (EtOH), the medium containing 2 µM Z-LEHD-FMK (LEHD), or the medium containing 5.0% ethanol plus 2 µM LEHD for 30 min. Protein was extracted and analyzed by Western blotting. The membranes were probed for <t>CASP8,</t> CASP9, CASP3, or GAPDH. B . Quantitative analyses of CASP8, CASP9, and CASP3 expression against GAPDH in HEEC cells. * indicates a significant change compared to the control (DMSO). C . An equal number of HEEC cells was seeded on the coverslips and incubated with the complete medium (control) or the medium containing 5.0% ethanol for 5–30 min, or 2, 6, and 12 h. Cells were fixed in 4% paraformaldehyde and stained for endoG. An FITC-conjugated secondary antibody was used to develop the signal. Cell nuclei were counterstained with DAPI. Scale bar = 5 μm. D . Quantitative analyses of endoG nuclear translocation in HEEC cells (%). * indicates a significant change compared to the control. E . An equal number of HEEC cells was seeded in 96-well plates and incubated with the medium containing 5.0% ethanol (EtOH) or the medium containing 5.0% ethanol plus 2 µM LEHD for 5 min, 30 min, 2 h, 6 h, or 12 h. Cell viability was assessed using CCK-8 kits. * indicates a significant change between EtOH and EtOH/LEHD. F . An equal number of Het1A cells was seeded in 96-well plates and incubated with the medium containing 5.0% ethanol (EtOH) or the medium containing 5.0% ethanol plus 2 µM LEHD for 5 min, 30 min, 2 h, 6 h, or 12 h. Cell viability was assessed using CCK-8 kits. * indicates a significant change between EtOH and EtOH/LEHD
Casp8, supplied by OriGene, 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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Cell Signaling Technology Inc anti cleaved caspase 8
Long-term exposure to 5.0% ethanol triggers apoptosis, which undermines cell growth. A . An equal number of HEEC cells was seeded in 6-well plates and incubated with the complete medium containing DMSO (control), the medium containing 5.0% ethanol (EtOH), the medium containing 2 µM Z-LEHD-FMK (LEHD), or the medium containing 5.0% ethanol plus 2 µM LEHD for 30 min. Protein was extracted and analyzed by Western blotting. The membranes were probed for <t>CASP8,</t> CASP9, CASP3, or GAPDH. B . Quantitative analyses of CASP8, CASP9, and CASP3 expression against GAPDH in HEEC cells. * indicates a significant change compared to the control (DMSO). C . An equal number of HEEC cells was seeded on the coverslips and incubated with the complete medium (control) or the medium containing 5.0% ethanol for 5–30 min, or 2, 6, and 12 h. Cells were fixed in 4% paraformaldehyde and stained for endoG. An FITC-conjugated secondary antibody was used to develop the signal. Cell nuclei were counterstained with DAPI. Scale bar = 5 μm. D . Quantitative analyses of endoG nuclear translocation in HEEC cells (%). * indicates a significant change compared to the control. E . An equal number of HEEC cells was seeded in 96-well plates and incubated with the medium containing 5.0% ethanol (EtOH) or the medium containing 5.0% ethanol plus 2 µM LEHD for 5 min, 30 min, 2 h, 6 h, or 12 h. Cell viability was assessed using CCK-8 kits. * indicates a significant change between EtOH and EtOH/LEHD. F . An equal number of Het1A cells was seeded in 96-well plates and incubated with the medium containing 5.0% ethanol (EtOH) or the medium containing 5.0% ethanol plus 2 µM LEHD for 5 min, 30 min, 2 h, 6 h, or 12 h. Cell viability was assessed using CCK-8 kits. * indicates a significant change between EtOH and EtOH/LEHD
Anti Cleaved Caspase 8, supplied by Cell Signaling Technology Inc, 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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Santa Cruz Biotechnology caspase 8
Zn-SaCDs@Ap inhibits tumor growth and promotes necroptosis in tumor tissues. (A) Schematic diagram of the process of treating animal models with transplanted tumors and liver in situ tumors using Zn-SaCDs@Ap. (B) Live animal imaging of transplanted tumors. (C) Fluorescence live imaging of liver in situ tumors. (D) Statistics of fluorescence intensity of transplanted tumors. (E) Statistics of tumor size of transplanted tumors. (F) Statistics of fluorescence intensity of liver in situ tumors. (G) Immunofluorescence analysis revealed that the localization of Zn-SaCDs@Ap within tissue sections overlapped with areas of tumor necrosis. GPC3 and AFP, two well-established markers for hepatocellular carcinoma malignancy, were used to verify the aggressive nature of the tumor tissue. (H) HE staining of tumor tissues from transplanted tumors. Quantification of tumor necroptosis area in mice with transplanted tumors. (I) HE staining of tumors from liver in situ tumor mice. Quantification of tumor necroptosis area in liver in situ tumor mice. (J) IHC of necroptosis-related markers in liver in situ tumor mice. And the IHC score of necroptosis-related markers in liver in situ tumor mice. (K) IHC for proliferation marker Ki67 and apoptosis-related marker <t>cleaved</t> <t>caspase-8</t> (Casp8) in tumor tissues. (L) Statistics of fluorescence intensity of apoptosis and proliferation-related markers in liver in situ tumor mice. N = 6 biologically independent animals. Statistical analysis was analyzed by one-way/two-way ANOVA. ∗P < 0.05, ∗∗P < 0.01, n. s. = not significant.
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Proteintech caspase 8 polyclonal antibody
Zn-SaCDs@Ap inhibits tumor growth and promotes necroptosis in tumor tissues. (A) Schematic diagram of the process of treating animal models with transplanted tumors and liver in situ tumors using Zn-SaCDs@Ap. (B) Live animal imaging of transplanted tumors. (C) Fluorescence live imaging of liver in situ tumors. (D) Statistics of fluorescence intensity of transplanted tumors. (E) Statistics of tumor size of transplanted tumors. (F) Statistics of fluorescence intensity of liver in situ tumors. (G) Immunofluorescence analysis revealed that the localization of Zn-SaCDs@Ap within tissue sections overlapped with areas of tumor necrosis. GPC3 and AFP, two well-established markers for hepatocellular carcinoma malignancy, were used to verify the aggressive nature of the tumor tissue. (H) HE staining of tumor tissues from transplanted tumors. Quantification of tumor necroptosis area in mice with transplanted tumors. (I) HE staining of tumors from liver in situ tumor mice. Quantification of tumor necroptosis area in liver in situ tumor mice. (J) IHC of necroptosis-related markers in liver in situ tumor mice. And the IHC score of necroptosis-related markers in liver in situ tumor mice. (K) IHC for proliferation marker Ki67 and apoptosis-related marker <t>cleaved</t> <t>caspase-8</t> (Casp8) in tumor tissues. (L) Statistics of fluorescence intensity of apoptosis and proliferation-related markers in liver in situ tumor mice. N = 6 biologically independent animals. Statistical analysis was analyzed by one-way/two-way ANOVA. ∗P < 0.05, ∗∗P < 0.01, n. s. = not significant.
Caspase 8 Polyclonal Antibody, 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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Cell Signaling Technology Inc clcaspase 8
Zn-SaCDs@Ap inhibits tumor growth and promotes necroptosis in tumor tissues. (A) Schematic diagram of the process of treating animal models with transplanted tumors and liver in situ tumors using Zn-SaCDs@Ap. (B) Live animal imaging of transplanted tumors. (C) Fluorescence live imaging of liver in situ tumors. (D) Statistics of fluorescence intensity of transplanted tumors. (E) Statistics of tumor size of transplanted tumors. (F) Statistics of fluorescence intensity of liver in situ tumors. (G) Immunofluorescence analysis revealed that the localization of Zn-SaCDs@Ap within tissue sections overlapped with areas of tumor necrosis. GPC3 and AFP, two well-established markers for hepatocellular carcinoma malignancy, were used to verify the aggressive nature of the tumor tissue. (H) HE staining of tumor tissues from transplanted tumors. Quantification of tumor necroptosis area in mice with transplanted tumors. (I) HE staining of tumors from liver in situ tumor mice. Quantification of tumor necroptosis area in liver in situ tumor mice. (J) IHC of necroptosis-related markers in liver in situ tumor mice. And the IHC score of necroptosis-related markers in liver in situ tumor mice. (K) IHC for proliferation marker Ki67 and apoptosis-related marker <t>cleaved</t> <t>caspase-8</t> (Casp8) in tumor tissues. (L) Statistics of fluorescence intensity of apoptosis and proliferation-related markers in liver in situ tumor mice. N = 6 biologically independent animals. Statistical analysis was analyzed by one-way/two-way ANOVA. ∗P < 0.05, ∗∗P < 0.01, n. s. = not significant.
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Zn-SaCDs@Ap inhibits tumor growth and promotes necroptosis in tumor tissues. (A) Schematic diagram of the process of treating animal models with transplanted tumors and liver in situ tumors using Zn-SaCDs@Ap. (B) Live animal imaging of transplanted tumors. (C) Fluorescence live imaging of liver in situ tumors. (D) Statistics of fluorescence intensity of transplanted tumors. (E) Statistics of tumor size of transplanted tumors. (F) Statistics of fluorescence intensity of liver in situ tumors. (G) Immunofluorescence analysis revealed that the localization of Zn-SaCDs@Ap within tissue sections overlapped with areas of tumor necrosis. GPC3 and AFP, two well-established markers for hepatocellular carcinoma malignancy, were used to verify the aggressive nature of the tumor tissue. (H) HE staining of tumor tissues from transplanted tumors. Quantification of tumor necroptosis area in mice with transplanted tumors. (I) HE staining of tumors from liver in situ tumor mice. Quantification of tumor necroptosis area in liver in situ tumor mice. (J) IHC of necroptosis-related markers in liver in situ tumor mice. And the IHC score of necroptosis-related markers in liver in situ tumor mice. (K) IHC for proliferation marker Ki67 and apoptosis-related marker <t>cleaved</t> <t>caspase-8</t> (Casp8) in tumor tissues. (L) Statistics of fluorescence intensity of apoptosis and proliferation-related markers in liver in situ tumor mice. N = 6 biologically independent animals. Statistical analysis was analyzed by one-way/two-way ANOVA. ∗P < 0.05, ∗∗P < 0.01, n. s. = not significant.
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Zn-SaCDs@Ap inhibits tumor growth and promotes necroptosis in tumor tissues. (A) Schematic diagram of the process of treating animal models with transplanted tumors and liver in situ tumors using Zn-SaCDs@Ap. (B) Live animal imaging of transplanted tumors. (C) Fluorescence live imaging of liver in situ tumors. (D) Statistics of fluorescence intensity of transplanted tumors. (E) Statistics of tumor size of transplanted tumors. (F) Statistics of fluorescence intensity of liver in situ tumors. (G) Immunofluorescence analysis revealed that the localization of Zn-SaCDs@Ap within tissue sections overlapped with areas of tumor necrosis. GPC3 and AFP, two well-established markers for hepatocellular carcinoma malignancy, were used to verify the aggressive nature of the tumor tissue. (H) HE staining of tumor tissues from transplanted tumors. Quantification of tumor necroptosis area in mice with transplanted tumors. (I) HE staining of tumors from liver in situ tumor mice. Quantification of tumor necroptosis area in liver in situ tumor mice. (J) IHC of necroptosis-related markers in liver in situ tumor mice. And the IHC score of necroptosis-related markers in liver in situ tumor mice. (K) IHC for proliferation marker Ki67 and apoptosis-related marker <t>cleaved</t> <t>caspase-8</t> (Casp8) in tumor tissues. (L) Statistics of fluorescence intensity of apoptosis and proliferation-related markers in liver in situ tumor mice. N = 6 biologically independent animals. Statistical analysis was analyzed by one-way/two-way ANOVA. ∗P < 0.05, ∗∗P < 0.01, n. s. = not significant.
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Long-term exposure to 5.0% ethanol triggers apoptosis, which undermines cell growth. A . An equal number of HEEC cells was seeded in 6-well plates and incubated with the complete medium containing DMSO (control), the medium containing 5.0% ethanol (EtOH), the medium containing 2 µM Z-LEHD-FMK (LEHD), or the medium containing 5.0% ethanol plus 2 µM LEHD for 30 min. Protein was extracted and analyzed by Western blotting. The membranes were probed for CASP8, CASP9, CASP3, or GAPDH. B . Quantitative analyses of CASP8, CASP9, and CASP3 expression against GAPDH in HEEC cells. * indicates a significant change compared to the control (DMSO). C . An equal number of HEEC cells was seeded on the coverslips and incubated with the complete medium (control) or the medium containing 5.0% ethanol for 5–30 min, or 2, 6, and 12 h. Cells were fixed in 4% paraformaldehyde and stained for endoG. An FITC-conjugated secondary antibody was used to develop the signal. Cell nuclei were counterstained with DAPI. Scale bar = 5 μm. D . Quantitative analyses of endoG nuclear translocation in HEEC cells (%). * indicates a significant change compared to the control. E . An equal number of HEEC cells was seeded in 96-well plates and incubated with the medium containing 5.0% ethanol (EtOH) or the medium containing 5.0% ethanol plus 2 µM LEHD for 5 min, 30 min, 2 h, 6 h, or 12 h. Cell viability was assessed using CCK-8 kits. * indicates a significant change between EtOH and EtOH/LEHD. F . An equal number of Het1A cells was seeded in 96-well plates and incubated with the medium containing 5.0% ethanol (EtOH) or the medium containing 5.0% ethanol plus 2 µM LEHD for 5 min, 30 min, 2 h, 6 h, or 12 h. Cell viability was assessed using CCK-8 kits. * indicates a significant change between EtOH and EtOH/LEHD

Journal: BMC Molecular and Cell Biology

Article Title: Alcohol exposure induces ferroptosis-dominated programmed cell death in esophageal epithelial cells

doi: 10.1186/s12860-026-00589-5

Figure Lengend Snippet: Long-term exposure to 5.0% ethanol triggers apoptosis, which undermines cell growth. A . An equal number of HEEC cells was seeded in 6-well plates and incubated with the complete medium containing DMSO (control), the medium containing 5.0% ethanol (EtOH), the medium containing 2 µM Z-LEHD-FMK (LEHD), or the medium containing 5.0% ethanol plus 2 µM LEHD for 30 min. Protein was extracted and analyzed by Western blotting. The membranes were probed for CASP8, CASP9, CASP3, or GAPDH. B . Quantitative analyses of CASP8, CASP9, and CASP3 expression against GAPDH in HEEC cells. * indicates a significant change compared to the control (DMSO). C . An equal number of HEEC cells was seeded on the coverslips and incubated with the complete medium (control) or the medium containing 5.0% ethanol for 5–30 min, or 2, 6, and 12 h. Cells were fixed in 4% paraformaldehyde and stained for endoG. An FITC-conjugated secondary antibody was used to develop the signal. Cell nuclei were counterstained with DAPI. Scale bar = 5 μm. D . Quantitative analyses of endoG nuclear translocation in HEEC cells (%). * indicates a significant change compared to the control. E . An equal number of HEEC cells was seeded in 96-well plates and incubated with the medium containing 5.0% ethanol (EtOH) or the medium containing 5.0% ethanol plus 2 µM LEHD for 5 min, 30 min, 2 h, 6 h, or 12 h. Cell viability was assessed using CCK-8 kits. * indicates a significant change between EtOH and EtOH/LEHD. F . An equal number of Het1A cells was seeded in 96-well plates and incubated with the medium containing 5.0% ethanol (EtOH) or the medium containing 5.0% ethanol plus 2 µM LEHD for 5 min, 30 min, 2 h, 6 h, or 12 h. Cell viability was assessed using CCK-8 kits. * indicates a significant change between EtOH and EtOH/LEHD

Article Snippet: The following primary antibodies were used: Beclin-1 (Origene, #TA502643), PCNA, CASP1 (Abcam, #ab179515), CASP3 (Santa Cruz Biotechnology, #sc-271759), CASP8 (Origene, #TA374288), CASP9 (Origene, #TA4227045), endoG, GPX4 (Origene, #TA423164M), GSDMD, IL-1β (Santa Cruz Biotechnology, #sc-12742), MLKL, phosphor-MLKL (Abcam, #ab196436), SLC7A11 (Origene, #TA423232), LC3B, BAX, GAPDH (OriGene, #TA800894), and β-actin (Santa Cruz Biotechnology, Inc. #sc-69879).

Techniques: Incubation, Control, Western Blot, Expressing, Staining, Translocation Assay, CCK-8 Assay

Zn-SaCDs@Ap inhibits tumor growth and promotes necroptosis in tumor tissues. (A) Schematic diagram of the process of treating animal models with transplanted tumors and liver in situ tumors using Zn-SaCDs@Ap. (B) Live animal imaging of transplanted tumors. (C) Fluorescence live imaging of liver in situ tumors. (D) Statistics of fluorescence intensity of transplanted tumors. (E) Statistics of tumor size of transplanted tumors. (F) Statistics of fluorescence intensity of liver in situ tumors. (G) Immunofluorescence analysis revealed that the localization of Zn-SaCDs@Ap within tissue sections overlapped with areas of tumor necrosis. GPC3 and AFP, two well-established markers for hepatocellular carcinoma malignancy, were used to verify the aggressive nature of the tumor tissue. (H) HE staining of tumor tissues from transplanted tumors. Quantification of tumor necroptosis area in mice with transplanted tumors. (I) HE staining of tumors from liver in situ tumor mice. Quantification of tumor necroptosis area in liver in situ tumor mice. (J) IHC of necroptosis-related markers in liver in situ tumor mice. And the IHC score of necroptosis-related markers in liver in situ tumor mice. (K) IHC for proliferation marker Ki67 and apoptosis-related marker cleaved caspase-8 (Casp8) in tumor tissues. (L) Statistics of fluorescence intensity of apoptosis and proliferation-related markers in liver in situ tumor mice. N = 6 biologically independent animals. Statistical analysis was analyzed by one-way/two-way ANOVA. ∗P < 0.05, ∗∗P < 0.01, n. s. = not significant.

Journal: Materials Today Bio

Article Title: Apoptotic body-encapsulated zinc-doped Salvia miltiorrhiza carbon dots trigger PANoptosis for targeted therapy of hepatocellular carcinoma

doi: 10.1016/j.mtbio.2026.102984

Figure Lengend Snippet: Zn-SaCDs@Ap inhibits tumor growth and promotes necroptosis in tumor tissues. (A) Schematic diagram of the process of treating animal models with transplanted tumors and liver in situ tumors using Zn-SaCDs@Ap. (B) Live animal imaging of transplanted tumors. (C) Fluorescence live imaging of liver in situ tumors. (D) Statistics of fluorescence intensity of transplanted tumors. (E) Statistics of tumor size of transplanted tumors. (F) Statistics of fluorescence intensity of liver in situ tumors. (G) Immunofluorescence analysis revealed that the localization of Zn-SaCDs@Ap within tissue sections overlapped with areas of tumor necrosis. GPC3 and AFP, two well-established markers for hepatocellular carcinoma malignancy, were used to verify the aggressive nature of the tumor tissue. (H) HE staining of tumor tissues from transplanted tumors. Quantification of tumor necroptosis area in mice with transplanted tumors. (I) HE staining of tumors from liver in situ tumor mice. Quantification of tumor necroptosis area in liver in situ tumor mice. (J) IHC of necroptosis-related markers in liver in situ tumor mice. And the IHC score of necroptosis-related markers in liver in situ tumor mice. (K) IHC for proliferation marker Ki67 and apoptosis-related marker cleaved caspase-8 (Casp8) in tumor tissues. (L) Statistics of fluorescence intensity of apoptosis and proliferation-related markers in liver in situ tumor mice. N = 6 biologically independent animals. Statistical analysis was analyzed by one-way/two-way ANOVA. ∗P < 0.05, ∗∗P < 0.01, n. s. = not significant.

Article Snippet: After blocking, the membranes were incubated overnight at 4 °C with primary antibodies against Caspase-1 (Santa Cruz, USA), GSDMD (Zenbio, China), GSDME (Zenbio, China), Caspase-8 (Santa Cruz), Caspase-3 (Santa Cruz), Caspase-7 (Santa Cruz, USA), pMLKL (Zenbio, China), tMLKL (Zenbio, China), pRIPK3 (Zenbio, China), and tRIPK3 (Zenbio, China).

Techniques: In Situ, Imaging, Fluorescence, Immunofluorescence, Staining, Marker

Zn-SaCDs@Ap suppresses malignancy in HCC by inducing PANoptosis in tumors. (A) Schematic diagram of cell pyroptosis. (B) Expression of pyroptosis-related proteins caspase-1 (CASP1), GSDMD, and GSDME in Zn-SaCDs@Ap-treated Hep3B cells, as determined by Western blot analysis (C) IHC showing expression of pyroptosis markers in Zn-SaCDs@Ap treated in situ tumors. (D) Expression of pyroptosis markers in three cases of liver in situ tumors. (E) Schematic diagram of cell apoptosis. (F) Expression of apoptosis-related proteins caspase-3 (CASP3), caspase-8 (CASP8), and caspase-7 (CASP7) in Hep3B cells. (G) IHC showing expression of apoptosis markers in liver in situ tumors. (H) Expression of apoptosis markers in three cases of liver in situ tumors. (I) Schematic diagram of cell necroptosis. (J) Expression of necroptosis markers in Hep3B cells. (K) IHC showing expression of necroptosis markers in liver in situ tumors. (L) Expression of necroptosis markers in three cases of liver in situ tumors. (M) Multicolor immunofluorescence data demonstrate that Zn-SaCDs@Ap concurrently induces apoptosis, pyroptosis, and necroptosis. N = 6 biologically independent animals.

Journal: Materials Today Bio

Article Title: Apoptotic body-encapsulated zinc-doped Salvia miltiorrhiza carbon dots trigger PANoptosis for targeted therapy of hepatocellular carcinoma

doi: 10.1016/j.mtbio.2026.102984

Figure Lengend Snippet: Zn-SaCDs@Ap suppresses malignancy in HCC by inducing PANoptosis in tumors. (A) Schematic diagram of cell pyroptosis. (B) Expression of pyroptosis-related proteins caspase-1 (CASP1), GSDMD, and GSDME in Zn-SaCDs@Ap-treated Hep3B cells, as determined by Western blot analysis (C) IHC showing expression of pyroptosis markers in Zn-SaCDs@Ap treated in situ tumors. (D) Expression of pyroptosis markers in three cases of liver in situ tumors. (E) Schematic diagram of cell apoptosis. (F) Expression of apoptosis-related proteins caspase-3 (CASP3), caspase-8 (CASP8), and caspase-7 (CASP7) in Hep3B cells. (G) IHC showing expression of apoptosis markers in liver in situ tumors. (H) Expression of apoptosis markers in three cases of liver in situ tumors. (I) Schematic diagram of cell necroptosis. (J) Expression of necroptosis markers in Hep3B cells. (K) IHC showing expression of necroptosis markers in liver in situ tumors. (L) Expression of necroptosis markers in three cases of liver in situ tumors. (M) Multicolor immunofluorescence data demonstrate that Zn-SaCDs@Ap concurrently induces apoptosis, pyroptosis, and necroptosis. N = 6 biologically independent animals.

Article Snippet: After blocking, the membranes were incubated overnight at 4 °C with primary antibodies against Caspase-1 (Santa Cruz, USA), GSDMD (Zenbio, China), GSDME (Zenbio, China), Caspase-8 (Santa Cruz), Caspase-3 (Santa Cruz), Caspase-7 (Santa Cruz, USA), pMLKL (Zenbio, China), tMLKL (Zenbio, China), pRIPK3 (Zenbio, China), and tRIPK3 (Zenbio, China).

Techniques: Expressing, Western Blot, In Situ, Immunofluorescence