35-8200

antibody from Invitrogen Antibodies

Targeting: PTGS2 COX2

Provider product page for 35-8200

Western blot

ELISA

Immunocytochemistry

Immunohistochemistry

Other assay

Antibody data

Antibody Data
Antigen structure
References [33]
Comments [0]
Validations
Immunocytochemistry [1]
Other assay [14]

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Product number: 35-8200 - Provider product page
Provider: Invitrogen Antibodies
Product name: COX2 Monoclonal Antibody (COX 229)
Antibody type: Monoclonal
Antigen: Synthetic peptide
Reactivity: Human, Mouse
Host: Mouse
Isotype: IgG
Antibody clone number: COX 229
Vial size: 100 µg
Concentration: 0.5 mg/mL
Storage: -20°C

PTGS2 protein structure - 35-8200 shown in red.

Supportive validation

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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: NULL

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
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Experimental details: Figure 4 Fluorescent immunocytochemistry was performed on cytospun BAL-cells using monoclonal antibodies against COX-1, COX-2, 15-LOX-1 and PPARgamma coupled with secondary antibodies labeled with fluorescent dyes Alexa488 (green) and Cy5 (red). Nuclear counter-staining was performed using DAPI (blue). Representative micrographs from a healthy and an asthmatic individual are shown for both the control air (A) and subway air (B) exposures. Semi-quantitative evaluation of staining intensities was performed using ImageJ software [24] .

Supportive validation

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Experimental details: Figure 3 Analysis of IL-1 beta , COX-2, IL-6 and C3 expression in PC3 cells cocultured with hFOB1.19 cells. ( A ) The mRNA expression of the four osteoclastogenesis-related genes, IL-1 beta , COX-2, IL-6 and C3, in PC-3 cells following coculture under contact and bilayer conditions, was analysed using RT-PCR. Consistent with the cDNA microarray results, these genes were upregulated in contact cocultured PC-3 cells compared with bilayer cocultured cells. The primers used for RT-PCR are shown in Table 1 . ( B ) Measurement of IL-6 and IL-1 beta levels in PC-3 cells using ELISA. The level of IL-6 was significantly higher ( P

Supportive validation

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Experimental details: Figure 3 GRSF1 Is Required for Mitochondrial Gene Expression (A) Left panel, immunoblot analysis of 143B cells treated with control (Ctrl) or GRSF1 RNAi1. Right panel, immunoblot analysis of 143B cells infected with lentiviruses carrying an empty vector (pLKO) or a shRNA (RNAi2) against GRSF1. COX1 and COX2 are mitochondrially encoded proteins. SDHB and Tom20 are nuclear-encoded mitochondrial proteins. Actin is a nuclear-encoded cytosolic protein. (B) Acidification of the culture medium in GRSF1 RNAi1-treated 143B cells. The number of cells was the same in both conditions. Similar results were obtained in GRSF1 RNAi2-infected cells (data not shown). (C) NanoString analysis of 11 mitochondrially encoded ORFs in control (Ctrl) or GRSF1 RNAi1-treated 143B cells. RNA14 corresponds to bicistronic MTATP8 - MTATP6 RNA. Data are shown as mean +- SEM (n = 3). (D) NanoString analysis of GRSF1 in control (Ctrl) or GRSF1 RNAi1-treated 143B cells. Data are shown as mean +- SEM (n = 3). (E) NanoString analysis of 11 nuclear-encoded proteins in control (Ctrl) or GRSF1 RNAi1-treated 143B cells. Data are shown as mean +- SEM (n = 3). (F) Northern blot analysis of 12S and 16S rRNA in control (Ctrl) or GRSF1 RNAi1-treated cells. TUB, tubulin. (G) Phosphorimager quantification of (E). Data are shown as mean +- SEM (n = 3). (H) 35 S-labeling of mitochondrial translation of 143B cells infected with lentiviruses carrying an empty vector (pLKO) or a shRNA (RNAi2) against GRSF1. (I) Phosphorimager qu

Supportive validation

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Experimental details: Figure 3 Cyclooxygenase-2 (COX-2) mRNA expression ( A ) and protein production ( B, and C ). COX-2 mRNA expression was determined by RT-PCR ( A ), and COX-2 protein production was determined using Western blot ( B : representative immunoblot; C: protein expression calculated as Arbitrary Densitometric Units; A.D.U.) in the NCTC 2544 72 h after the addition of M. MeOH (50 ug/mL) with INF-gamma + H. * Significantly different than control; deg significantly different than INF-gamma/H-treated samples ( p < 0.05).

Supportive validation

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Experimental details: Fig. 1 Immunohistochemical staining demonstrates the intensity of COX-2 expression in the cytoplasm of follicular carcinoma cases. ( A ) score 0; ( B ) score 1; ( C ) score 2; ( D ) score 3 (x400).

Supportive validation

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Experimental details: Fig. 3 Loss of N-AS generation by Abeta reduces COX2 acetylation and SPMs production in neurons and microglia, except astrocyte. a The primary culture of neuron, microglia, and astrocyte was prepared from C57BL/6 mice, and N-AS were detected by LC-MS/MS in these cells. Representative chromatograms of N-AS and quantification in neuron, microglia, and astrocyte treated 10 muM Abeta or not ( n = 6 per group). b Western blotting for ac-S565 and total COX2 in neuron, microglia, and astrocyte treated 10 muM Abeta or not ( n = 6 per group). c Immunofluorescence images and quantification of neuron (NeuN, red), microglia (Iba1, red), or astrocyte (GFAP, red) with ac-S565 (green) and COX2 (blue) ( n = 6 per group, scale bars, 50 mum). d SphK activity in neuron and microglia treated 10 muM Abeta or not ( n = 6 per group). e Analysis of acetyl-CoA in neuron and microglia treated 10 muM Abeta or not using assay kit ( n = 6 per group). f Detection of sphingosine in neuron and microglia treated 10 muM Abeta or not using UPLC ( n = 6 per group). g Quantification of N-AS by LC-MS/MS in neuron and microglia treated 10 muM Abeta or not in presence of acetyl-CoA, sphingosine, or SphK1 each ( n = 6 per group). h Western blotting for ac-S565 in microglia and neuron treated 10 muM Abeta or not in presence of N-AS, acetyl-CoA, sphingosine, or SphK1 each ( n = 6 per group). i Quantification of 15R-LXA 4 , RvE1, and RvD1 using systematic LC-MS/MS in microglia and neuron treated 10 muM Abeta or not in

Supportive validation

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Experimental details: Fig. 2 Inhibition of CDH1 increases the susceptibility of HNC cells to ferroptosis inducers. ( A ) Immunoblotting of vimentin, ZEB1, GPX4, Nrf2, and E-cadherin with or without CDH1 silencing in HN4 cancer cells. Ctr, control; scr, scrambled. ( B - C ) Cell death was measured using PI staining, in HN4 with or without CDH1 gene silencing and exposure to 1 muM RSL3 or 0.5 mM sulfasalazine (SAS) treatment for 72 h. Original magnification, x 200. Scale bar, 50 mum. ( D ) Labile iron pool (LIP) was measured by calcein-AM (8 mug/ml) after 1 muM RSL3 or 0.5 mM SAS; all data were quantified by the Image J software. ( E , F ) Lipid and cytosolic ROS were measured using flow cytometry with staining BODIPY C11 and DCFDA, respectively, after 1 muM RSL3 or 0.5 mM SAS treatment, or cyst(e)ine deprivation for 24 h. ( G ) Immunoblotting of vimentin, ZEB1, GPX4, Nrf2, and E-cadherin with or without transfection of CDH1 overexpression or control vector. ( H ) Immunoblotting of 4-HNE, PTGS2, and CDH1 in HN6 cells with or without CDH1 overexpression. ( I - L ) PI staining, LIP assay, lipid peroxidation (BODIPY C11), and total ROS (DCFDA) measurements in HN6 cells transfected with or without CDH-1 overexpression and then exposure to 1 muM RSL3 or 0.5 mM SAS, or cyst(e)ine deprivation. Scale bar 50 mum. The error bars represent standard errors from three replicates. ** P < 0.01, *** P < 0.001 between the control and CDH1 overexpression. ( M - N ) Tumor volume, glutathione (GSH) content, and NAD/NAD

Supportive validation

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Experimental details: Fig. 3 ZEB-1 regulates ferroptosis sensitivity. ( A ) Immunoblotting of E-cadherin, vimentin, GPX4, Nrf2, and ZEB1 in HN6 cells with or without ZEB1 silencing. ( B - E ) Cell death, labile iron pool (LIP), lipid peroxidation, and total ROS assays were measured in HN6 cancer cells with or without ZEB1 gene silencing after 1 muM RSL3 or 0.5 mM SAS or cyst(e)ine deprivation. ( F ) Immunoblotting of E-cadherin, ZEB1, vimentin, Nrf2 and GPX4 in HN4 cells with or without ZEB1 overexpression. ( G ) Immunoblotting of 4-HNE, PTGS2, and ZEB1 in HN4 cells with or without ZEB1 overexpression. ( H - L ) Cell death, LIP, lipid peroxidation, and total ROS assays were also measured in HN4 cancer cells with or without ZEB1 overexpression after exposure to 1 muM RSL3 and 0.5 mM SAS. Original magnification, x 200. Scale bar, 50 mum. The error bars represent standard errors from three technical replicates. ** P < 0.01, *** P < 0.001 between the control and ZEB1 overexpression. ( M - N ) GSH content and NAD/NADH ratio were measured in HN3 and HN4 cells with ZEB1 overexpression or control vector. ( O - Q ) Tumor volume, GSH content, and NAD/NADH ratio were assessed in HN4 tumors with or without ZEB overexpression that were transplanted and grown in nude mice. * P < 0.05, ** P < 0.01, *** P < 0.001 between the vector control and ZEB1 overexpression or between the vehicle control and SAS treatment groups. Fig. 3

Supportive validation

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Experimental details: Fig. S4 CDH1 or ZEB1 regulation modulates the susceptibility to sulfasalazine in vivo . ( A - D ) Representative images, weights, and immunoblotting of tumors grown in mice with HN9 cells transfected with CDH1 overexpression or control vector. The mice were subjected to vehicle or SAS (250 mg/kg daily per intraperitoneal route) for 21 days. Immunoblotting was performed from tumors extracted at 21 days with the primary antibodies of vimentin, ZEB1, PTGS2, 4HNE, E-cadherin, GSH, and beta-actin. ( E - H ) Representative images, weights, and immunoblotting of tumors harvested in mice HN4 cells with or without ZEB1 overexpression or control vector. The mice were also subjected to SAS or vehicle for 21 days. * P < 0.05, * P < 0.01, *** P < 0.001 between the vector control and CDH1 or ZEB1 overexpression or between vehicle or SAS treatment. Fig. S4

Supportive validation

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Experimental details: Figure 2 Palmitate and IL-26 synergistically induced the production of inflammatory factors by HACs. Primary HACs were treated with 0.25 mM palmitate alone, 100 ng/mL of IL-26, or a combination of both for 24 h. Total protein was extracted, and inflammatory or extracellular matrix proteins (COX-2, IL-6, MMP-1, and COL-II) were quantified by Western blot analysis. Data are presented as the mean +- SD. Significant differences were detected between the control and palmitate and/or IL-26 groups ( n = 3).

Supportive validation

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Experimental details: Figure 5 HET0016 decreases lipid peroxidation level after ICH mice. Glutathione (GSH) (A) , malondialdehyde (MDA) (B) , and 4-hydroxy-2-nonenal (4-HNE) (C) content in brain 3 days after ICH. HET0016 reversed the ICH-induced reduction in GSH and increases in MDA and 4-HNE. n = 9 (A,C) or 5 (B) per group. (D) Brain tissue surrounding the hematoma was harvested 3 days after ICH, and total protein was extracted for western blotting. After ICH, cyclooxygenase-2 (COX-2) levels increased to a similar extent in the vehicle and HET0016 groups relative to that in the Sham group. n = 7/group. * P < 0.05, ** P < 0.01 vs. Vehicle group. Mann-Whitney U -test (B) or unpaired t -test (A,C,D) was applied. Data are expressed as median with confidence interval (B) or mean +- SD (A,C,D) .