ceacam1 (Abcam)

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Abcam ceacam1

The relationship between DcR3 and <t>CEACAM1.</t> A. Cellular component analysis showed that 8 plasma membrane proteins were correlated with DcR3. B. TCGA database showed that CEACAM1 and CDH11 were upregulated in pancreatic cancer tissues (n=179) compared with control (n=171) (***P<0.001) while TNFRSF10B showed no significant difference between the two groups (P>0.05). Mann-Whitney test was used to analyze the differences between groups, data were presented as the median with range. C. Western blot assays showed changes in the levels of CEACAM1 and CDH11 in DcR3 knockdown or DcR3-overexpressing cells. D. DcR3 TPM was associated with CEACAM1 TPM (*P=0.037) but not with CDH11 (P=0.27) in TCGA database. E. ChIP assay showed PCR products targeting P1-P2 of the CEACAM1 promoter. Specific anti-IRF1 or control normal mouse IgG was used for immunoprecipitations, whereas genomic DNA was used as the input control. F. Luciferase assay showed that IRF1 could bind to the two CEACAM1 promoter sites. G. Western blot was used to examine the expression of DcR3 and CEACAM1 after manipulating IRF1 expression. The data were represented as the mean ± S.D. of three independent experiments in vitro. Significant differences are indicated as follows: *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001.

Ceacam1, supplied by Abcam, used in various techniques. Bioz Stars score: 99/100, based on 2153 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/spatial+transcriptomics+cell-type+deconvolution/pmc06943350-77-5-19?v=Abcam
Average 99 stars, based on 2153 article reviews

ceacam1 - by Bioz Stars, 2026-08

99/100 stars

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1) Product Images from "DcR3 promotes proliferation and invasion of pancreatic cancer via a DcR3/STAT1/IRF1 feedback loop"

Article Title: DcR3 promotes proliferation and invasion of pancreatic cancer via a DcR3/STAT1/IRF1 feedback loop

Journal: American Journal of Cancer Research

doi:

The relationship between DcR3 and CEACAM1. A. Cellular component analysis showed that 8 plasma membrane proteins were correlated with DcR3. B. TCGA database showed that CEACAM1 and CDH11 were upregulated in pancreatic cancer tissues (n=179) compared with control (n=171) (***P<0.001) while TNFRSF10B showed no significant difference between the two groups (P>0.05). Mann-Whitney test was used to analyze the differences between groups, data were presented as the median with range. C. Western blot assays showed changes in the levels of CEACAM1 and CDH11 in DcR3 knockdown or DcR3-overexpressing cells. D. DcR3 TPM was associated with CEACAM1 TPM (*P=0.037) but not with CDH11 (P=0.27) in TCGA database. E. ChIP assay showed PCR products targeting P1-P2 of the CEACAM1 promoter. Specific anti-IRF1 or control normal mouse IgG was used for immunoprecipitations, whereas genomic DNA was used as the input control. F. Luciferase assay showed that IRF1 could bind to the two CEACAM1 promoter sites. G. Western blot was used to examine the expression of DcR3 and CEACAM1 after manipulating IRF1 expression. The data were represented as the mean ± S.D. of three independent experiments in vitro. Significant differences are indicated as follows: *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001.

Figure Legend Snippet: The relationship between DcR3 and CEACAM1. A. Cellular component analysis showed that 8 plasma membrane proteins were correlated with DcR3. B. TCGA database showed that CEACAM1 and CDH11 were upregulated in pancreatic cancer tissues (n=179) compared with control (n=171) (***P<0.001) while TNFRSF10B showed no significant difference between the two groups (P>0.05). Mann-Whitney test was used to analyze the differences between groups, data were presented as the median with range. C. Western blot assays showed changes in the levels of CEACAM1 and CDH11 in DcR3 knockdown or DcR3-overexpressing cells. D. DcR3 TPM was associated with CEACAM1 TPM (*P=0.037) but not with CDH11 (P=0.27) in TCGA database. E. ChIP assay showed PCR products targeting P1-P2 of the CEACAM1 promoter. Specific anti-IRF1 or control normal mouse IgG was used for immunoprecipitations, whereas genomic DNA was used as the input control. F. Luciferase assay showed that IRF1 could bind to the two CEACAM1 promoter sites. G. Western blot was used to examine the expression of DcR3 and CEACAM1 after manipulating IRF1 expression. The data were represented as the mean ± S.D. of three independent experiments in vitro. Significant differences are indicated as follows: *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001.

Techniques Used: MANN-WHITNEY, Western Blot, Luciferase, Expressing, In Vitro

Relationship between DcR3/STAT1/IRF1 and CEACAM1 in pancreatic cancer tissues. A. IHC for p-STAT1, IRF1 and CEACAM1 was performed between DcR3 negative group (left panel) and DcR3 positive group (right panel) in 64 pancreatic cancer tissue samples. Representative cases show stains of the same cohorts of pancreatic cancer sections. Magnification ×100. B-D. Correlation analysis of the expression of DcR3 with that of p-STAT1 (r=0.3904, **P=0.0014), IRF1 (r=0.2998, *P=0.0161) and CEACAM1 (r=0.3523, **P=0.0043). E. Schematic illustration showing that DcR3/STAT1/IRF1 forms a feedback loop to reinforce DcR3 and CEACAM1 expression.

Figure Legend Snippet: Relationship between DcR3/STAT1/IRF1 and CEACAM1 in pancreatic cancer tissues. A. IHC for p-STAT1, IRF1 and CEACAM1 was performed between DcR3 negative group (left panel) and DcR3 positive group (right panel) in 64 pancreatic cancer tissue samples. Representative cases show stains of the same cohorts of pancreatic cancer sections. Magnification ×100. B-D. Correlation analysis of the expression of DcR3 with that of p-STAT1 (r=0.3904, **P=0.0014), IRF1 (r=0.2998, *P=0.0161) and CEACAM1 (r=0.3523, **P=0.0043). E. Schematic illustration showing that DcR3/STAT1/IRF1 forms a feedback loop to reinforce DcR3 and CEACAM1 expression.

Techniques Used: Expressing

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ceacam1 (Abcam)

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