Structured Review

Enzo Biochem necroptosis inhibitor necrostatin 1
DAMP release and monocyte attraction occur during secondary necrosis upon irradiation in combination with HSP90i treatment. (A) Induction of cell death, THP-1 cell attraction, and DAMP release in HCT116 subclones with or without functional Bax and/or hyperactive Kras G 13 D . Parental HCT116 Kras +/ G 13 D Bax +/+ cells (upper row), HCT116 Kras +/ G 13 D Bax –/– cells (middle row), and HCT116 Kras +/– Bax +/+ cells (lower panel) were treated with 5 Gy plus 625 nM HSP90i or left untreated. At the indicated time points, induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration, ATP release) or means ± SD of triplicates of one representative experiment (HSP70 release) are shown. (B) Impact of different cell death inhibitors on apoptosis and necrosis induction, THP-1 cell attraction, and DAMP release in HCT116 cells upon treatment with radiotherapy and HSP90i. HCT116 cells were treated with 5 Gy plus 625 nM HSP90i in the presence of the poly-caspase inhibitor zVAD-fmk or the <t>necroptosis</t> inhibitor necrostatin-1, respectively (upper panel). Untreated cells served as controls (lower panel). Induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration) or means ± SD of triplicates of one representative experiment (release of HSP70 and ATP) are shown.
Necroptosis Inhibitor Necrostatin 1, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/necroptosis inhibitor necrostatin 1/product/Enzo Biochem
Average 93 stars, based on 6 article reviews
Price from $9.99 to $1999.99
necroptosis inhibitor necrostatin 1 - by Bioz Stars, 2022-10
93/100 stars

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1) Product Images from "Priming of Anti-tumor Immune Mechanisms by Radiotherapy Is Augmented by Inhibition of Heat Shock Protein 90"

Article Title: Priming of Anti-tumor Immune Mechanisms by Radiotherapy Is Augmented by Inhibition of Heat Shock Protein 90

Journal: Frontiers in Oncology

doi: 10.3389/fonc.2020.01668

DAMP release and monocyte attraction occur during secondary necrosis upon irradiation in combination with HSP90i treatment. (A) Induction of cell death, THP-1 cell attraction, and DAMP release in HCT116 subclones with or without functional Bax and/or hyperactive Kras G 13 D . Parental HCT116 Kras +/ G 13 D Bax +/+ cells (upper row), HCT116 Kras +/ G 13 D Bax –/– cells (middle row), and HCT116 Kras +/– Bax +/+ cells (lower panel) were treated with 5 Gy plus 625 nM HSP90i or left untreated. At the indicated time points, induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration, ATP release) or means ± SD of triplicates of one representative experiment (HSP70 release) are shown. (B) Impact of different cell death inhibitors on apoptosis and necrosis induction, THP-1 cell attraction, and DAMP release in HCT116 cells upon treatment with radiotherapy and HSP90i. HCT116 cells were treated with 5 Gy plus 625 nM HSP90i in the presence of the poly-caspase inhibitor zVAD-fmk or the necroptosis inhibitor necrostatin-1, respectively (upper panel). Untreated cells served as controls (lower panel). Induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration) or means ± SD of triplicates of one representative experiment (release of HSP70 and ATP) are shown.
Figure Legend Snippet: DAMP release and monocyte attraction occur during secondary necrosis upon irradiation in combination with HSP90i treatment. (A) Induction of cell death, THP-1 cell attraction, and DAMP release in HCT116 subclones with or without functional Bax and/or hyperactive Kras G 13 D . Parental HCT116 Kras +/ G 13 D Bax +/+ cells (upper row), HCT116 Kras +/ G 13 D Bax –/– cells (middle row), and HCT116 Kras +/– Bax +/+ cells (lower panel) were treated with 5 Gy plus 625 nM HSP90i or left untreated. At the indicated time points, induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration, ATP release) or means ± SD of triplicates of one representative experiment (HSP70 release) are shown. (B) Impact of different cell death inhibitors on apoptosis and necrosis induction, THP-1 cell attraction, and DAMP release in HCT116 cells upon treatment with radiotherapy and HSP90i. HCT116 cells were treated with 5 Gy plus 625 nM HSP90i in the presence of the poly-caspase inhibitor zVAD-fmk or the necroptosis inhibitor necrostatin-1, respectively (upper panel). Untreated cells served as controls (lower panel). Induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration) or means ± SD of triplicates of one representative experiment (release of HSP70 and ATP) are shown.

Techniques Used: Irradiation, Functional Assay, Migration

2) Product Images from "Circadian rhythm disruption impairs tissue homeostasis and exacerbates chronic inflammation in the intestine"

Article Title: Circadian rhythm disruption impairs tissue homeostasis and exacerbates chronic inflammation in the intestine

Journal: The FASEB Journal

doi: 10.1096/fj.201700141RR

RIP3-dependent necroptotic cell death is increased in arrhythmic mice.  A ) Western blot analysis for RIP3 production in intestinal biopsy samples from DSS- and TNF-α-treated mice. Biopsy samples from DSS-treated mice were taken from the colon, and samples from TNF-α-treated mice were taken from the ileum. β-Actin served as the loading control.  B ) Wee1 mRNA transcript levels were determined by qPCR, using colonic tissue samples from rhythmic ( n  = 5) or arrhythmic ( n  = 3) mice. Wee1 mRNA levels were normalized to β-actin mRNA levels.  C ) Rip3 mRNA transcript levels were evaluated by qPCR, using ileal tissue samples from rhythmic or arrhythmic mice treated with TNF-α or left untreated ( n  = 4 per strain and treatment). Rip3 mRNA levels were normalized to β-actin mRNA levels.  D ) Western blot for RIP3 with ileal biopsy samples. β-Actin served as a control.  E ) Representative images of TUNEL +  dying cells in ileal tissue after intraperitoneal injection of TNF-α, with or without coinjection of Nec1. Insets: lower crypt of arrhythmic (LL) mice showing fewer TUNEL +  cells after Nec1 treatment. LD, rhythmic mice.  F ) Quantification of TUNEL +  cells in the lower crypt ( n >  8 per strain).  G ) KC-specific ELISA with serum samples collected from rhythmic and arrhythmic mice. Mice underwent intraperitoneal injection of TNF-α, with or without coinjection of necrostatin 1 (Nec1; rhythmic,  n  = 3; arrhythmic,  n  = 6; rhythmic+TNF-α,  n  = 6; arrhythmic+TNF-α,  n  = 6; rhythmic+TNF-α+Nec1,  n  = 9; and arrhythmic+TNF-α+Nec1,  n  = 6). * P  ≤ 0.05, ** P  ≤ 0.01, *** P  ≤ 0.001.
Figure Legend Snippet: RIP3-dependent necroptotic cell death is increased in arrhythmic mice. A ) Western blot analysis for RIP3 production in intestinal biopsy samples from DSS- and TNF-α-treated mice. Biopsy samples from DSS-treated mice were taken from the colon, and samples from TNF-α-treated mice were taken from the ileum. β-Actin served as the loading control. B ) Wee1 mRNA transcript levels were determined by qPCR, using colonic tissue samples from rhythmic ( n = 5) or arrhythmic ( n = 3) mice. Wee1 mRNA levels were normalized to β-actin mRNA levels. C ) Rip3 mRNA transcript levels were evaluated by qPCR, using ileal tissue samples from rhythmic or arrhythmic mice treated with TNF-α or left untreated ( n = 4 per strain and treatment). Rip3 mRNA levels were normalized to β-actin mRNA levels. D ) Western blot for RIP3 with ileal biopsy samples. β-Actin served as a control. E ) Representative images of TUNEL + dying cells in ileal tissue after intraperitoneal injection of TNF-α, with or without coinjection of Nec1. Insets: lower crypt of arrhythmic (LL) mice showing fewer TUNEL + cells after Nec1 treatment. LD, rhythmic mice. F ) Quantification of TUNEL + cells in the lower crypt ( n > 8 per strain). G ) KC-specific ELISA with serum samples collected from rhythmic and arrhythmic mice. Mice underwent intraperitoneal injection of TNF-α, with or without coinjection of necrostatin 1 (Nec1; rhythmic, n = 3; arrhythmic, n = 6; rhythmic+TNF-α, n = 6; arrhythmic+TNF-α, n = 6; rhythmic+TNF-α+Nec1, n = 9; and arrhythmic+TNF-α+Nec1, n = 6). * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001.

Techniques Used: Mouse Assay, Western Blot, Real-time Polymerase Chain Reaction, TUNEL Assay, Injection, Enzyme-linked Immunosorbent Assay

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    Enzo Biochem necroptosis inhibitor necrostatin 1
    DAMP release and monocyte attraction occur during secondary necrosis upon irradiation in combination with HSP90i treatment. (A) Induction of cell death, THP-1 cell attraction, and DAMP release in HCT116 subclones with or without functional Bax and/or hyperactive Kras G 13 D . Parental HCT116 Kras +/ G 13 D Bax +/+ cells (upper row), HCT116 Kras +/ G 13 D Bax –/– cells (middle row), and HCT116 Kras +/– Bax +/+ cells (lower panel) were treated with 5 Gy plus 625 nM HSP90i or left untreated. At the indicated time points, induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration, ATP release) or means ± SD of triplicates of one representative experiment (HSP70 release) are shown. (B) Impact of different cell death inhibitors on apoptosis and necrosis induction, THP-1 cell attraction, and DAMP release in HCT116 cells upon treatment with radiotherapy and HSP90i. HCT116 cells were treated with 5 Gy plus 625 nM HSP90i in the presence of the poly-caspase inhibitor zVAD-fmk or the <t>necroptosis</t> inhibitor necrostatin-1, respectively (upper panel). Untreated cells served as controls (lower panel). Induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration) or means ± SD of triplicates of one representative experiment (release of HSP70 and ATP) are shown.
    Necroptosis Inhibitor Necrostatin 1, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/necroptosis inhibitor necrostatin 1/product/Enzo Biochem
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    necroptosis inhibitor necrostatin 1 - by Bioz Stars, 2022-10
    94/100 stars
      Buy from Supplier

    90
    Enzo Biochem necrostatin 1
    Autophagy prevents fragmented mtDNA-induced macrophage necroptosis. ( a ) Flow cytometric plots and analysis of cell death (AnnexinV-positive, 7-AAD-positive) in WT or LC3 −/− BMDM stimulated by 40 μ l/ml BCM for 24 h. ( b ) Western blot of whole-cell lysates showing RIPK1 phosphorylation (p-RIPK1) in WT or LC3 −/− BMDM stimulated by 40 μ l/ml BCM for 24 h. ( c ) Confocal microscopy images and analysis showing colocalization of RIPK1 (green) and RIPK3 (red) in WT or LC3 −/− BMDM treated with BCM (40 μ l/ml) or CIRP (10 μ g/ml) for 24 h. ( d ) Flow cytometric plots and analysis of cell death (AnnexinV-positive, 7-AAD-positive) in LC3 −/− BMDM treated with BCM (40 μ l/ml) or CIRP (10 μ g/ml) +/− 30 μ M <t>necrostatin-1</t> <t>(Nec-1)</t> for 24 h. All results are representative of three independent experiments. The graphs show the mean and S.E.M., n =3. Significances between groups were determined by using independent samples two-tailed Student’s t -test. * P
    Necrostatin 1, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/necrostatin 1/product/Enzo Biochem
    Average 90 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    necrostatin 1 - by Bioz Stars, 2022-10
    90/100 stars
      Buy from Supplier

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    DAMP release and monocyte attraction occur during secondary necrosis upon irradiation in combination with HSP90i treatment. (A) Induction of cell death, THP-1 cell attraction, and DAMP release in HCT116 subclones with or without functional Bax and/or hyperactive Kras G 13 D . Parental HCT116 Kras +/ G 13 D Bax +/+ cells (upper row), HCT116 Kras +/ G 13 D Bax –/– cells (middle row), and HCT116 Kras +/– Bax +/+ cells (lower panel) were treated with 5 Gy plus 625 nM HSP90i or left untreated. At the indicated time points, induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration, ATP release) or means ± SD of triplicates of one representative experiment (HSP70 release) are shown. (B) Impact of different cell death inhibitors on apoptosis and necrosis induction, THP-1 cell attraction, and DAMP release in HCT116 cells upon treatment with radiotherapy and HSP90i. HCT116 cells were treated with 5 Gy plus 625 nM HSP90i in the presence of the poly-caspase inhibitor zVAD-fmk or the necroptosis inhibitor necrostatin-1, respectively (upper panel). Untreated cells served as controls (lower panel). Induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration) or means ± SD of triplicates of one representative experiment (release of HSP70 and ATP) are shown.

    Journal: Frontiers in Oncology

    Article Title: Priming of Anti-tumor Immune Mechanisms by Radiotherapy Is Augmented by Inhibition of Heat Shock Protein 90

    doi: 10.3389/fonc.2020.01668

    Figure Lengend Snippet: DAMP release and monocyte attraction occur during secondary necrosis upon irradiation in combination with HSP90i treatment. (A) Induction of cell death, THP-1 cell attraction, and DAMP release in HCT116 subclones with or without functional Bax and/or hyperactive Kras G 13 D . Parental HCT116 Kras +/ G 13 D Bax +/+ cells (upper row), HCT116 Kras +/ G 13 D Bax –/– cells (middle row), and HCT116 Kras +/– Bax +/+ cells (lower panel) were treated with 5 Gy plus 625 nM HSP90i or left untreated. At the indicated time points, induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration, ATP release) or means ± SD of triplicates of one representative experiment (HSP70 release) are shown. (B) Impact of different cell death inhibitors on apoptosis and necrosis induction, THP-1 cell attraction, and DAMP release in HCT116 cells upon treatment with radiotherapy and HSP90i. HCT116 cells were treated with 5 Gy plus 625 nM HSP90i in the presence of the poly-caspase inhibitor zVAD-fmk or the necroptosis inhibitor necrostatin-1, respectively (upper panel). Untreated cells served as controls (lower panel). Induction of apoptosis (first column) and necrosis (second column), THP-1 cell transwell migration (third column), and release of HSP70 (fourth column) and ATP (last column) were measured as in Figure 1 . Data points of n = 3–5 independent experiments (apoptosis, necrosis, transwell migration) or means ± SD of triplicates of one representative experiment (release of HSP70 and ATP) are shown.

    Article Snippet: For analyses of secondary necrosis and necroptosis, the poly-caspase inhibitor zVAD-fmk (50 μM; Bachem, Bubendorf, Switzerland) or the necroptosis inhibitor necrostatin-1 (50 μM; Enzo Life Sciences, Loerrach, Germany) were used in addition to irradiation and HSP90i treatment.

    Techniques: Irradiation, Functional Assay, Migration

    RIP3-dependent necroptotic cell death is increased in arrhythmic mice.  A ) Western blot analysis for RIP3 production in intestinal biopsy samples from DSS- and TNF-α-treated mice. Biopsy samples from DSS-treated mice were taken from the colon, and samples from TNF-α-treated mice were taken from the ileum. β-Actin served as the loading control.  B ) Wee1 mRNA transcript levels were determined by qPCR, using colonic tissue samples from rhythmic ( n  = 5) or arrhythmic ( n  = 3) mice. Wee1 mRNA levels were normalized to β-actin mRNA levels.  C ) Rip3 mRNA transcript levels were evaluated by qPCR, using ileal tissue samples from rhythmic or arrhythmic mice treated with TNF-α or left untreated ( n  = 4 per strain and treatment). Rip3 mRNA levels were normalized to β-actin mRNA levels.  D ) Western blot for RIP3 with ileal biopsy samples. β-Actin served as a control.  E ) Representative images of TUNEL +  dying cells in ileal tissue after intraperitoneal injection of TNF-α, with or without coinjection of Nec1. Insets: lower crypt of arrhythmic (LL) mice showing fewer TUNEL +  cells after Nec1 treatment. LD, rhythmic mice.  F ) Quantification of TUNEL +  cells in the lower crypt ( n >  8 per strain).  G ) KC-specific ELISA with serum samples collected from rhythmic and arrhythmic mice. Mice underwent intraperitoneal injection of TNF-α, with or without coinjection of necrostatin 1 (Nec1; rhythmic,  n  = 3; arrhythmic,  n  = 6; rhythmic+TNF-α,  n  = 6; arrhythmic+TNF-α,  n  = 6; rhythmic+TNF-α+Nec1,  n  = 9; and arrhythmic+TNF-α+Nec1,  n  = 6). * P  ≤ 0.05, ** P  ≤ 0.01, *** P  ≤ 0.001.

    Journal: The FASEB Journal

    Article Title: Circadian rhythm disruption impairs tissue homeostasis and exacerbates chronic inflammation in the intestine

    doi: 10.1096/fj.201700141RR

    Figure Lengend Snippet: RIP3-dependent necroptotic cell death is increased in arrhythmic mice. A ) Western blot analysis for RIP3 production in intestinal biopsy samples from DSS- and TNF-α-treated mice. Biopsy samples from DSS-treated mice were taken from the colon, and samples from TNF-α-treated mice were taken from the ileum. β-Actin served as the loading control. B ) Wee1 mRNA transcript levels were determined by qPCR, using colonic tissue samples from rhythmic ( n = 5) or arrhythmic ( n = 3) mice. Wee1 mRNA levels were normalized to β-actin mRNA levels. C ) Rip3 mRNA transcript levels were evaluated by qPCR, using ileal tissue samples from rhythmic or arrhythmic mice treated with TNF-α or left untreated ( n = 4 per strain and treatment). Rip3 mRNA levels were normalized to β-actin mRNA levels. D ) Western blot for RIP3 with ileal biopsy samples. β-Actin served as a control. E ) Representative images of TUNEL + dying cells in ileal tissue after intraperitoneal injection of TNF-α, with or without coinjection of Nec1. Insets: lower crypt of arrhythmic (LL) mice showing fewer TUNEL + cells after Nec1 treatment. LD, rhythmic mice. F ) Quantification of TUNEL + cells in the lower crypt ( n > 8 per strain). G ) KC-specific ELISA with serum samples collected from rhythmic and arrhythmic mice. Mice underwent intraperitoneal injection of TNF-α, with or without coinjection of necrostatin 1 (Nec1; rhythmic, n = 3; arrhythmic, n = 6; rhythmic+TNF-α, n = 6; arrhythmic+TNF-α, n = 6; rhythmic+TNF-α+Nec1, n = 9; and arrhythmic+TNF-α+Nec1, n = 6). * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001.

    Article Snippet: Mice were either treated with recombinant murine TNF-α (ImmunoTools, Friesoythe, Germany; 200 ng/g body weight, i.p.) in the presence or absence of the necroptosis inhibitor necrostatin 1 (Nec-1; Enzo Life Sciences, Lörrach, Germany; intraperitoneal injection; 1.65 µg/g body weight) or were left untreated.

    Techniques: Mouse Assay, Western Blot, Real-time Polymerase Chain Reaction, TUNEL Assay, Injection, Enzyme-linked Immunosorbent Assay

    Autophagy prevents fragmented mtDNA-induced macrophage necroptosis. ( a ) Flow cytometric plots and analysis of cell death (AnnexinV-positive, 7-AAD-positive) in WT or LC3 −/− BMDM stimulated by 40 μ l/ml BCM for 24 h. ( b ) Western blot of whole-cell lysates showing RIPK1 phosphorylation (p-RIPK1) in WT or LC3 −/− BMDM stimulated by 40 μ l/ml BCM for 24 h. ( c ) Confocal microscopy images and analysis showing colocalization of RIPK1 (green) and RIPK3 (red) in WT or LC3 −/− BMDM treated with BCM (40 μ l/ml) or CIRP (10 μ g/ml) for 24 h. ( d ) Flow cytometric plots and analysis of cell death (AnnexinV-positive, 7-AAD-positive) in LC3 −/− BMDM treated with BCM (40 μ l/ml) or CIRP (10 μ g/ml) +/− 30 μ M necrostatin-1 (Nec-1) for 24 h. All results are representative of three independent experiments. The graphs show the mean and S.E.M., n =3. Significances between groups were determined by using independent samples two-tailed Student’s t -test. * P

    Journal: Cell Death & Disease

    Article Title: Cold-inducible RNA-binding protein through TLR4 signaling induces mitochondrial DNA fragmentation and regulates macrophage cell death after trauma

    doi: 10.1038/cddis.2017.187

    Figure Lengend Snippet: Autophagy prevents fragmented mtDNA-induced macrophage necroptosis. ( a ) Flow cytometric plots and analysis of cell death (AnnexinV-positive, 7-AAD-positive) in WT or LC3 −/− BMDM stimulated by 40 μ l/ml BCM for 24 h. ( b ) Western blot of whole-cell lysates showing RIPK1 phosphorylation (p-RIPK1) in WT or LC3 −/− BMDM stimulated by 40 μ l/ml BCM for 24 h. ( c ) Confocal microscopy images and analysis showing colocalization of RIPK1 (green) and RIPK3 (red) in WT or LC3 −/− BMDM treated with BCM (40 μ l/ml) or CIRP (10 μ g/ml) for 24 h. ( d ) Flow cytometric plots and analysis of cell death (AnnexinV-positive, 7-AAD-positive) in LC3 −/− BMDM treated with BCM (40 μ l/ml) or CIRP (10 μ g/ml) +/− 30 μ M necrostatin-1 (Nec-1) for 24 h. All results are representative of three independent experiments. The graphs show the mean and S.E.M., n =3. Significances between groups were determined by using independent samples two-tailed Student’s t -test. * P

    Article Snippet: Transfect reagents, Lipofectamine LTX Reagent with PLUS Reagent (15338100) was purchased from Thermo Fisher Scientific; siNC and siEndoG was purchased from Integrated DNA Technologies (Coralville, IA, USA); Necroptosis inhibitor Necrostatin-1 (BML-AP309-0020) was purchased from Enzo Life Sciences (Farmingdale, NY, USA).

    Techniques: Western Blot, Confocal Microscopy, Two Tailed Test