rabbit twist1 Search Results


95
Cell Signaling Technology Inc rabbit anti twist antibody
Patient and disease characteristics and <t> TWIST </t> levels in CD34 + cells
Rabbit Anti Twist Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti twist antibody/product/Cell Signaling Technology Inc
Average 95 stars, based on 1 article reviews
rabbit anti twist antibody - by Bioz Stars, 2026-03
95/100 stars
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95
Cell Signaling Technology Inc twist1
Reagents used for western blot staining of cells.
Twist1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/twist1/product/Cell Signaling Technology Inc
Average 95 stars, based on 1 article reviews
twist1 - by Bioz Stars, 2026-03
95/100 stars
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94
Cell Signaling Technology Inc anti twist1 antibody
E. coli stimulation alters TLR, NF-κB and EndMT pathways and promotes migration in LSECs. ( A ) PCA analysis showing different gene expression signatures between TMNK1 treated with PBS and with E coli . ( B ) KEGG enrichment analysis showing the pathway related to TLR and NF-κB in RNA sequencing data set. ( C ) Representative image showing immunocyfluorescence (ICC) staining for CD31 and α-SMA in primary LSECs of NAFLD mice with PBS and E coli . ( D ) Representative image showing ICC staining for CD31 and <t>TWIST1</t> in primary LSECs of NAFLD mice with PBS and E coli . ( E ) Representative image showing ICC staining for CD31 and TLR5 in primary LSECs of NAFLD mice with PBS and E coli. ( F ) Representative image showing ICC staining for CD31 and E-cadherin in primary LSECs of NAFLD mice with PBS and E coli . ( G ) Wound healing test showing the mitigation of TMNK1 treated with flagellin and TH1020. Statistical chart is on the right side. CD31 ( green ) was the marker of LSECs.
Anti Twist1 Antibody, supplied by Cell Signaling Technology Inc, 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/anti twist1 antibody/product/Cell Signaling Technology Inc
Average 94 stars, based on 1 article reviews
anti twist1 antibody - by Bioz Stars, 2026-03
94/100 stars
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92
Cusabio anti snail
E. coli stimulation alters TLR, NF-κB and EndMT pathways and promotes migration in LSECs. ( A ) PCA analysis showing different gene expression signatures between TMNK1 treated with PBS and with E coli . ( B ) KEGG enrichment analysis showing the pathway related to TLR and NF-κB in RNA sequencing data set. ( C ) Representative image showing immunocyfluorescence (ICC) staining for CD31 and α-SMA in primary LSECs of NAFLD mice with PBS and E coli . ( D ) Representative image showing ICC staining for CD31 and <t>TWIST1</t> in primary LSECs of NAFLD mice with PBS and E coli . ( E ) Representative image showing ICC staining for CD31 and TLR5 in primary LSECs of NAFLD mice with PBS and E coli. ( F ) Representative image showing ICC staining for CD31 and E-cadherin in primary LSECs of NAFLD mice with PBS and E coli . ( G ) Wound healing test showing the mitigation of TMNK1 treated with flagellin and TH1020. Statistical chart is on the right side. CD31 ( green ) was the marker of LSECs.
Anti Snail, supplied by Cusabio, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti snail/product/Cusabio
Average 92 stars, based on 1 article reviews
anti snail - by Bioz Stars, 2026-03
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91
Bio-Rad rabbit anti twist
E. coli stimulation alters TLR, NF-κB and EndMT pathways and promotes migration in LSECs. ( A ) PCA analysis showing different gene expression signatures between TMNK1 treated with PBS and with E coli . ( B ) KEGG enrichment analysis showing the pathway related to TLR and NF-κB in RNA sequencing data set. ( C ) Representative image showing immunocyfluorescence (ICC) staining for CD31 and α-SMA in primary LSECs of NAFLD mice with PBS and E coli . ( D ) Representative image showing ICC staining for CD31 and <t>TWIST1</t> in primary LSECs of NAFLD mice with PBS and E coli . ( E ) Representative image showing ICC staining for CD31 and TLR5 in primary LSECs of NAFLD mice with PBS and E coli. ( F ) Representative image showing ICC staining for CD31 and E-cadherin in primary LSECs of NAFLD mice with PBS and E coli . ( G ) Wound healing test showing the mitigation of TMNK1 treated with flagellin and TH1020. Statistical chart is on the right side. CD31 ( green ) was the marker of LSECs.
Rabbit Anti Twist, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti twist/product/Bio-Rad
Average 91 stars, based on 1 article reviews
rabbit anti twist - by Bioz Stars, 2026-03
91/100 stars
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90
Signalway Antibody twist1 antibody
E. coli stimulation alters TLR, NF-κB and EndMT pathways and promotes migration in LSECs. ( A ) PCA analysis showing different gene expression signatures between TMNK1 treated with PBS and with E coli . ( B ) KEGG enrichment analysis showing the pathway related to TLR and NF-κB in RNA sequencing data set. ( C ) Representative image showing immunocyfluorescence (ICC) staining for CD31 and α-SMA in primary LSECs of NAFLD mice with PBS and E coli . ( D ) Representative image showing ICC staining for CD31 and <t>TWIST1</t> in primary LSECs of NAFLD mice with PBS and E coli . ( E ) Representative image showing ICC staining for CD31 and TLR5 in primary LSECs of NAFLD mice with PBS and E coli. ( F ) Representative image showing ICC staining for CD31 and E-cadherin in primary LSECs of NAFLD mice with PBS and E coli . ( G ) Wound healing test showing the mitigation of TMNK1 treated with flagellin and TH1020. Statistical chart is on the right side. CD31 ( green ) was the marker of LSECs.
Twist1 Antibody, supplied by Signalway Antibody, 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/twist1 antibody/product/Signalway Antibody
Average 90 stars, based on 1 article reviews
twist1 antibody - by Bioz Stars, 2026-03
90/100 stars
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90
OriGene twist (twist1) rabbit polyclonal antibody
E. coli stimulation alters TLR, NF-κB and EndMT pathways and promotes migration in LSECs. ( A ) PCA analysis showing different gene expression signatures between TMNK1 treated with PBS and with E coli . ( B ) KEGG enrichment analysis showing the pathway related to TLR and NF-κB in RNA sequencing data set. ( C ) Representative image showing immunocyfluorescence (ICC) staining for CD31 and α-SMA in primary LSECs of NAFLD mice with PBS and E coli . ( D ) Representative image showing ICC staining for CD31 and <t>TWIST1</t> in primary LSECs of NAFLD mice with PBS and E coli . ( E ) Representative image showing ICC staining for CD31 and TLR5 in primary LSECs of NAFLD mice with PBS and E coli. ( F ) Representative image showing ICC staining for CD31 and E-cadherin in primary LSECs of NAFLD mice with PBS and E coli . ( G ) Wound healing test showing the mitigation of TMNK1 treated with flagellin and TH1020. Statistical chart is on the right side. CD31 ( green ) was the marker of LSECs.
Twist (Twist1) Rabbit Polyclonal Antibody, supplied by OriGene, 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/twist (twist1) rabbit polyclonal antibody/product/OriGene
Average 90 stars, based on 1 article reviews
twist (twist1) rabbit polyclonal antibody - by Bioz Stars, 2026-03
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Image Search Results


Patient and disease characteristics and  TWIST  levels in CD34 + cells

Journal: Blood

Article Title: The helix-loop-helix transcription factor TWIST is dysregulated in myelodysplastic syndromes

doi: 10.1182/blood-2009-09-242313

Figure Lengend Snippet: Patient and disease characteristics and TWIST levels in CD34 + cells

Article Snippet: The membranes were blocked in 5% nonfat dry milk diluted in Tris-buffered saline containing 0.1% Tween-20 (TBS-T) for 1 hour at room temperature and then incubated overnight at 4°C in 5% nonfat dry milk /TBS-T containing either rabbit anti-P53 antibody (1:1000; Cell Signaling Technology Inc), rabbit anti-TWIST antibody (1:1000; Cell Signaling Inc), rabbit anti– intercellular adhesion molecule-1 (ICAM1) antibody (1:1000; Cell Signaling Inc) or rabbit anti-PYCARD antibody (1:1000; Sigma).

Techniques: Expressing

Expression of TWIST in patients with MDS and in healthy donors. (A) Stroma cells. mRNA levels were determined by quantitative real-time PCR. TWIST levels were lower in MDS than in healthy controls (see text). (B) CD34+ cells. Samples from 56 patients with MDS and from 17 healthy donors were analyzed. TWIST mRNA levels were significantly higher in patients with advanced MDS (P < .001). Shown are the means and SEM. The gel shows actual mRNA levels in 14 patients with MDS and 5 healthy controls. (C) TWIST levels in patients with MDS and healthy donors. Relative mRNA levels of TWIST were significantly higher in patients with low-grade (P < .001) and advanced MDS (P < .001) than in healthy donors. (D) Ratio of relative TWIST and p53 levels in patients with MDS and healthy donors. The ratio of TWIST to p53 mRNA differed significantly between cells from healthy donors and cells from patients with low-grade (P < .001) and advanced MDS (P < .001), respectively. Horizontal lines indicate median values.

Journal: Blood

Article Title: The helix-loop-helix transcription factor TWIST is dysregulated in myelodysplastic syndromes

doi: 10.1182/blood-2009-09-242313

Figure Lengend Snippet: Expression of TWIST in patients with MDS and in healthy donors. (A) Stroma cells. mRNA levels were determined by quantitative real-time PCR. TWIST levels were lower in MDS than in healthy controls (see text). (B) CD34+ cells. Samples from 56 patients with MDS and from 17 healthy donors were analyzed. TWIST mRNA levels were significantly higher in patients with advanced MDS (P < .001). Shown are the means and SEM. The gel shows actual mRNA levels in 14 patients with MDS and 5 healthy controls. (C) TWIST levels in patients with MDS and healthy donors. Relative mRNA levels of TWIST were significantly higher in patients with low-grade (P < .001) and advanced MDS (P < .001) than in healthy donors. (D) Ratio of relative TWIST and p53 levels in patients with MDS and healthy donors. The ratio of TWIST to p53 mRNA differed significantly between cells from healthy donors and cells from patients with low-grade (P < .001) and advanced MDS (P < .001), respectively. Horizontal lines indicate median values.

Article Snippet: The membranes were blocked in 5% nonfat dry milk diluted in Tris-buffered saline containing 0.1% Tween-20 (TBS-T) for 1 hour at room temperature and then incubated overnight at 4°C in 5% nonfat dry milk /TBS-T containing either rabbit anti-P53 antibody (1:1000; Cell Signaling Technology Inc), rabbit anti-TWIST antibody (1:1000; Cell Signaling Inc), rabbit anti– intercellular adhesion molecule-1 (ICAM1) antibody (1:1000; Cell Signaling Inc) or rabbit anti-PYCARD antibody (1:1000; Sigma).

Techniques: Expressing, Real-time Polymerase Chain Reaction

TWIST expression and interactions with p53 in primary CD34+ marrow cells and myeloid cell lines. (A) Primary CD34+ marrow cells from healthy donors and patients with MDS. Healthy CD34+cells (control) cultured without stroma (Not-CC) or with stroma contact (CC) showed no change in the expression of p53 or TWIST. In cells from patients with MDS, p53 showed prominent up-regulation on stroma contact (CC), whereas levels of TWIST declined. (B) Immunoprecipitation (IP) of TWIST from KG1a, MDS-L, HL-60, and PL-21 cell lysates. p53 was contained in the complex precipitated from all myeloid cell lines by anti-TWIST antibody; DJ-1 served as positive (+) and Stro-1 as negative (−) control. (C) IP as in panel B, but using KG1a cells without and with coculture, normalizing for TWIST content in the cell lysate. IgG indicates immunoglobulin G.

Journal: Blood

Article Title: The helix-loop-helix transcription factor TWIST is dysregulated in myelodysplastic syndromes

doi: 10.1182/blood-2009-09-242313

Figure Lengend Snippet: TWIST expression and interactions with p53 in primary CD34+ marrow cells and myeloid cell lines. (A) Primary CD34+ marrow cells from healthy donors and patients with MDS. Healthy CD34+cells (control) cultured without stroma (Not-CC) or with stroma contact (CC) showed no change in the expression of p53 or TWIST. In cells from patients with MDS, p53 showed prominent up-regulation on stroma contact (CC), whereas levels of TWIST declined. (B) Immunoprecipitation (IP) of TWIST from KG1a, MDS-L, HL-60, and PL-21 cell lysates. p53 was contained in the complex precipitated from all myeloid cell lines by anti-TWIST antibody; DJ-1 served as positive (+) and Stro-1 as negative (−) control. (C) IP as in panel B, but using KG1a cells without and with coculture, normalizing for TWIST content in the cell lysate. IgG indicates immunoglobulin G.

Article Snippet: The membranes were blocked in 5% nonfat dry milk diluted in Tris-buffered saline containing 0.1% Tween-20 (TBS-T) for 1 hour at room temperature and then incubated overnight at 4°C in 5% nonfat dry milk /TBS-T containing either rabbit anti-P53 antibody (1:1000; Cell Signaling Technology Inc), rabbit anti-TWIST antibody (1:1000; Cell Signaling Inc), rabbit anti– intercellular adhesion molecule-1 (ICAM1) antibody (1:1000; Cell Signaling Inc) or rabbit anti-PYCARD antibody (1:1000; Sigma).

Techniques: Expressing, Control, Cell Culture, Immunoprecipitation, Negative Control

Inhibition of TWIST in KG1a cells and its effect on apoptosis. Early stage apoptosis (annexin V+, propidium iodide−) in KG1a and PL-21 cell lines transfected with either a scrambled siRNA sequence (SCR) or siRNA specific for TWIST (siTWIST), and exposed overnight to normal medium (veh) versus exogenous TNFα (25 ng/mL, A) or TRAIL (100 ng/mL, B), respectively. Apoptosis was determined by flow cytometry. (C) Cell preparation as in panels A and B, but cultured in normal medium (veh) or in the presence of the soluble TNF receptor etanercept (10 μg/mL for 24 hours [concentration based on ancillary studies]). Error bars indicate SEM. (D) Protein lysates from the same cell preparations were separated on 4% to 12% Bis-Tris gels and immunoblotted with antibodies against TWIST, p53-ser46, Bax, and caspase 9, respectively. β-Actin served as loading control. (E) TWIST and p53 levels in primary CD34+ MDS cells in which TWIST was silenced by specific siRNA (KD TWIST) compared with levels in unmodified cells from the same primary CD34+ MDS sample.

Journal: Blood

Article Title: The helix-loop-helix transcription factor TWIST is dysregulated in myelodysplastic syndromes

doi: 10.1182/blood-2009-09-242313

Figure Lengend Snippet: Inhibition of TWIST in KG1a cells and its effect on apoptosis. Early stage apoptosis (annexin V+, propidium iodide−) in KG1a and PL-21 cell lines transfected with either a scrambled siRNA sequence (SCR) or siRNA specific for TWIST (siTWIST), and exposed overnight to normal medium (veh) versus exogenous TNFα (25 ng/mL, A) or TRAIL (100 ng/mL, B), respectively. Apoptosis was determined by flow cytometry. (C) Cell preparation as in panels A and B, but cultured in normal medium (veh) or in the presence of the soluble TNF receptor etanercept (10 μg/mL for 24 hours [concentration based on ancillary studies]). Error bars indicate SEM. (D) Protein lysates from the same cell preparations were separated on 4% to 12% Bis-Tris gels and immunoblotted with antibodies against TWIST, p53-ser46, Bax, and caspase 9, respectively. β-Actin served as loading control. (E) TWIST and p53 levels in primary CD34+ MDS cells in which TWIST was silenced by specific siRNA (KD TWIST) compared with levels in unmodified cells from the same primary CD34+ MDS sample.

Article Snippet: The membranes were blocked in 5% nonfat dry milk diluted in Tris-buffered saline containing 0.1% Tween-20 (TBS-T) for 1 hour at room temperature and then incubated overnight at 4°C in 5% nonfat dry milk /TBS-T containing either rabbit anti-P53 antibody (1:1000; Cell Signaling Technology Inc), rabbit anti-TWIST antibody (1:1000; Cell Signaling Inc), rabbit anti– intercellular adhesion molecule-1 (ICAM1) antibody (1:1000; Cell Signaling Inc) or rabbit anti-PYCARD antibody (1:1000; Sigma).

Techniques: Inhibition, Transfection, Sequencing, Flow Cytometry, Cell Culture, Concentration Assay, Control

TWIST and p53 expression and apoptosis in primary CD34+ cells. (A) Apoptosis in CD34+ marrow cells from healthy normal bone marrow donors (NBM) and patients with MDS cocultured with either unmodified HS5 stroma or HS5 with suppression of TWIST by siRNA (KD TWIST). Apoptosis was determined by flow cytometry. Error bars indicate SEM. (B) Levels of TWIST and p53 mRNA in CD34+ cells from healthy donors (NBM) and patients with MDS cocultured with either unmodified HS5 stroma (WT) or HS5 stroma with inhibition of TWIST (KD TWIST).

Journal: Blood

Article Title: The helix-loop-helix transcription factor TWIST is dysregulated in myelodysplastic syndromes

doi: 10.1182/blood-2009-09-242313

Figure Lengend Snippet: TWIST and p53 expression and apoptosis in primary CD34+ cells. (A) Apoptosis in CD34+ marrow cells from healthy normal bone marrow donors (NBM) and patients with MDS cocultured with either unmodified HS5 stroma or HS5 with suppression of TWIST by siRNA (KD TWIST). Apoptosis was determined by flow cytometry. Error bars indicate SEM. (B) Levels of TWIST and p53 mRNA in CD34+ cells from healthy donors (NBM) and patients with MDS cocultured with either unmodified HS5 stroma (WT) or HS5 stroma with inhibition of TWIST (KD TWIST).

Article Snippet: The membranes were blocked in 5% nonfat dry milk diluted in Tris-buffered saline containing 0.1% Tween-20 (TBS-T) for 1 hour at room temperature and then incubated overnight at 4°C in 5% nonfat dry milk /TBS-T containing either rabbit anti-P53 antibody (1:1000; Cell Signaling Technology Inc), rabbit anti-TWIST antibody (1:1000; Cell Signaling Inc), rabbit anti– intercellular adhesion molecule-1 (ICAM1) antibody (1:1000; Cell Signaling Inc) or rabbit anti-PYCARD antibody (1:1000; Sigma).

Techniques: Expressing, Flow Cytometry, Inhibition

Inhibition of TWIST and ICAM1 (CD54) expression in HS5 cells. (A) FACS analysis of ICAM1 expression in HS5 cells transfected with scrambled siRNA (SCR) or TWIST-specific siRNA (KD TWIST). The cells were stained with FITC conjugated anti–human CD54 antibody (AB) for 30 minutes (a indicates isotype control; b, HS5 transfected with scrambled siRNA sequences; c, HS5 transfected with TWIST-specific siRNA.) (B) Western blot of TWIST and ICAM1 proteins in HS5 cells transfected with scrambled siRNA (SCR) or with 1 of 3 TWIST-specific siRNAs (KD TWIST in HS5). β-Actin served as loading control. (C) IACM1 expression in primary MDS stroma cells; a indicates normal bone marrow stroma labeled with isotype control antibody; b, normal bone marrow stroma labeled with CD54+-allophycocyanin flow antibody; c1, patients with RA MDS; c2, patients with RAEB-2 MDS. (D) Early stage apoptosis (annexin V+/propidium iodide−) in KG1a cells in control cultures containing unmodified HS5 cells (WT) or HS5 cells pretreated with either 5 or 10 μg of anti-ICAM1 antibody. Cells were cultured in the absence or presence of TNFα (25 ng/mL). Apoptosis was determined by flow cytometry. Only CD45+ (KG1a) cells were considered. (E) Early-stage apoptosis in PL-21 and KG1a cells cultured with either unmodified stroma or stroma pretreated with anti-IACM1 antibody, and apoptosis in PL-21 or KG1a cells treated with anti-CD11b antibody. Error bars indicate SEM.

Journal: Blood

Article Title: The helix-loop-helix transcription factor TWIST is dysregulated in myelodysplastic syndromes

doi: 10.1182/blood-2009-09-242313

Figure Lengend Snippet: Inhibition of TWIST and ICAM1 (CD54) expression in HS5 cells. (A) FACS analysis of ICAM1 expression in HS5 cells transfected with scrambled siRNA (SCR) or TWIST-specific siRNA (KD TWIST). The cells were stained with FITC conjugated anti–human CD54 antibody (AB) for 30 minutes (a indicates isotype control; b, HS5 transfected with scrambled siRNA sequences; c, HS5 transfected with TWIST-specific siRNA.) (B) Western blot of TWIST and ICAM1 proteins in HS5 cells transfected with scrambled siRNA (SCR) or with 1 of 3 TWIST-specific siRNAs (KD TWIST in HS5). β-Actin served as loading control. (C) IACM1 expression in primary MDS stroma cells; a indicates normal bone marrow stroma labeled with isotype control antibody; b, normal bone marrow stroma labeled with CD54+-allophycocyanin flow antibody; c1, patients with RA MDS; c2, patients with RAEB-2 MDS. (D) Early stage apoptosis (annexin V+/propidium iodide−) in KG1a cells in control cultures containing unmodified HS5 cells (WT) or HS5 cells pretreated with either 5 or 10 μg of anti-ICAM1 antibody. Cells were cultured in the absence or presence of TNFα (25 ng/mL). Apoptosis was determined by flow cytometry. Only CD45+ (KG1a) cells were considered. (E) Early-stage apoptosis in PL-21 and KG1a cells cultured with either unmodified stroma or stroma pretreated with anti-IACM1 antibody, and apoptosis in PL-21 or KG1a cells treated with anti-CD11b antibody. Error bars indicate SEM.

Article Snippet: The membranes were blocked in 5% nonfat dry milk diluted in Tris-buffered saline containing 0.1% Tween-20 (TBS-T) for 1 hour at room temperature and then incubated overnight at 4°C in 5% nonfat dry milk /TBS-T containing either rabbit anti-P53 antibody (1:1000; Cell Signaling Technology Inc), rabbit anti-TWIST antibody (1:1000; Cell Signaling Inc), rabbit anti– intercellular adhesion molecule-1 (ICAM1) antibody (1:1000; Cell Signaling Inc) or rabbit anti-PYCARD antibody (1:1000; Sigma).

Techniques: Inhibition, Expressing, Transfection, Staining, Control, Western Blot, Labeling, Cell Culture, Flow Cytometry

Reagents used for western blot staining of cells.

Journal: Oncology Reports

Article Title: Unravelling heterogeneous effects of cancer‑associated fibroblasts on poor prognosis markers in breast cancer EM‑G3 cell line: In vitro ‑targeted treatment (anti‑IL-6, anti‑VEGF-A, anti‑MFGE8) based on transcriptomic profiling

doi: 10.3892/or.2023.8662

Figure Lengend Snippet: Reagents used for western blot staining of cells.

Article Snippet: TWIST1 , Rabbit , IgG , Monoclonal , 1:1,000 , 69366 , Cell Signaling Technology, Inc..

Techniques: Western Blot, Staining, Produced

Western blot analysis of EM-G3 cells. Protein expression analysis in indirect (CM) co-culture of EM-G3 cells with HDFs, BCCFs, SCCFs and BCMFs. The studied conditions for each studied fibroblast type included: Control culture of EM-G3 cells, EM-G3 cells cultured in CM derived from respective fibroblasts, EM-G3 cells cultured in CM enriched with neutralizing antibodies against either IL-6 or VEGF-A or MFGE8 or combination of all three tested antibodies (anti-IL-6 + anti-VEGF-A + anti-MFGE8). The expression profile of the following markers related to cell differentiation and epithelial-to-mesenchymal transition was evaluated: keratin-8, keratin-14, keratin-18, keratin-19, vimentin, SLUG, SNAIL, TWIST1, ZEB1, E-cadherin, N-cadherin, VE-cadherin. β-Actin was used as sample loading control (representative beta-actin controls are shown). HDFs, human dermal fibroblasts; BCCFs, basal cell carcinoma fibroblasts; SCCFs, squamous cell carcinoma fibroblasts; BCMFs, breast cancer metastasis fibroblasts; CM, conditioned media.

Journal: Oncology Reports

Article Title: Unravelling heterogeneous effects of cancer‑associated fibroblasts on poor prognosis markers in breast cancer EM‑G3 cell line: In vitro ‑targeted treatment (anti‑IL-6, anti‑VEGF-A, anti‑MFGE8) based on transcriptomic profiling

doi: 10.3892/or.2023.8662

Figure Lengend Snippet: Western blot analysis of EM-G3 cells. Protein expression analysis in indirect (CM) co-culture of EM-G3 cells with HDFs, BCCFs, SCCFs and BCMFs. The studied conditions for each studied fibroblast type included: Control culture of EM-G3 cells, EM-G3 cells cultured in CM derived from respective fibroblasts, EM-G3 cells cultured in CM enriched with neutralizing antibodies against either IL-6 or VEGF-A or MFGE8 or combination of all three tested antibodies (anti-IL-6 + anti-VEGF-A + anti-MFGE8). The expression profile of the following markers related to cell differentiation and epithelial-to-mesenchymal transition was evaluated: keratin-8, keratin-14, keratin-18, keratin-19, vimentin, SLUG, SNAIL, TWIST1, ZEB1, E-cadherin, N-cadherin, VE-cadherin. β-Actin was used as sample loading control (representative beta-actin controls are shown). HDFs, human dermal fibroblasts; BCCFs, basal cell carcinoma fibroblasts; SCCFs, squamous cell carcinoma fibroblasts; BCMFs, breast cancer metastasis fibroblasts; CM, conditioned media.

Article Snippet: TWIST1 , Rabbit , IgG , Monoclonal , 1:1,000 , 69366 , Cell Signaling Technology, Inc..

Techniques: Western Blot, Expressing, Co-Culture Assay, Control, Cell Culture, Derivative Assay, Cell Differentiation

E. coli stimulation alters TLR, NF-κB and EndMT pathways and promotes migration in LSECs. ( A ) PCA analysis showing different gene expression signatures between TMNK1 treated with PBS and with E coli . ( B ) KEGG enrichment analysis showing the pathway related to TLR and NF-κB in RNA sequencing data set. ( C ) Representative image showing immunocyfluorescence (ICC) staining for CD31 and α-SMA in primary LSECs of NAFLD mice with PBS and E coli . ( D ) Representative image showing ICC staining for CD31 and TWIST1 in primary LSECs of NAFLD mice with PBS and E coli . ( E ) Representative image showing ICC staining for CD31 and TLR5 in primary LSECs of NAFLD mice with PBS and E coli. ( F ) Representative image showing ICC staining for CD31 and E-cadherin in primary LSECs of NAFLD mice with PBS and E coli . ( G ) Wound healing test showing the mitigation of TMNK1 treated with flagellin and TH1020. Statistical chart is on the right side. CD31 ( green ) was the marker of LSECs.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: E. coli stimulation alters TLR, NF-κB and EndMT pathways and promotes migration in LSECs. ( A ) PCA analysis showing different gene expression signatures between TMNK1 treated with PBS and with E coli . ( B ) KEGG enrichment analysis showing the pathway related to TLR and NF-κB in RNA sequencing data set. ( C ) Representative image showing immunocyfluorescence (ICC) staining for CD31 and α-SMA in primary LSECs of NAFLD mice with PBS and E coli . ( D ) Representative image showing ICC staining for CD31 and TWIST1 in primary LSECs of NAFLD mice with PBS and E coli . ( E ) Representative image showing ICC staining for CD31 and TLR5 in primary LSECs of NAFLD mice with PBS and E coli. ( F ) Representative image showing ICC staining for CD31 and E-cadherin in primary LSECs of NAFLD mice with PBS and E coli . ( G ) Wound healing test showing the mitigation of TMNK1 treated with flagellin and TH1020. Statistical chart is on the right side. CD31 ( green ) was the marker of LSECs.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Migration, Gene Expression, RNA Sequencing, Staining, Marker

E coli up-regulates TLR5 and EndMT associated genes in TMNK1 and primary LSECs. ( A ) Gene set enrichment analysis results showing the pathway related to TLR and EndMT in TMNK1 treated with PBS and E coli . ( B ) Heatmap analysis showing genes involved in TLR pathway (eg, Tlr2, Tlr4, Tlr5, and Myd88) and inflammation (eg, Il1β, Tnf, Nfκb1, and Nfκb2). ( C ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the TMNK1 treated with PBS and E coli . ( D ) Representative image showing immunocytofluorescence staining for CD31 and TLR5, α-SMA, TWIST1 in primary LSECs (original magnification, ×400). ( E ) Western blot analysis of α-SMA, N-cadherin, E-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the primary LSECs of NAFLD mice with PBS and E coli . ( F ) Representative image showing immunofluorescence staining for TLR5 and CD31, α-SMA, E-cadherin in NAFLD mice with PBS and E coli . ( G ) Representative image showing immunofluorescence staining for α-SMA, TLR5, and CD31 in the liver of controls and NAFLD patients with advanced fibrosis. CD31 ( green ) was the marker of LSECs.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: E coli up-regulates TLR5 and EndMT associated genes in TMNK1 and primary LSECs. ( A ) Gene set enrichment analysis results showing the pathway related to TLR and EndMT in TMNK1 treated with PBS and E coli . ( B ) Heatmap analysis showing genes involved in TLR pathway (eg, Tlr2, Tlr4, Tlr5, and Myd88) and inflammation (eg, Il1β, Tnf, Nfκb1, and Nfκb2). ( C ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the TMNK1 treated with PBS and E coli . ( D ) Representative image showing immunocytofluorescence staining for CD31 and TLR5, α-SMA, TWIST1 in primary LSECs (original magnification, ×400). ( E ) Western blot analysis of α-SMA, N-cadherin, E-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the primary LSECs of NAFLD mice with PBS and E coli . ( F ) Representative image showing immunofluorescence staining for TLR5 and CD31, α-SMA, E-cadherin in NAFLD mice with PBS and E coli . ( G ) Representative image showing immunofluorescence staining for α-SMA, TLR5, and CD31 in the liver of controls and NAFLD patients with advanced fibrosis. CD31 ( green ) was the marker of LSECs.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Western Blot, Staining, Immunofluorescence, Marker

E coli activates TLR5 and induces the EndMT of LSECs in NAFLD mice. ( A ) Representative image showing immunofluorescence staining for CD31 and TLR5 in NAFLD mice with PBS and E coli . ( B ) Representative image showing immunofluorescence staining for CD31 and α-SMA in NAFLD mice with PBS and E coli . ( C ) Representative image showing immunofluorescence staining for CD31 and E-cadherin in NAFLD mice with PBS and E coli . ( D ) Representative image showing immunofluorescence staining for CD31 and N-cadherin in NAFLD mice with PBS and E coli . ( E ) Representative image showing immunofluorescence staining for CD31 and TWIST1 in NAFLD mice with PBS and E coli. CD31 ( green ) was the marker of LSECs.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: E coli activates TLR5 and induces the EndMT of LSECs in NAFLD mice. ( A ) Representative image showing immunofluorescence staining for CD31 and TLR5 in NAFLD mice with PBS and E coli . ( B ) Representative image showing immunofluorescence staining for CD31 and α-SMA in NAFLD mice with PBS and E coli . ( C ) Representative image showing immunofluorescence staining for CD31 and E-cadherin in NAFLD mice with PBS and E coli . ( D ) Representative image showing immunofluorescence staining for CD31 and N-cadherin in NAFLD mice with PBS and E coli . ( E ) Representative image showing immunofluorescence staining for CD31 and TWIST1 in NAFLD mice with PBS and E coli. CD31 ( green ) was the marker of LSECs.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Immunofluorescence, Staining, Marker

TLR5 inhibitor attenuates E coli –induced EndMT of LSECs in NAFLD mice. ( A ) Representative image showing immunofluorescence staining for CD31 and TLR5 in NAFLD mice with E coli+ DMSO and E coli+ TH1020. ( B ) Representative image showing immunofluorescence staining for CD31 and α-SMA in NAFLD mice with E coli+ DMSO and E coli+ TH1020. ( C ) Representative image showing immunofluorescence staining for CD31 and E-cadherin in NAFLD mice with E coli+ DMSO and E coli+ TH1020. ( D ) Representative image showing immunofluorescence staining for CD31 and N-cadherin in NAFLD mice with E coli+ DMSO and E coli+ TH1020. ( E ) Representative image showing immunofluorescence staining for CD31 and TWIST1 in NAFLD mice with E coli+ DMSO and E coli+ TH1020. CD31 ( green ) was the marker of LSECs.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: TLR5 inhibitor attenuates E coli –induced EndMT of LSECs in NAFLD mice. ( A ) Representative image showing immunofluorescence staining for CD31 and TLR5 in NAFLD mice with E coli+ DMSO and E coli+ TH1020. ( B ) Representative image showing immunofluorescence staining for CD31 and α-SMA in NAFLD mice with E coli+ DMSO and E coli+ TH1020. ( C ) Representative image showing immunofluorescence staining for CD31 and E-cadherin in NAFLD mice with E coli+ DMSO and E coli+ TH1020. ( D ) Representative image showing immunofluorescence staining for CD31 and N-cadherin in NAFLD mice with E coli+ DMSO and E coli+ TH1020. ( E ) Representative image showing immunofluorescence staining for CD31 and TWIST1 in NAFLD mice with E coli+ DMSO and E coli+ TH1020. CD31 ( green ) was the marker of LSECs.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Immunofluorescence, Staining, Marker

TLR5 inhibitor attenuates E coli –induced EndMT in TMNK1 and primary LSECs. ( A ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the TMNK1 treated with E coli and TH1020. ( B ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in primary LSECs treated with flagellin and TH1020. ( C ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the TMNK1 treated with flagellin and TH1020. ( D ) Representative image showing immunofluorescence staining for α-SMA, TLR5, TWIST1, and CD31 in primary LSECs treated with E coli and TH1020 (original magnification, ×400). ( E ) Representative image showing immunofluorescence staining for α-SMA, TLR5, TWIST1, and CD31 in primary LSECs treated with flagellin and TH1020 (original magnification, ×400). ( F ) Western blot analysis of α-SMA, N-cadherin, E-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in primary LSECs of NAFLD mice with DMSO and TH1020. ( G ) Representative image showing immunofluorescence staining for α-SMA, TLR5, TWIST1, and CD31 in livers of NAFLD mice with DMSO and TH1020. Statistical chart is on the right . CD31 ( green ) was the marker of LSECs.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: TLR5 inhibitor attenuates E coli –induced EndMT in TMNK1 and primary LSECs. ( A ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the TMNK1 treated with E coli and TH1020. ( B ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in primary LSECs treated with flagellin and TH1020. ( C ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the TMNK1 treated with flagellin and TH1020. ( D ) Representative image showing immunofluorescence staining for α-SMA, TLR5, TWIST1, and CD31 in primary LSECs treated with E coli and TH1020 (original magnification, ×400). ( E ) Representative image showing immunofluorescence staining for α-SMA, TLR5, TWIST1, and CD31 in primary LSECs treated with flagellin and TH1020 (original magnification, ×400). ( F ) Western blot analysis of α-SMA, N-cadherin, E-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in primary LSECs of NAFLD mice with DMSO and TH1020. ( G ) Representative image showing immunofluorescence staining for α-SMA, TLR5, TWIST1, and CD31 in livers of NAFLD mice with DMSO and TH1020. Statistical chart is on the right . CD31 ( green ) was the marker of LSECs.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Western Blot, Immunofluorescence, Staining, Marker

Flagellin deficiency in E coli reduces EndMT in TMNK1 and primary LSECs . ( A ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the TMNK1 treated with E coli and E coli Δ(FliC). ( B ) Representative image showing immunocytofluorescence staining for α-SMA, TLR5, TWIST1, and CD31 in primary LSECs treated with E coli and E coli Δ(FliC). ( C ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in LSECs of NAFLD mice with E coli and E coli Δ(FliC). ( D ) Representative image showing immunofluorescence staining for CD31 and TLR5 in NAFLD mice with E coli and E coli Δ(FliC). Statistical chart is on the right . ( E ) Representative image showing immunofluorescence staining for α-SMA, E-cadherin, N-cadherin, TWIST1, and CD31 in NAFLD mice with E coli and E coli Δ(FliC). Statistical chart is on the right . CD31 ( green ) was the marker of LSECs.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: Flagellin deficiency in E coli reduces EndMT in TMNK1 and primary LSECs . ( A ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in the TMNK1 treated with E coli and E coli Δ(FliC). ( B ) Representative image showing immunocytofluorescence staining for α-SMA, TLR5, TWIST1, and CD31 in primary LSECs treated with E coli and E coli Δ(FliC). ( C ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR5, MYD88, and TUBULIN in LSECs of NAFLD mice with E coli and E coli Δ(FliC). ( D ) Representative image showing immunofluorescence staining for CD31 and TLR5 in NAFLD mice with E coli and E coli Δ(FliC). Statistical chart is on the right . ( E ) Representative image showing immunofluorescence staining for α-SMA, E-cadherin, N-cadherin, TWIST1, and CD31 in NAFLD mice with E coli and E coli Δ(FliC). Statistical chart is on the right . CD31 ( green ) was the marker of LSECs.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Western Blot, Staining, Immunofluorescence, Marker

Flagellin deficiency in E coli reduces EndMT of LSECs in NAFLD mice. ( A ) Representative image showing immunofluorescence staining for CD31 and TLR5 in NAFLD mice with E coli and E coli Δ(FliC). ( B ) Representative image showing immunofluorescence staining for CD31 and α-SMA in NAFLD mice with E coli and E coli Δ(FliC). ( C ) Representative image showing immunofluorescence staining for CD31 and E-cadherin in NAFLD mice with E coli and E coli Δ(FliC). ( D ) Representative image showing immunofluorescence staining for CD31 and N-cadherin in NAFLD mice with E coli and E coli Δ(FliC). ( E ) Representative image showing immunofluorescence staining for CD31 and TWIST1 in NAFLD mice with E coli and E coli Δ(FliC). CD31 ( green ) was the marker of LSECs.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: Flagellin deficiency in E coli reduces EndMT of LSECs in NAFLD mice. ( A ) Representative image showing immunofluorescence staining for CD31 and TLR5 in NAFLD mice with E coli and E coli Δ(FliC). ( B ) Representative image showing immunofluorescence staining for CD31 and α-SMA in NAFLD mice with E coli and E coli Δ(FliC). ( C ) Representative image showing immunofluorescence staining for CD31 and E-cadherin in NAFLD mice with E coli and E coli Δ(FliC). ( D ) Representative image showing immunofluorescence staining for CD31 and N-cadherin in NAFLD mice with E coli and E coli Δ(FliC). ( E ) Representative image showing immunofluorescence staining for CD31 and TWIST1 in NAFLD mice with E coli and E coli Δ(FliC). CD31 ( green ) was the marker of LSECs.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Immunofluorescence, Staining, Marker

E coli promotes phosphorylation and nuclear translocation of P65 in LSECs via TLR5 pathway. ( A ) Western blot analysis of p-P65 and P65 in TMNK1 treated with E coli+ DMSO and E coli+ TH1020. ( B ) Western blot analysis of p-P65 and P65 in TMNK1 treated with flagellin and flagellin + TH1020. ( C ) Western blot analysis of p-P65 and P65 in TMNK1 treated with E coli and E coli Δ(FliC). ( D ) Western blot analysis of p-P65 and P65 in primary LSECs isolated from NAFLD mice fed with PBS, E coli , TH1020, and E coli Δ(FliC), and from both wild-type (WT) and TLR5-KO (KO) NAFLD mice. ( E ) Western blot analysis of P65 expression in cytoplasm and nucleus of TMNK1 treated with E coli+ DMSO and E coli+ TH1020 or treated with E coli and E coli Δ(FliC). ( F ) Representative image showing immunofluorescence staining for P65 in TMNK1 treated with E coli , E coli+ TH1020, and E coli Δ(FliC) (original magnification, ×200). Statistical chart is on the lower side. ( G ) Representative image showing immunofluorescence staining for P65 in primary LSECs treated with E coli , E coli+ TH1020, and E coli Δ(FliC) (original magnification, ×400). Statistical chart is on the lower side. ( H ) Luciferase reporter activity for wild-type and p65-binding element–mutated Twist1 promoter luciferase in TMNK1 treated with E coli and E coli+ TH1020.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: E coli promotes phosphorylation and nuclear translocation of P65 in LSECs via TLR5 pathway. ( A ) Western blot analysis of p-P65 and P65 in TMNK1 treated with E coli+ DMSO and E coli+ TH1020. ( B ) Western blot analysis of p-P65 and P65 in TMNK1 treated with flagellin and flagellin + TH1020. ( C ) Western blot analysis of p-P65 and P65 in TMNK1 treated with E coli and E coli Δ(FliC). ( D ) Western blot analysis of p-P65 and P65 in primary LSECs isolated from NAFLD mice fed with PBS, E coli , TH1020, and E coli Δ(FliC), and from both wild-type (WT) and TLR5-KO (KO) NAFLD mice. ( E ) Western blot analysis of P65 expression in cytoplasm and nucleus of TMNK1 treated with E coli+ DMSO and E coli+ TH1020 or treated with E coli and E coli Δ(FliC). ( F ) Representative image showing immunofluorescence staining for P65 in TMNK1 treated with E coli , E coli+ TH1020, and E coli Δ(FliC) (original magnification, ×200). Statistical chart is on the lower side. ( G ) Representative image showing immunofluorescence staining for P65 in primary LSECs treated with E coli , E coli+ TH1020, and E coli Δ(FliC) (original magnification, ×400). Statistical chart is on the lower side. ( H ) Luciferase reporter activity for wild-type and p65-binding element–mutated Twist1 promoter luciferase in TMNK1 treated with E coli and E coli+ TH1020.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Phospho-proteomics, Translocation Assay, Western Blot, Isolation, Expressing, Immunofluorescence, Staining, Luciferase, Activity Assay, Binding Assay

E coli and LPS up-regulate TLR4 and EndMT associated genes in TMNK1. ( A ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR4, and TUBULIN in the TMNK1 treated with LPS (10 ng/mL and 100 ng/mL). ( B ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR4, and TUBULIN in the TMNK1 treated with E coli (MOI100) and Resatorvid.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: E coli and LPS up-regulate TLR4 and EndMT associated genes in TMNK1. ( A ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR4, and TUBULIN in the TMNK1 treated with LPS (10 ng/mL and 100 ng/mL). ( B ) Western blot analysis of α-SMA, E-cadherin, N-cadherin, TWIST1, TLR4, and TUBULIN in the TMNK1 treated with E coli (MOI100) and Resatorvid.

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: Western Blot

Primary Antibodies

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Escherichia coli Promotes Endothelial to Mesenchymal Transformation of Liver Sinusoidal Endothelial Cells and Exacerbates Nonalcoholic Fatty Liver Disease Via Its Flagellin

doi: 10.1016/j.jcmgh.2023.08.001

Figure Lengend Snippet: Primary Antibodies

Article Snippet: Anti-TWIST1 antibody (31174) , CST, USA.

Techniques: