Review

antibodies anti cebpb (Proteintech)

Proteintech is a verified supplier

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Proteintech antibodies anti cebpb

<t>CEBPB</t> regulates gastric plasticity through its global enhancer-binding function. <t>(A)</t> <t>H3K27ac</t> modification levels, chromosomal accessibility (defined by ATAC-seq signals), and the number of CEBPB-binding sites across the genome in the NCI-N87 ( n = 2). (B) CEBPB Cut&Tag, H3K27ac Cut&Tag, and ATAC-seq peak signal levels flanking ±5 kb of the CEBPB binding sites (indicated by the black box) in NCI-N87 ( n = 2). (C) Venn diagrams showing the overlap between putative enhancers and CEBPB binding sites. (D) Gene set enrichment analysis of malignant and nonmalignant cell clusters using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (E) Gene set enrichment analysis of transcriptome profiles of GC cell lines derived from GCLM (red) and primary GC tissues (blue) using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (F) Gene set enrichment analysis of transcriptome profiles of CTCs using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (G to I) Expression levels of liver-specific genes ( SLC27A5 , F12 , and DECR2 ) in malignant and nonmalignant cells (G), CTCs (H), and GC cell lines (I). (J) ATAC-seq, H3K27ac Cut&Tag, and CEBPB Cut&Tag signal levels, along with putative enhancer and CEBPB binding regions, in the gene regions of SLC27A5 , F12 , and DECR2 in NCI-N87 ( n = 2). Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: ATAC-seq, assay for transposase-accessible chromatin using sequencing; CEBPB, CCAAT enhancer-binding protein beta; CPM, counts per million; Cut&Tag, cleavage under targets and tagmentation; CTC, circulating tumor cell; CTC-LM, CTC associated with liver metastasis; CTC-N, CTC not associated with liver metastasis; DECR2, 2,4-dienoyl-CoA reductase 2; F12, coagulation factor XII; GC, gastric cancer; GCLM, gastric cancer liver metastasis; Mag, malignant; Rep, replicate; SLC27A5, solute carrier family 27 member 5; TPM, transcripts per million.

Antibodies Anti Cebpb, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 76 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cebpb/CEBPB+Antibody/pmc12981248-191-7-11
Average 95 stars, based on 76 article reviews

antibodies anti cebpb - by Bioz Stars, 2026-10

95/100 stars

Images

1) Product Images from "CEBPB-Regulated Gastric Cell Plasticity Promotes Liver Metastasis of Gastric Cancer"

Article Title: CEBPB-Regulated Gastric Cell Plasticity Promotes Liver Metastasis of Gastric Cancer

Journal: Cancer Communications

doi: 10.34133/cancomm.0016

CEBPB regulates gastric plasticity through its global enhancer-binding function. (A) H3K27ac modification levels, chromosomal accessibility (defined by ATAC-seq signals), and the number of CEBPB-binding sites across the genome in the NCI-N87 ( n = 2). (B) CEBPB Cut&Tag, H3K27ac Cut&Tag, and ATAC-seq peak signal levels flanking ±5 kb of the CEBPB binding sites (indicated by the black box) in NCI-N87 ( n = 2). (C) Venn diagrams showing the overlap between putative enhancers and CEBPB binding sites. (D) Gene set enrichment analysis of malignant and nonmalignant cell clusters using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (E) Gene set enrichment analysis of transcriptome profiles of GC cell lines derived from GCLM (red) and primary GC tissues (blue) using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (F) Gene set enrichment analysis of transcriptome profiles of CTCs using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (G to I) Expression levels of liver-specific genes ( SLC27A5 , F12 , and DECR2 ) in malignant and nonmalignant cells (G), CTCs (H), and GC cell lines (I). (J) ATAC-seq, H3K27ac Cut&Tag, and CEBPB Cut&Tag signal levels, along with putative enhancer and CEBPB binding regions, in the gene regions of SLC27A5 , F12 , and DECR2 in NCI-N87 ( n = 2). Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: ATAC-seq, assay for transposase-accessible chromatin using sequencing; CEBPB, CCAAT enhancer-binding protein beta; CPM, counts per million; Cut&Tag, cleavage under targets and tagmentation; CTC, circulating tumor cell; CTC-LM, CTC associated with liver metastasis; CTC-N, CTC not associated with liver metastasis; DECR2, 2,4-dienoyl-CoA reductase 2; F12, coagulation factor XII; GC, gastric cancer; GCLM, gastric cancer liver metastasis; Mag, malignant; Rep, replicate; SLC27A5, solute carrier family 27 member 5; TPM, transcripts per million.

Figure Legend Snippet: CEBPB regulates gastric plasticity through its global enhancer-binding function. (A) H3K27ac modification levels, chromosomal accessibility (defined by ATAC-seq signals), and the number of CEBPB-binding sites across the genome in the NCI-N87 ( n = 2). (B) CEBPB Cut&Tag, H3K27ac Cut&Tag, and ATAC-seq peak signal levels flanking ±5 kb of the CEBPB binding sites (indicated by the black box) in NCI-N87 ( n = 2). (C) Venn diagrams showing the overlap between putative enhancers and CEBPB binding sites. (D) Gene set enrichment analysis of malignant and nonmalignant cell clusters using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (E) Gene set enrichment analysis of transcriptome profiles of GC cell lines derived from GCLM (red) and primary GC tissues (blue) using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (F) Gene set enrichment analysis of transcriptome profiles of CTCs using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (G to I) Expression levels of liver-specific genes ( SLC27A5 , F12 , and DECR2 ) in malignant and nonmalignant cells (G), CTCs (H), and GC cell lines (I). (J) ATAC-seq, H3K27ac Cut&Tag, and CEBPB Cut&Tag signal levels, along with putative enhancer and CEBPB binding regions, in the gene regions of SLC27A5 , F12 , and DECR2 in NCI-N87 ( n = 2). Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: ATAC-seq, assay for transposase-accessible chromatin using sequencing; CEBPB, CCAAT enhancer-binding protein beta; CPM, counts per million; Cut&Tag, cleavage under targets and tagmentation; CTC, circulating tumor cell; CTC-LM, CTC associated with liver metastasis; CTC-N, CTC not associated with liver metastasis; DECR2, 2,4-dienoyl-CoA reductase 2; F12, coagulation factor XII; GC, gastric cancer; GCLM, gastric cancer liver metastasis; Mag, malignant; Rep, replicate; SLC27A5, solute carrier family 27 member 5; TPM, transcripts per million.

Techniques Used: Binding Assay, Modification, Derivative Assay, Expressing, Sequencing, Coagulation

Cebpb-regulated gastric plasticity evades CD8 + T cell surveillance by CD155–TIGIT interaction in vivo. (A) Schematic of in vivo mouse experiments to determine the immune-regulatory role of Cebpb ( n = 5 for each group). The healthy control group denoted the group without cancer cell transplantation, and the NC group denoted the group transplanted with MFC. (B) Tumor volume of liver metastases inferred from in vivo bioluminescence imaging results performed every 7 days from day 3 to day 50 (left) since cell transplantation, and liver metastases visualized using a bioluminescence imaging system on day 50 (right). (C) Representative H&E staining and immunohistochemistry results for Cebpb in liver metastasis tissues from the control group, MFC Cebpb-OE group, and Cebpb-OE plus anti-TIGIT mAbs treatment group. Arrows denote the representative areas of GC liver metastasis within the hepatic tissue. (D) Levels of IFN-γ, TNF-α, and the proportion of CD8 + T cells and NK cells among CD45 + immune cells in the healthy control group (green), MFC control group (gray), Cebpb-OE group (red), and Cebpb-OE plus anti-TIGIT mAbs treatment group (blue). (E) Multiplex immunofluorescence showing CD8 (green), IFN-γ (red), and nuclei (blue) in the MFC control group, Cebpb-OE group, and Cebpb-OE plus anti-TIGIT mAbs treatment group. Data were presented as the mean ± standard deviation. Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: Cebpb, CCAAT enhancer binding protein beta; H&E, hematoxylin and eosin; IFN-γ, interferon-gamma; mAb, monoclonal antibody; NC, negative control; OE, overexpression; TNF-α, tumor necrosis factor alpha; TIGIT, T cell immunoreceptor with Ig and ITIM domains.

Figure Legend Snippet: Cebpb-regulated gastric plasticity evades CD8 + T cell surveillance by CD155–TIGIT interaction in vivo. (A) Schematic of in vivo mouse experiments to determine the immune-regulatory role of Cebpb ( n = 5 for each group). The healthy control group denoted the group without cancer cell transplantation, and the NC group denoted the group transplanted with MFC. (B) Tumor volume of liver metastases inferred from in vivo bioluminescence imaging results performed every 7 days from day 3 to day 50 (left) since cell transplantation, and liver metastases visualized using a bioluminescence imaging system on day 50 (right). (C) Representative H&E staining and immunohistochemistry results for Cebpb in liver metastasis tissues from the control group, MFC Cebpb-OE group, and Cebpb-OE plus anti-TIGIT mAbs treatment group. Arrows denote the representative areas of GC liver metastasis within the hepatic tissue. (D) Levels of IFN-γ, TNF-α, and the proportion of CD8 + T cells and NK cells among CD45 + immune cells in the healthy control group (green), MFC control group (gray), Cebpb-OE group (red), and Cebpb-OE plus anti-TIGIT mAbs treatment group (blue). (E) Multiplex immunofluorescence showing CD8 (green), IFN-γ (red), and nuclei (blue) in the MFC control group, Cebpb-OE group, and Cebpb-OE plus anti-TIGIT mAbs treatment group. Data were presented as the mean ± standard deviation. Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: Cebpb, CCAAT enhancer binding protein beta; H&E, hematoxylin and eosin; IFN-γ, interferon-gamma; mAb, monoclonal antibody; NC, negative control; OE, overexpression; TNF-α, tumor necrosis factor alpha; TIGIT, T cell immunoreceptor with Ig and ITIM domains.

Techniques Used: In Vivo, Control, Transplantation Assay, Imaging, Staining, Immunohistochemistry, Multiplex Assay, Immunofluorescence, Standard Deviation, Binding Assay, Negative Control, Over Expression

Incubation:

Article Title: Dynamic remodelling of epithelial plasticity in colorectal cancer from single-cell and spatially resolved perspectives
Article Snippet: .. Sections were then sequentially incubated with primary antibodies against S100A4 (1:500, Proteintech, 16105–1-AP), CEBPB (1:500, Proteintech, 83791–6-RR), and ARGLU1 (1:500, Proteintech, 28155–1-AP), PanCK (1:400, ZSGB, ZM0069, 1:200), FOSL1(Proteintech, Ag25788), followed by species-matched secondary antibodies. ..

Article Title: Targeted Inhibition of CD74 + Macrophages by Luteolin via CEBPB/P65 Signaling Ameliorates Osteoarthritis Progression
Article Snippet: .. After blocking, the membranes were incubated overnight at 4 °C with primary antibodies targeting CD74 (1:1000, Servicebio, GB115427 , China), MMP13 (1:1000, Servicebio, GB11247‐1, China), iNOS (1:1000, Servicebio, GB125703 , China), CEBPB (1:1000, Proteintech, 23431‐1‐AP, China), P65 (1:1000, CST, 8242, USA), COL2A1 (1:1000, Abcam, ab34712, USA), and IL6 (1:000, CST, 12912, USA). ..

Article Title: Dynamic remodelling of epithelial plasticity in colorectal cancer from single-cell and spatially resolved perspectives.
Article Snippet: .. Sections were then sequentially incubated with primary antibodies against S100A4 (1:500, Proteintech, 16105–1-AP), CEBPB (1:500, Proteintech, 83791–6-RR), and ARGLU1 (1:500, Proteintech, 28155–1-AP), PanCK (1:400, ZSGB, ZM0069, 1:200), FOSL1(Proteintech, Ag25788), followed by speciesmatched secondary antibodies. ..

Blocking Assay:

other:

Article Title: Identification of monomethylsulochrin as a novel agent to ameliorate DSS-induced ulcerative colitis through dual modulation of the IL-17/TNF pathway and gut microbiota.
Article Snippet: Novel therapeutic agents with improved safety and efficacy are urgently required for ulcerative colitis (UC), a refractory inflammatory bowel disease.. Mangrove-derived natural products represent a promising reservoir for drug discovery.. Monomethylsulochrin (MMSC) is a type II polyketide isolated from the endophytic fungus Aspergillus fumigatus of the mangrove plant Aegiceras corniculatum.

Immunoprecipitation:

Article Title: Super enhancer-driven LINC01013 mediates hypoxia-induced mitochondrial dysfunction by HSPA9 to determine pulmonary arterial smooth muscle cell fate
Article Snippet: .. Antibodies against H3K27ac (A7253, 1:100, ABclonal, Wuhan, China), H3K4me1 (A2355, 1:100, ABclonal, Wuhan, China), CEBPB (18311-1-AP, 1:150, Proteintech, IL, USA) and normal rabbit IgG were used for immunoprecipitation. ..

Western Blot:

Article Title: Corticosterone reprograms splenic responses to avian pathogenic Escherichia coli infection in broiler chickens
Article Snippet: .. Western blot analysis of RAB7A (Starter Biotechnology Co., Ltd., S0B0791, Hangzhou, China), ATP6V0D1 (ABclonal Biotechnology Co., Ltd., A4271, Wuhan, China), CSF3R (ABclonal Biotechnology Co., Ltd., A7661, Wuhan, China), and CEBPB (Proteintech Group, Inc., 23431-1-AP, Wuhan, China) was conducted following the manufaturer’s instruction. .. Tubulin-α (Bioworld Technology, Inc., BS1699, Minnesota, USA) was employed as the internal control.

Image Search Results

C/EBP-β is downregulated in sorafenib-resistant hepatocellular carcinoma cells. ( A ) The inhibition ratio (%) of parental (HepG2, Huh7) and sorafenib-resistant (HepG2-R, Huh7-R) HCC cells was measured by CCK-8 assay after treatment with a gradient of sorafenib concentrations for 48 h. The calculated IC 50 values are indicated on the dose-response curves. Data are presented as mean ± SD (n=3). ( B ) The relative mRNA and protein expression levels of C/EBP-β in parental and sorafenib-resistant cell lines were determined by RT-qPCR (bar graphs) and Western blot (gel images), respectively. GAPDH was used as an internal control. Data in the bar graphs are presented as mean ± SD from three independent experiments. ** P < 0.01 compared to the corresponding parental cells.

Journal: Journal of Hepatocellular Carcinoma

Article Title: C/EBP-β Mediates the Reversal of Sorafenib Resistance by Tunicamycin in Hepatocellular Carcinoma

doi: 10.2147/JHC.S587037

Figure Lengend Snippet: C/EBP-β is downregulated in sorafenib-resistant hepatocellular carcinoma cells. ( A ) The inhibition ratio (%) of parental (HepG2, Huh7) and sorafenib-resistant (HepG2-R, Huh7-R) HCC cells was measured by CCK-8 assay after treatment with a gradient of sorafenib concentrations for 48 h. The calculated IC 50 values are indicated on the dose-response curves. Data are presented as mean ± SD (n=3). ( B ) The relative mRNA and protein expression levels of C/EBP-β in parental and sorafenib-resistant cell lines were determined by RT-qPCR (bar graphs) and Western blot (gel images), respectively. GAPDH was used as an internal control. Data in the bar graphs are presented as mean ± SD from three independent experiments. ** P < 0.01 compared to the corresponding parental cells.

Article Snippet: The following primary antibodies were used for Western blot and immunohistochemistry: C/EBP-β (A0711, Abclonal, China), p53 (ET1601-13, HUABIO, China), Bax (ET1603-34, HUABIO, China), Bcl-2 (ET1702-53, HUABIO, China), Cleaved Caspase-3 (ET1602-47, HUABIO, China), GAPDH (K200102M, Solarbio, China), and Ki-67 (PT0321R, Immunoway, China).

Techniques: Inhibition, CCK-8 Assay, Expressing, Quantitative RT-PCR, Western Blot, Control

Tunicamycin (TM) reverses sorafenib resistance by upregulating C/EBP-β. ( A ) Western blot analysis of C/EBP-β protein levels in parental Huh7 and resistant Huh7-R cells treated with increasing concentrations of TM (0, 2, 4, 8 μM) for 48 h. ( B ) RT-qPCR analysis of relative C/EBP-β mRNA levels in cells treated as in ( A ). ( C ) Cell viability of Huh7-R cells was measured by CCK-8 assay. Cells were treated with 8 μM sorafenib alone or in combination with TM (2, 4, 8 μM) for the indicated durations. Parental Huh7 cells treated with 8 μM sorafenib served as a sensitive control. ( D ) Clonogenic potential of cells treated as in ( C ). Representative images (left) and quantification (right) are shown. ( E ) Western blot validation of C/EBP-β overexpression (C/EBP-β-oe) and knockdown (shC/EBP-β) in Huh7-R cells under various treatment conditions. ( F ) Cell viability (CCK-8) of genetically modified or unmodified Huh7-R cells treated with sorafenib (8 μM) with or without TM (4 μM) for 48 h. ( G ) Cell viability (CCK-8) of HepG2-R cells treated as in ( F ). ( H ) Clonogenic potential of Huh7-R cells treated as in ( F ). ( I ) Clonogenic potential of HepG2-R cells treated as in ( F ). The “+” and “-” signs indicate the presence or absence of the specified treatment, respectively. All quantitative data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared between indicated groups.

Journal: Journal of Hepatocellular Carcinoma

Article Title: C/EBP-β Mediates the Reversal of Sorafenib Resistance by Tunicamycin in Hepatocellular Carcinoma

doi: 10.2147/JHC.S587037

Figure Lengend Snippet: Tunicamycin (TM) reverses sorafenib resistance by upregulating C/EBP-β. ( A ) Western blot analysis of C/EBP-β protein levels in parental Huh7 and resistant Huh7-R cells treated with increasing concentrations of TM (0, 2, 4, 8 μM) for 48 h. ( B ) RT-qPCR analysis of relative C/EBP-β mRNA levels in cells treated as in ( A ). ( C ) Cell viability of Huh7-R cells was measured by CCK-8 assay. Cells were treated with 8 μM sorafenib alone or in combination with TM (2, 4, 8 μM) for the indicated durations. Parental Huh7 cells treated with 8 μM sorafenib served as a sensitive control. ( D ) Clonogenic potential of cells treated as in ( C ). Representative images (left) and quantification (right) are shown. ( E ) Western blot validation of C/EBP-β overexpression (C/EBP-β-oe) and knockdown (shC/EBP-β) in Huh7-R cells under various treatment conditions. ( F ) Cell viability (CCK-8) of genetically modified or unmodified Huh7-R cells treated with sorafenib (8 μM) with or without TM (4 μM) for 48 h. ( G ) Cell viability (CCK-8) of HepG2-R cells treated as in ( F ). ( H ) Clonogenic potential of Huh7-R cells treated as in ( F ). ( I ) Clonogenic potential of HepG2-R cells treated as in ( F ). The “+” and “-” signs indicate the presence or absence of the specified treatment, respectively. All quantitative data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared between indicated groups.

Techniques: Western Blot, Quantitative RT-PCR, CCK-8 Assay, Control, Biomarker Discovery, Over Expression, Knockdown, Genetically Modified

TM and C/EBP-β overexpression cooperatively suppress sorafenib-resistant tumor growth in vivo. Nude mice were treated with sorafenib (15 mg/kg/day) alone (control), sorafenib plus tunicamycin (TM, 0.04 mg/kg/day), sorafenib plus C/EBP-β overexpression (C/EBP-β-oe), or a combination of sorafenib, TM, and C/EBP-β-oe. ( A – D ) Subcutaneous xenograft model using Huh7-R cells. ( A ) Representative images of excised tumors from each treatment group on day 38. ( B ) Tumor growth curves measured over a 38-day treatment period. Data are presented as mean ± SD (n=6 mice per group). **P< 0.01 and ***P< 0.001 compared with the sorafenib-only group. ## P< 0.01 compared between indicated groups. ( C ) H&E staining of tumor sections showing tumor morphology and cell density. Scale bars, 50 μm. ( D ) Immunohistochemical staining for C/EBP-β and proliferation marker Ki-67 in tumor tissues. Scale bars, 50 μm. ( E and F ) Orthotopic xenograft model of Huh7-R cells. ( E ) Representative images of the liver illustrating intrahepatic tumor burden at the experimental endpoint. ( F ) Representative H&E staining of liver sections from the orthotopic model, with insets providing magnified views of tumor foci. Scale bars: 100 μm (main) and 50 μm (inset). The “+” and “-” signs indicate the presence or absence of the specified treatment, respectively.

Journal: Journal of Hepatocellular Carcinoma

Article Title: C/EBP-β Mediates the Reversal of Sorafenib Resistance by Tunicamycin in Hepatocellular Carcinoma

doi: 10.2147/JHC.S587037

Figure Lengend Snippet: TM and C/EBP-β overexpression cooperatively suppress sorafenib-resistant tumor growth in vivo. Nude mice were treated with sorafenib (15 mg/kg/day) alone (control), sorafenib plus tunicamycin (TM, 0.04 mg/kg/day), sorafenib plus C/EBP-β overexpression (C/EBP-β-oe), or a combination of sorafenib, TM, and C/EBP-β-oe. ( A – D ) Subcutaneous xenograft model using Huh7-R cells. ( A ) Representative images of excised tumors from each treatment group on day 38. ( B ) Tumor growth curves measured over a 38-day treatment period. Data are presented as mean ± SD (n=6 mice per group). **P< 0.01 and ***P< 0.001 compared with the sorafenib-only group. ## P< 0.01 compared between indicated groups. ( C ) H&E staining of tumor sections showing tumor morphology and cell density. Scale bars, 50 μm. ( D ) Immunohistochemical staining for C/EBP-β and proliferation marker Ki-67 in tumor tissues. Scale bars, 50 μm. ( E and F ) Orthotopic xenograft model of Huh7-R cells. ( E ) Representative images of the liver illustrating intrahepatic tumor burden at the experimental endpoint. ( F ) Representative H&E staining of liver sections from the orthotopic model, with insets providing magnified views of tumor foci. Scale bars: 100 μm (main) and 50 μm (inset). The “+” and “-” signs indicate the presence or absence of the specified treatment, respectively.

Techniques: Over Expression, In Vivo, Control, Staining, Immunohistochemical staining, Marker

The C/EBP-β axis overcomes sorafenib resistance by inducing ROS production and apoptosis in Huh7-R cells. Huh7-R cells were treated for 48 h with sorafenib (8 μM) alone or in combination with C/EBP-β overexpression (C/EBP-β-oe), tunicamycin (TM, 4 μM), TM plus shC/EBP-β, or TM plus NAC (5 mM). Hydrogen peroxide (H 2 O 2 , 2 mM) was included as a positive control for ROS generation. ( A ) Intracellular ROS levels were detected using DCFDA staining and visualized using fluorescence microscopy. Scale bar, 200 μm. ( B ) Quantification of the relative fluorescence intensity from ( A ). ( C ) Apoptosis was detected using the TUNEL assay, with TUNEL-positive nuclei stained green and all nuclei counterstained with DAPI (blue). Scale bar, 100 μm. ( D ) Percentage of TUNEL-positive cells from ( C ). ( E ) Western blot analysis of C/EBP-β, p53, Bax, Bcl-2, and cleaved caspase-3 protein levels. GAPDH was used as an internal control. The “+” and “-” signs indicate the presence or absence of the specified treatment, respectively. All quantitative data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared between indicated groups.

Journal: Journal of Hepatocellular Carcinoma

Article Title: C/EBP-β Mediates the Reversal of Sorafenib Resistance by Tunicamycin in Hepatocellular Carcinoma

doi: 10.2147/JHC.S587037

Figure Lengend Snippet: The C/EBP-β axis overcomes sorafenib resistance by inducing ROS production and apoptosis in Huh7-R cells. Huh7-R cells were treated for 48 h with sorafenib (8 μM) alone or in combination with C/EBP-β overexpression (C/EBP-β-oe), tunicamycin (TM, 4 μM), TM plus shC/EBP-β, or TM plus NAC (5 mM). Hydrogen peroxide (H 2 O 2 , 2 mM) was included as a positive control for ROS generation. ( A ) Intracellular ROS levels were detected using DCFDA staining and visualized using fluorescence microscopy. Scale bar, 200 μm. ( B ) Quantification of the relative fluorescence intensity from ( A ). ( C ) Apoptosis was detected using the TUNEL assay, with TUNEL-positive nuclei stained green and all nuclei counterstained with DAPI (blue). Scale bar, 100 μm. ( D ) Percentage of TUNEL-positive cells from ( C ). ( E ) Western blot analysis of C/EBP-β, p53, Bax, Bcl-2, and cleaved caspase-3 protein levels. GAPDH was used as an internal control. The “+” and “-” signs indicate the presence or absence of the specified treatment, respectively. All quantitative data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01, and *** P < 0.001 compared between indicated groups.

Techniques: Over Expression, Positive Control, Staining, Fluorescence, Microscopy, TUNEL Assay, Western Blot, Control

Integrated bioinformatic analyses define the C/EBP-β-dependent transcriptomic mechanism of tunicamycin in HCC. ( A ) Representative Gene Set Enrichment Analysis (GSEA) plots from the TCGA-LIHC dataset showing positive enrichment of apoptosis (TWEAK signaling) and ER stress (ATF4 activation) pathways in tumors with high C/EBP-β expression. ( B ) Venn diagram illustrating the identification of 185 intersecting genes between potential Tunicamycin (TM) targets (from SwissTarget, Pharmmapper, and DrugBank) and known hepatocellular carcinoma (HCC) disease genes (from GeneCards and OMIM). ( C ) GO (Biological Process) and KEGG pathway enrichment analysis of the 185 intersecting genes identified in (B). The bubble plot displays top enriched terms, with bubble size corresponding to gene count and color intensity reflecting the adjusted P -value. ( D ) GO enrichment analysis (Biological Process) of the 13 core genes at the intersection of TM’s potential targets and C/EBP-β-regulated differentially expressed genes. The bar chart highlights “intrinsic apoptotic signaling pathway in response to ER stress” and “multiple cell differentiation-related pathways” as the key convergent mechanisms.

Journal: Journal of Hepatocellular Carcinoma

Article Title: C/EBP-β Mediates the Reversal of Sorafenib Resistance by Tunicamycin in Hepatocellular Carcinoma

doi: 10.2147/JHC.S587037

Figure Lengend Snippet: Integrated bioinformatic analyses define the C/EBP-β-dependent transcriptomic mechanism of tunicamycin in HCC. ( A ) Representative Gene Set Enrichment Analysis (GSEA) plots from the TCGA-LIHC dataset showing positive enrichment of apoptosis (TWEAK signaling) and ER stress (ATF4 activation) pathways in tumors with high C/EBP-β expression. ( B ) Venn diagram illustrating the identification of 185 intersecting genes between potential Tunicamycin (TM) targets (from SwissTarget, Pharmmapper, and DrugBank) and known hepatocellular carcinoma (HCC) disease genes (from GeneCards and OMIM). ( C ) GO (Biological Process) and KEGG pathway enrichment analysis of the 185 intersecting genes identified in (B). The bubble plot displays top enriched terms, with bubble size corresponding to gene count and color intensity reflecting the adjusted P -value. ( D ) GO enrichment analysis (Biological Process) of the 13 core genes at the intersection of TM’s potential targets and C/EBP-β-regulated differentially expressed genes. The bar chart highlights “intrinsic apoptotic signaling pathway in response to ER stress” and “multiple cell differentiation-related pathways” as the key convergent mechanisms.

Techniques: Activation Assay, Expressing, Cell Differentiation

Journal: Cancer Communications

Article Title: CEBPB-Regulated Gastric Cell Plasticity Promotes Liver Metastasis of Gastric Cancer

doi: 10.34133/cancomm.0016

Figure Lengend Snippet: CEBPB regulates gastric plasticity through its global enhancer-binding function. (A) H3K27ac modification levels, chromosomal accessibility (defined by ATAC-seq signals), and the number of CEBPB-binding sites across the genome in the NCI-N87 ( n = 2). (B) CEBPB Cut&Tag, H3K27ac Cut&Tag, and ATAC-seq peak signal levels flanking ±5 kb of the CEBPB binding sites (indicated by the black box) in NCI-N87 ( n = 2). (C) Venn diagrams showing the overlap between putative enhancers and CEBPB binding sites. (D) Gene set enrichment analysis of malignant and nonmalignant cell clusters using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (E) Gene set enrichment analysis of transcriptome profiles of GC cell lines derived from GCLM (red) and primary GC tissues (blue) using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (F) Gene set enrichment analysis of transcriptome profiles of CTCs using the top 200 most active CEBPB-binding enhancer genes derived from NCI-N87 H3K27ac Cut&Tag data. (G to I) Expression levels of liver-specific genes ( SLC27A5 , F12 , and DECR2 ) in malignant and nonmalignant cells (G), CTCs (H), and GC cell lines (I). (J) ATAC-seq, H3K27ac Cut&Tag, and CEBPB Cut&Tag signal levels, along with putative enhancer and CEBPB binding regions, in the gene regions of SLC27A5 , F12 , and DECR2 in NCI-N87 ( n = 2). Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: ATAC-seq, assay for transposase-accessible chromatin using sequencing; CEBPB, CCAAT enhancer-binding protein beta; CPM, counts per million; Cut&Tag, cleavage under targets and tagmentation; CTC, circulating tumor cell; CTC-LM, CTC associated with liver metastasis; CTC-N, CTC not associated with liver metastasis; DECR2, 2,4-dienoyl-CoA reductase 2; F12, coagulation factor XII; GC, gastric cancer; GCLM, gastric cancer liver metastasis; Mag, malignant; Rep, replicate; SLC27A5, solute carrier family 27 member 5; TPM, transcripts per million.

Article Snippet: The cells were incubated overnight with primary antibodies anti-CEBPB (Cat. #23431-1-AP, Proteintech), anti-H3K27ac (Cat. #13-0059, EpiCypher), and IgG negative control (Cat. #13-0047, EpiCypher).

Techniques: Binding Assay, Modification, Derivative Assay, Expressing, Sequencing, Coagulation

Journal: Cancer Communications

Article Title: CEBPB-Regulated Gastric Cell Plasticity Promotes Liver Metastasis of Gastric Cancer

doi: 10.34133/cancomm.0016

Figure Lengend Snippet: Cebpb-regulated gastric plasticity evades CD8 + T cell surveillance by CD155–TIGIT interaction in vivo. (A) Schematic of in vivo mouse experiments to determine the immune-regulatory role of Cebpb ( n = 5 for each group). The healthy control group denoted the group without cancer cell transplantation, and the NC group denoted the group transplanted with MFC. (B) Tumor volume of liver metastases inferred from in vivo bioluminescence imaging results performed every 7 days from day 3 to day 50 (left) since cell transplantation, and liver metastases visualized using a bioluminescence imaging system on day 50 (right). (C) Representative H&E staining and immunohistochemistry results for Cebpb in liver metastasis tissues from the control group, MFC Cebpb-OE group, and Cebpb-OE plus anti-TIGIT mAbs treatment group. Arrows denote the representative areas of GC liver metastasis within the hepatic tissue. (D) Levels of IFN-γ, TNF-α, and the proportion of CD8 + T cells and NK cells among CD45 + immune cells in the healthy control group (green), MFC control group (gray), Cebpb-OE group (red), and Cebpb-OE plus anti-TIGIT mAbs treatment group (blue). (E) Multiplex immunofluorescence showing CD8 (green), IFN-γ (red), and nuclei (blue) in the MFC control group, Cebpb-OE group, and Cebpb-OE plus anti-TIGIT mAbs treatment group. Data were presented as the mean ± standard deviation. Statistical significance, * P < 0.05, ** P < 0.01, *** P < 0.001. Abbreviations: Cebpb, CCAAT enhancer binding protein beta; H&E, hematoxylin and eosin; IFN-γ, interferon-gamma; mAb, monoclonal antibody; NC, negative control; OE, overexpression; TNF-α, tumor necrosis factor alpha; TIGIT, T cell immunoreceptor with Ig and ITIM domains.

Techniques: In Vivo, Control, Transplantation Assay, Imaging, Staining, Immunohistochemistry, Multiplex Assay, Immunofluorescence, Standard Deviation, Binding Assay, Negative Control, Over Expression

Review

antibodies anti cebpb (Proteintech)

Structured Review

Images

1) Product Images from "CEBPB-Regulated Gastric Cell Plasticity Promotes Liver Metastasis of Gastric Cancer"

Related Articles

Incubation:

Blocking Assay:

other:

Immunoprecipitation:

Western Blot:

Similar Products

Image Search Results