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94
MedChemExpress fasn inhibitor
Pathway enrichment analysis of the 25-gene signature. (A) Reactome enrichment analysis identified significant pathways, including fatty acid metabolism, cholesterol biosynthesis, and nuclear receptor signaling. (B) WikiPathways analysis corroborated the involvement of these genes in lipid metabolism pathways, including SREBF and MIR33 (microRNA 33) in cholesterol and lipid homeostasis. (C) Gene–pathway interaction network highlighting the central roles of lipid metabolism regulators fatty acid (FA) synthase ( <t>FASN</t> ) and stearoyl-coenzyme A (CoA) desaturase <t>(</t> <t>SCD</t> ) and other genes involved in the cell cycle and membrane trafficking, including TPD52 like 1 ( TPD52L1 ), leucine-rich repeats and immunoglobulin-like domains 1 ( LRIG1 ), keratin 7 ( KRT7 ), homeobox C4 ( HOXC4 ), and CDC42 effector protein 3 ( CDC42EP3 ).
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MedChemExpress vitro fasn inhibition fasn inhibitors tvb2640
Pathway enrichment analysis of the 25-gene signature. (A) Reactome enrichment analysis identified significant pathways, including fatty acid metabolism, cholesterol biosynthesis, and nuclear receptor signaling. (B) WikiPathways analysis corroborated the involvement of these genes in lipid metabolism pathways, including SREBF and MIR33 (microRNA 33) in cholesterol and lipid homeostasis. (C) Gene–pathway interaction network highlighting the central roles of lipid metabolism regulators fatty acid (FA) synthase ( <t>FASN</t> ) and stearoyl-coenzyme A (CoA) desaturase <t>(</t> <t>SCD</t> ) and other genes involved in the cell cycle and membrane trafficking, including TPD52 like 1 ( TPD52L1 ), leucine-rich repeats and immunoglobulin-like domains 1 ( LRIG1 ), keratin 7 ( KRT7 ), homeobox C4 ( HOXC4 ), and CDC42 effector protein 3 ( CDC42EP3 ).
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MedChemExpress fasn inhibitor tvb 2640
Therapeutic targeting of KAT2B-low RCC with a FASN inhibitor (A-B) Representative images of IHC staining of FASN in RCC cohort and statistical analysis. (C) Representative images of IHC staining for FASN and KAT2B in RCC tissues with high and low KAT2B expression. (D) Scatter plot of the relationship among KAT2B expression and FASN expression in advanced RCC tumors (n = 53). (E) The cell viability of ACHN and Caki-1 cells after treated <t>with</t> <t>TVB-2640</t> (n = 4). (F) The cell viability of 786O and 769P cells after treated with TVB-2640 (n = 10). Proteins from three independent sites in RCC tissues were extracted to detect KAT2B expression. (H) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM). 15 organoids were randomly selected from each group for statistical analysis. (I) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM) (n = 15). (J) Representative images of two PDOs with different KAT2B expression after treatment with TVB-2640 (n = 10). (K) Representative images of PRO-1 staining of PDOs. (L-M) The cell viability of ACHN cells (L) and case 1 primary RCC cells (M) with KAT2B knockdown after treated with TVB-2640 (n = 4). (N-O) The picture (N) of xenograft using 786O cells with KAT2B knockdown after treated with TVB-2640, and tumor growth curve (n = 4). Data were analyzed by unpaired t test (B, H, I, J), one-way ANOVA (O) or two-way ANOVA (E, F, G, L, M).
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MedChemExpress fasn inhibitor orlistat
Therapeutic targeting of KAT2B-low RCC with a FASN inhibitor (A-B) Representative images of IHC staining of FASN in RCC cohort and statistical analysis. (C) Representative images of IHC staining for FASN and KAT2B in RCC tissues with high and low KAT2B expression. (D) Scatter plot of the relationship among KAT2B expression and FASN expression in advanced RCC tumors (n = 53). (E) The cell viability of ACHN and Caki-1 cells after treated <t>with</t> <t>TVB-2640</t> (n = 4). (F) The cell viability of 786O and 769P cells after treated with TVB-2640 (n = 10). Proteins from three independent sites in RCC tissues were extracted to detect KAT2B expression. (H) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM). 15 organoids were randomly selected from each group for statistical analysis. (I) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM) (n = 15). (J) Representative images of two PDOs with different KAT2B expression after treatment with TVB-2640 (n = 10). (K) Representative images of PRO-1 staining of PDOs. (L-M) The cell viability of ACHN cells (L) and case 1 primary RCC cells (M) with KAT2B knockdown after treated with TVB-2640 (n = 4). (N-O) The picture (N) of xenograft using 786O cells with KAT2B knockdown after treated with TVB-2640, and tumor growth curve (n = 4). Data were analyzed by unpaired t test (B, H, I, J), one-way ANOVA (O) or two-way ANOVA (E, F, G, L, M).
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MedChemExpress fasn specific inhibitor cerulenin
Determine the roles of FASN in BoAHV-1 productive infection in MDBK cells using a chemical inhibitor. ( A and C ) MDBK cells in six-well plates were infected with BoAHV-1 (MOI = 1) and treated either with DMSO control or with the FASN-specific inhibitor <t>Cerulenin</t> at the indicated concentrations. At 24 hpi, the cells were collected either to prepare cell lysates for Western blotting using an antibody against virus-associated proteins (VMRD, cat# P170703-001, 1:5,000) ( A ) or to extract DNA for subsequent qPCR analysis using gB-specific primers ( C ). ( B ) The intensity of bands for virus-associated proteins was quantified using the freeware software Image J. Changes in the levels of individual bands upon treatment with the inhibitor were calculated relative to those of the DMSO control, which was set at 100%. ( D ) Virus titers in the supernatants were determined and expressed as TCID 50 /mL. ( E ) MDBK cells in six-well plates were infected with the virus at an MOI of 1 for 24 h and treated with either DMSO control or 10 µM Cerulenin. Total RNA was then extracted from the cells for the detection of viral mRNA using RT-qPCR. Primers specific for bICP27, viral DNA polymerase, and viral protein gC were used, respectively. The data shown are means of three independent experiments, with error bars representing standard deviations. Significance was assessed by a standard t -test (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001).
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Teva 1 4 substituted piperidine based fasn inhibitors
Determine the roles of FASN in BoAHV-1 productive infection in MDBK cells using a chemical inhibitor. ( A and C ) MDBK cells in six-well plates were infected with BoAHV-1 (MOI = 1) and treated either with DMSO control or with the FASN-specific inhibitor <t>Cerulenin</t> at the indicated concentrations. At 24 hpi, the cells were collected either to prepare cell lysates for Western blotting using an antibody against virus-associated proteins (VMRD, cat# P170703-001, 1:5,000) ( A ) or to extract DNA for subsequent qPCR analysis using gB-specific primers ( C ). ( B ) The intensity of bands for virus-associated proteins was quantified using the freeware software Image J. Changes in the levels of individual bands upon treatment with the inhibitor were calculated relative to those of the DMSO control, which was set at 100%. ( D ) Virus titers in the supernatants were determined and expressed as TCID 50 /mL. ( E ) MDBK cells in six-well plates were infected with the virus at an MOI of 1 for 24 h and treated with either DMSO control or 10 µM Cerulenin. Total RNA was then extracted from the cells for the detection of viral mRNA using RT-qPCR. Primers specific for bICP27, viral DNA polymerase, and viral protein gC were used, respectively. The data shown are means of three independent experiments, with error bars representing standard deviations. Significance was assessed by a standard t -test (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001).
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MedChemExpress fasn inhibitors tvb2640
Determine the roles of FASN in BoAHV-1 productive infection in MDBK cells using a chemical inhibitor. ( A and C ) MDBK cells in six-well plates were infected with BoAHV-1 (MOI = 1) and treated either with DMSO control or with the FASN-specific inhibitor <t>Cerulenin</t> at the indicated concentrations. At 24 hpi, the cells were collected either to prepare cell lysates for Western blotting using an antibody against virus-associated proteins (VMRD, cat# P170703-001, 1:5,000) ( A ) or to extract DNA for subsequent qPCR analysis using gB-specific primers ( C ). ( B ) The intensity of bands for virus-associated proteins was quantified using the freeware software Image J. Changes in the levels of individual bands upon treatment with the inhibitor were calculated relative to those of the DMSO control, which was set at 100%. ( D ) Virus titers in the supernatants were determined and expressed as TCID 50 /mL. ( E ) MDBK cells in six-well plates were infected with the virus at an MOI of 1 for 24 h and treated with either DMSO control or 10 µM Cerulenin. Total RNA was then extracted from the cells for the detection of viral mRNA using RT-qPCR. Primers specific for bICP27, viral DNA polymerase, and viral protein gC were used, respectively. The data shown are means of three independent experiments, with error bars representing standard deviations. Significance was assessed by a standard t -test (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001).
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Image Search Results


Pathway enrichment analysis of the 25-gene signature. (A) Reactome enrichment analysis identified significant pathways, including fatty acid metabolism, cholesterol biosynthesis, and nuclear receptor signaling. (B) WikiPathways analysis corroborated the involvement of these genes in lipid metabolism pathways, including SREBF and MIR33 (microRNA 33) in cholesterol and lipid homeostasis. (C) Gene–pathway interaction network highlighting the central roles of lipid metabolism regulators fatty acid (FA) synthase ( FASN ) and stearoyl-coenzyme A (CoA) desaturase ( SCD ) and other genes involved in the cell cycle and membrane trafficking, including TPD52 like 1 ( TPD52L1 ), leucine-rich repeats and immunoglobulin-like domains 1 ( LRIG1 ), keratin 7 ( KRT7 ), homeobox C4 ( HOXC4 ), and CDC42 effector protein 3 ( CDC42EP3 ).

Journal: Computational and Structural Biotechnology Journal

Article Title: Epigenomics-Guided Multi-Omics Integration Uncovers a Lipid-Metabolic Signature with Translational Utility in Bladder Cancer

doi: 10.34133/csbj.0139

Figure Lengend Snippet: Pathway enrichment analysis of the 25-gene signature. (A) Reactome enrichment analysis identified significant pathways, including fatty acid metabolism, cholesterol biosynthesis, and nuclear receptor signaling. (B) WikiPathways analysis corroborated the involvement of these genes in lipid metabolism pathways, including SREBF and MIR33 (microRNA 33) in cholesterol and lipid homeostasis. (C) Gene–pathway interaction network highlighting the central roles of lipid metabolism regulators fatty acid (FA) synthase ( FASN ) and stearoyl-coenzyme A (CoA) desaturase ( SCD ) and other genes involved in the cell cycle and membrane trafficking, including TPD52 like 1 ( TPD52L1 ), leucine-rich repeats and immunoglobulin-like domains 1 ( LRIG1 ), keratin 7 ( KRT7 ), homeobox C4 ( HOXC4 ), and CDC42 effector protein 3 ( CDC42EP3 ).

Article Snippet: In summary, 5,637 cells (1,000 cells per well) and J82 cells (500 cells per well) were seeded into 6-well plates and incubated at 37 °C for 24 h. The following day, one group served as the control and was maintained in the growth medium, while the experimental group received an addition of 50 μM FASN inhibitor (MedChemExpress, TVB-3664, catalog no. HY-120062) and SCD inhibitor (MedChemExpress, A939572, catalog no. HY-50709) to the growth medium and was cultured for a duration of 13 d. Subsequently, the cells were fixed with 4% formaldehyde (Sigma-Aldrich) and stained with 0.5% crystal violet (Sigma-Aldrich).

Techniques: Membrane

Prognostic validation and functional assessment of lipid metabolism regulators, fatty acid synthase ( FASN ) and stearoyl-coenzyme A desaturase ( SCD ). (A) Kaplan–Meier survival analysis indicating the prognostic significance of high expression levels of FASN (hazard ratio [HR] = 1.41) and SCD (HR = 1.8) in patients with bladder cancer (BLCA). (B) Expression analysis across stages revealed no significant variation (ANOVA, P = 0.3). (C) Colony formation assays demonstrating significantly reduced proliferation in BLCA cell lines (J82 and 5637) treated with the FASN inhibitor (FASNi; TVB-3664) and SCD inhibitor (SCDi; A939572). (D) Migration assays confirmed significantly impaired motility upon FASN and SCD inhibition, underscoring their roles in tumor aggressiveness. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Journal: Computational and Structural Biotechnology Journal

Article Title: Epigenomics-Guided Multi-Omics Integration Uncovers a Lipid-Metabolic Signature with Translational Utility in Bladder Cancer

doi: 10.34133/csbj.0139

Figure Lengend Snippet: Prognostic validation and functional assessment of lipid metabolism regulators, fatty acid synthase ( FASN ) and stearoyl-coenzyme A desaturase ( SCD ). (A) Kaplan–Meier survival analysis indicating the prognostic significance of high expression levels of FASN (hazard ratio [HR] = 1.41) and SCD (HR = 1.8) in patients with bladder cancer (BLCA). (B) Expression analysis across stages revealed no significant variation (ANOVA, P = 0.3). (C) Colony formation assays demonstrating significantly reduced proliferation in BLCA cell lines (J82 and 5637) treated with the FASN inhibitor (FASNi; TVB-3664) and SCD inhibitor (SCDi; A939572). (D) Migration assays confirmed significantly impaired motility upon FASN and SCD inhibition, underscoring their roles in tumor aggressiveness. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: In summary, 5,637 cells (1,000 cells per well) and J82 cells (500 cells per well) were seeded into 6-well plates and incubated at 37 °C for 24 h. The following day, one group served as the control and was maintained in the growth medium, while the experimental group received an addition of 50 μM FASN inhibitor (MedChemExpress, TVB-3664, catalog no. HY-120062) and SCD inhibitor (MedChemExpress, A939572, catalog no. HY-50709) to the growth medium and was cultured for a duration of 13 d. Subsequently, the cells were fixed with 4% formaldehyde (Sigma-Aldrich) and stained with 0.5% crystal violet (Sigma-Aldrich).

Techniques: Biomarker Discovery, Functional Assay, Expressing, Migration, Inhibition

Therapeutic targeting of KAT2B-low RCC with a FASN inhibitor (A-B) Representative images of IHC staining of FASN in RCC cohort and statistical analysis. (C) Representative images of IHC staining for FASN and KAT2B in RCC tissues with high and low KAT2B expression. (D) Scatter plot of the relationship among KAT2B expression and FASN expression in advanced RCC tumors (n = 53). (E) The cell viability of ACHN and Caki-1 cells after treated with TVB-2640 (n = 4). (F) The cell viability of 786O and 769P cells after treated with TVB-2640 (n = 10). Proteins from three independent sites in RCC tissues were extracted to detect KAT2B expression. (H) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM). 15 organoids were randomly selected from each group for statistical analysis. (I) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM) (n = 15). (J) Representative images of two PDOs with different KAT2B expression after treatment with TVB-2640 (n = 10). (K) Representative images of PRO-1 staining of PDOs. (L-M) The cell viability of ACHN cells (L) and case 1 primary RCC cells (M) with KAT2B knockdown after treated with TVB-2640 (n = 4). (N-O) The picture (N) of xenograft using 786O cells with KAT2B knockdown after treated with TVB-2640, and tumor growth curve (n = 4). Data were analyzed by unpaired t test (B, H, I, J), one-way ANOVA (O) or two-way ANOVA (E, F, G, L, M).

Journal: Journal of Advanced Research

Article Title: Epigenetically silenced KAT2B suppresses de novo lipogenesis through destroying HDAC5/LSD1 complex assembly in renal cell carcinoma

doi: 10.1016/j.jare.2025.08.007

Figure Lengend Snippet: Therapeutic targeting of KAT2B-low RCC with a FASN inhibitor (A-B) Representative images of IHC staining of FASN in RCC cohort and statistical analysis. (C) Representative images of IHC staining for FASN and KAT2B in RCC tissues with high and low KAT2B expression. (D) Scatter plot of the relationship among KAT2B expression and FASN expression in advanced RCC tumors (n = 53). (E) The cell viability of ACHN and Caki-1 cells after treated with TVB-2640 (n = 4). (F) The cell viability of 786O and 769P cells after treated with TVB-2640 (n = 10). Proteins from three independent sites in RCC tissues were extracted to detect KAT2B expression. (H) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM). 15 organoids were randomly selected from each group for statistical analysis. (I) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM) (n = 15). (J) Representative images of two PDOs with different KAT2B expression after treatment with TVB-2640 (n = 10). (K) Representative images of PRO-1 staining of PDOs. (L-M) The cell viability of ACHN cells (L) and case 1 primary RCC cells (M) with KAT2B knockdown after treated with TVB-2640 (n = 4). (N-O) The picture (N) of xenograft using 786O cells with KAT2B knockdown after treated with TVB-2640, and tumor growth curve (n = 4). Data were analyzed by unpaired t test (B, H, I, J), one-way ANOVA (O) or two-way ANOVA (E, F, G, L, M).

Article Snippet: Four days after inoculation, the mice were randomly divided into two groups and treated with either the vehicle (30 % PEG400) or the FASN inhibitor TVB-2640 (HY-112829, MCE, USA) (100 mg/kg) once daily by oral gavage for 3 consecutive weeks.

Techniques: Immunohistochemistry, Expressing, Staining, Knockdown

Determine the roles of FASN in BoAHV-1 productive infection in MDBK cells using a chemical inhibitor. ( A and C ) MDBK cells in six-well plates were infected with BoAHV-1 (MOI = 1) and treated either with DMSO control or with the FASN-specific inhibitor Cerulenin at the indicated concentrations. At 24 hpi, the cells were collected either to prepare cell lysates for Western blotting using an antibody against virus-associated proteins (VMRD, cat# P170703-001, 1:5,000) ( A ) or to extract DNA for subsequent qPCR analysis using gB-specific primers ( C ). ( B ) The intensity of bands for virus-associated proteins was quantified using the freeware software Image J. Changes in the levels of individual bands upon treatment with the inhibitor were calculated relative to those of the DMSO control, which was set at 100%. ( D ) Virus titers in the supernatants were determined and expressed as TCID 50 /mL. ( E ) MDBK cells in six-well plates were infected with the virus at an MOI of 1 for 24 h and treated with either DMSO control or 10 µM Cerulenin. Total RNA was then extracted from the cells for the detection of viral mRNA using RT-qPCR. Primers specific for bICP27, viral DNA polymerase, and viral protein gC were used, respectively. The data shown are means of three independent experiments, with error bars representing standard deviations. Significance was assessed by a standard t -test (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001).

Journal: Microbiology Spectrum

Article Title: Fatty acid synthase may facilitate the trafficking of bovine alpha herpesvirus 1 out of the Golgi apparatus, potentially promoting viral infection

doi: 10.1128/spectrum.01388-25

Figure Lengend Snippet: Determine the roles of FASN in BoAHV-1 productive infection in MDBK cells using a chemical inhibitor. ( A and C ) MDBK cells in six-well plates were infected with BoAHV-1 (MOI = 1) and treated either with DMSO control or with the FASN-specific inhibitor Cerulenin at the indicated concentrations. At 24 hpi, the cells were collected either to prepare cell lysates for Western blotting using an antibody against virus-associated proteins (VMRD, cat# P170703-001, 1:5,000) ( A ) or to extract DNA for subsequent qPCR analysis using gB-specific primers ( C ). ( B ) The intensity of bands for virus-associated proteins was quantified using the freeware software Image J. Changes in the levels of individual bands upon treatment with the inhibitor were calculated relative to those of the DMSO control, which was set at 100%. ( D ) Virus titers in the supernatants were determined and expressed as TCID 50 /mL. ( E ) MDBK cells in six-well plates were infected with the virus at an MOI of 1 for 24 h and treated with either DMSO control or 10 µM Cerulenin. Total RNA was then extracted from the cells for the detection of viral mRNA using RT-qPCR. Primers specific for bICP27, viral DNA polymerase, and viral protein gC were used, respectively. The data shown are means of three independent experiments, with error bars representing standard deviations. Significance was assessed by a standard t -test (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001).

Article Snippet: FASN-specific inhibitor Cerulenin (cat# HY-A0210) was ordered from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Infection, Control, Western Blot, Virus, Software, Quantitative RT-PCR

Determine the roles of FASN in BoAHV-1 productive infection in Neuro-2A cells using both siRNA and chemical inhibitor. ( A ) Neuro-2A cells in six-well plates were transfected with either scrambled siRNA (150 pmol) or individual siRNAs targeting FASN (150 pmol), referred to as siRNA1, siRNA2, siRNA3, and siRNA4, respectively. At 48 h post-transfection, cell lysates were prepared and subjected to Western blot analysis to detect FASN protein levels using an antibody against FASN (Proteintech, cat# 10624-2-AP, 1:10,000). ( C ) Neuro-2A cells in six-well plates were transfected with either scrambled siRNA (150 pmol) or siRNA1 (150 pmol). At 36 h post-transfection, the cells were infected with BoAHV-1 at an MOI of 10. After 24 h of infection, the cells were collected and subjected to Western blot analysis using a monoclonal antibody against viral protein gC (VMRD, cat#F2, 1:2,000). ( E ) Neuro-2A cells in six-well plates were infected with BoAHV-1 (MOI = 10) and treated either with DMSO control or with the FASN-specific inhibitor Cerulenin at the indicated concentrations. At 24 hpi, the cell lysates were prepared and subjected to Western blotting to detect viral protein gC. ( B, D, and F ) The band intensities were quantified using the free software Image J. The intensity of each band was first normalized to that of the respective loading control Tubulin, and then normalized to that of either DMSO-treated or scrambled siRNA-transfected control, which was arbitrarily set to 100%. The data shown are means of three independent experiments, with error bars representing standard deviations. Significance was assessed using a Student’s t -test (ns, not significant; * P < 0.05; ** P < 0.01).

Journal: Microbiology Spectrum

Article Title: Fatty acid synthase may facilitate the trafficking of bovine alpha herpesvirus 1 out of the Golgi apparatus, potentially promoting viral infection

doi: 10.1128/spectrum.01388-25

Figure Lengend Snippet: Determine the roles of FASN in BoAHV-1 productive infection in Neuro-2A cells using both siRNA and chemical inhibitor. ( A ) Neuro-2A cells in six-well plates were transfected with either scrambled siRNA (150 pmol) or individual siRNAs targeting FASN (150 pmol), referred to as siRNA1, siRNA2, siRNA3, and siRNA4, respectively. At 48 h post-transfection, cell lysates were prepared and subjected to Western blot analysis to detect FASN protein levels using an antibody against FASN (Proteintech, cat# 10624-2-AP, 1:10,000). ( C ) Neuro-2A cells in six-well plates were transfected with either scrambled siRNA (150 pmol) or siRNA1 (150 pmol). At 36 h post-transfection, the cells were infected with BoAHV-1 at an MOI of 10. After 24 h of infection, the cells were collected and subjected to Western blot analysis using a monoclonal antibody against viral protein gC (VMRD, cat#F2, 1:2,000). ( E ) Neuro-2A cells in six-well plates were infected with BoAHV-1 (MOI = 10) and treated either with DMSO control or with the FASN-specific inhibitor Cerulenin at the indicated concentrations. At 24 hpi, the cell lysates were prepared and subjected to Western blotting to detect viral protein gC. ( B, D, and F ) The band intensities were quantified using the free software Image J. The intensity of each band was first normalized to that of the respective loading control Tubulin, and then normalized to that of either DMSO-treated or scrambled siRNA-transfected control, which was arbitrarily set to 100%. The data shown are means of three independent experiments, with error bars representing standard deviations. Significance was assessed using a Student’s t -test (ns, not significant; * P < 0.05; ** P < 0.01).

Article Snippet: FASN-specific inhibitor Cerulenin (cat# HY-A0210) was ordered from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Infection, Transfection, Western Blot, Control, Software

Determine the effects of FASN inhibitor, Cerulenin, on the accumulation of gD in the Golgi apparatus. ( A ) Diagram shows the treatment manner of virus-infected cells by both Cerulenin and Monensin. ( B ) MDBK cells of either mock-infected or virus-infected were treated either with vehicle control DMSO or with Cerulenin (10 µM) or Monensin (10 µM) for a duration of 4 h prior to the termination of infection. At 24 hpi, the cells were collected to purify the Golgi apparatus using a commercial purification kit (Beijing Biolabo Technology, cat# HR0247-50T). Subsequently, Western blot analysis was performed to detect the protein levels of gD in the Golgi fractions. GOLGA1, a marker of the Golgi apparatus, was used as a loading control and for subsequent quantitative analysis. ( C ) The band intensity was analyzed with the free software Image J. The intensity of each band was first normalized to that of the respective loading control GOLGA1, and then normalized to that of the control treated with DMSO, which was arbitrarily set to 1. The data shown are means of three independent experiments with error bars indicating standard deviations. Significance was assessed with a Student’s t -test (* P < 0.05, ** P < 0.01).

Journal: Microbiology Spectrum

Article Title: Fatty acid synthase may facilitate the trafficking of bovine alpha herpesvirus 1 out of the Golgi apparatus, potentially promoting viral infection

doi: 10.1128/spectrum.01388-25

Figure Lengend Snippet: Determine the effects of FASN inhibitor, Cerulenin, on the accumulation of gD in the Golgi apparatus. ( A ) Diagram shows the treatment manner of virus-infected cells by both Cerulenin and Monensin. ( B ) MDBK cells of either mock-infected or virus-infected were treated either with vehicle control DMSO or with Cerulenin (10 µM) or Monensin (10 µM) for a duration of 4 h prior to the termination of infection. At 24 hpi, the cells were collected to purify the Golgi apparatus using a commercial purification kit (Beijing Biolabo Technology, cat# HR0247-50T). Subsequently, Western blot analysis was performed to detect the protein levels of gD in the Golgi fractions. GOLGA1, a marker of the Golgi apparatus, was used as a loading control and for subsequent quantitative analysis. ( C ) The band intensity was analyzed with the free software Image J. The intensity of each band was first normalized to that of the respective loading control GOLGA1, and then normalized to that of the control treated with DMSO, which was arbitrarily set to 1. The data shown are means of three independent experiments with error bars indicating standard deviations. Significance was assessed with a Student’s t -test (* P < 0.05, ** P < 0.01).

Article Snippet: FASN-specific inhibitor Cerulenin (cat# HY-A0210) was ordered from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Virus, Infection, Control, Purification, Western Blot, Marker, Software