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Journal: Tumour Virus Research
Article Title: PRMT5–mediated symmetric dimethylation of SHBs at Arg169 stabilizes SHBs and promotes angiogenesis and tumor growth
doi: 10.1016/j.tvr.2026.200340
Figure Lengend Snippet: SHBs is symmetrically dimethylated at arginine 169. (A–C) Huh7 and HepG2 cells were transfected with plasmids encoding SHBs–Strep–Flag or Strep–Flag control. Strep pull–down (IP:Strep) was performed, followed by Western blot (WB) with antibodies against (A) monomethylarginine (MMA), (B) asymmetric dimethylarginine (ADMA), or (C) symmetric dimethylarginine (SDMA). SHBs in the IP fraction and SHBs/β–actin in input lysates are shown as controls. (D) Cells expressing SHBs–Strep–Flag were treated with adenosine dialdehyde (ADOX, 40 μM) for 36 h, followed by Strep pull–down and WB for SDMA and SHBs. Densitometric ratios (SDMA/IP–SHBs and SHBs/β–actin) are shown above/below the blots. (E) Huh7 cells were transfected with plasmids encoding SHBs–Strep–Flag or the indicated R→K mutants (R73K, R78K, R79K, R169K). SDMA on immunoprecipitated SHBs was assessed by Strep pull–down and WB; densitometric SDMA/IP–SHBs ratios are shown above the blots. (F–G) HepG2 cells were transfected with plasmids encoding SHBs–Strep–Flag or SHBs/R169K–Strep–Flag (F) and SHBs/R169A–Strep–Flag (G) and analyzed by Strep pull–down and WB as in (E).
Article Snippet:
Techniques: Transfection, Control, Western Blot, Expressing, Immunoprecipitation
Journal: Tumour Virus Research
Article Title: PRMT5–mediated symmetric dimethylation of SHBs at Arg169 stabilizes SHBs and promotes angiogenesis and tumor growth
doi: 10.1016/j.tvr.2026.200340
Figure Lengend Snippet: PRMT interacts with SHBs. (A) Huh7 cells were co–transfected with plasmids encoding SHBs–Strep–Flag (or Strep–Flag control) together with Flag–PRMT9. Strep pull–down was followed by WB with anti–Flag and anti–SHBs to assess co–precipitation. (B) Huh7 and HepG2 cells were co–transfected with plasmids encoding SHBs–Strep–Flag (or Strep–Flag control) together with Flag–PRMT5 and analyzed by Strep pull–down and WB as in (A). (C) Huh7 and HepG2 cells were co–transfected with plasmids encoding Strep–Flag–PRMT5 and SHBs–myc. Strep pull–down was performed and precipitates were immunoblotted for SHBs and Flag to validate the interaction. (D) Direct interaction between SHBs and PRMT5 was tested by GST pull–down. Purified GST or GST–PRMT5 (Coomassie–stained gel, left) was incubated with in vitro–translated SHBs–Flag, and bound SHBs was detected by WB using anti–Flag (right). (E) Confocal microscopy showing subcellular localization of SHBs (red) and PRMT5 (green) with nuclear DAPI staining (blue). Merged images and a representative line–scan fluorescence intensity profile (right) are shown.
Article Snippet:
Techniques: Transfection, Control, Purification, Staining, Incubation, In Vitro, Confocal Microscopy, Fluorescence
Journal: Tumour Virus Research
Article Title: PRMT5–mediated symmetric dimethylation of SHBs at Arg169 stabilizes SHBs and promotes angiogenesis and tumor growth
doi: 10.1016/j.tvr.2026.200340
Figure Lengend Snippet: PRMT5 stabilizes SHBs protein expression in an Arg169–dependent manner. (A) Huh7 and HepG2 cells were co–transfected with plasmids encoding SHBs–Strep–Flag or SHBs/R169K–Strep–Flag together with increasing amounts of Flag–PRMT5 (0, 1, 3 μg). Whole–cell lysates were immunoblotted for SHBs, Flag, and β–actin; SHBs/β–actin ratios are shown above the blots. (B) Cells expressing SHBs–Strep–Flag or SHBs/R169K–Strep–Flag were transfected with NC or PRMT5 siRNAs (#1, #2). Lysates were immunoblotted for SHBs, PRMT5, and β–actin; SHBs/β–actin ratios are shown. (C–D) Cycloheximide (CHX) chase assays in (C) Huh7 and (D) HepG2 cells. Cells expressing SHBs or SHBs/R169K with vector or Flag–PRMT5 were treated with CHX for the indicated times (0–120 min), followed by WB for SHBs, Flag, and β–actin. Plots show relative SHBs levels normalized to time 0 with fitted linear regression (equations displayed). (E) HepG2 cells were co–transfected with plasmids encoding SHBs–Strep, HA–K48Ub, together with or without Flag–PRMT5, and treated with MG132 (20 μM) for 8 h, the ubiquitination levels of SHBs was evaluated via ubiquitination assay analysis. (F) HepG2 cells were co–transfected with plasmid encoding SHBs–Strep and TRIM21–myc (or control vector) and Flag–PRMT5 (or control vector), the cell lysates were subjected to immunoprecipitation using Strep–Tactin and analyzed by immunoblotting.
Article Snippet:
Techniques: Expressing, Transfection, Plasmid Preparation, Ubiquitin Proteomics, Control, Immunoprecipitation, Western Blot
Journal: Tumour Virus Research
Article Title: PRMT5–mediated symmetric dimethylation of SHBs at Arg169 stabilizes SHBs and promotes angiogenesis and tumor growth
doi: 10.1016/j.tvr.2026.200340
Figure Lengend Snippet: Arg169 symmetric dimethylation is required for SHBs–driven angiogenesis and tumor growth. (A) WB analysis of SHBs and BIP expression in stably transduced Huh7 and HepG2 cells (Vector, SHBs, and SHBs/R169K). (B) ELISA measurement of VEGFA levels in the supernatants of Huh7/HepG2–Vector, Huh7/HepG2–SHBs, or Huh7/HepG2–SHBs/R169K cells. (C) Endothelial tube formation assay. EA.hy926 cells were cultured with conditioned media (CM) from Huh7 or HepG2 stable lines (Vector, SHBs, SHBs/R169K). Representative images and quantification of mesh numbers are shown. (D) Transwell migration assay. EA.hy926 cells were assessed for migration in response to CM from the indicated stable lines. Representative images and quantification of migrated cell numbers per field are shown. (E) Representative images of excised subcutaneous xenograft tumors derived from Huh7–Vector, Huh7–SHBs, or Huh7–SHBs/R169K cells. (F) Tumor growth curves (tumor volume over time) for the indicated xenograft groups. (G) Tumor weights at endpoint. (H) Representative immunohistochemical staining of xenograft tumors for CD31 and SHBs, with quantification of microvessel density (MVD) based on CD31 staining. Data are presented as mean ± SD; ∗ P < 0.05 as indicated.
Article Snippet:
Techniques: Expressing, Stable Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Endothelial Tube Formation Assay, Cell Culture, Transwell Migration Assay, Migration, Derivative Assay, Immunohistochemical staining, Staining
Journal: Food Chemistry: Molecular Sciences
Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways
doi: 10.1016/j.fochms.2026.100387
Figure Lengend Snippet: Sangyod rice extract demonstrated a reduction in cytotoxicity and ROS levels in OA-induced HepG2 cells. (A) Viability of HepG2 cells exposed to different concentrations of Sangyod rice extract. (B) Viability of Sangyod rice extract treatment after OA-induced HepG2 cells. (C) ROS generation in OA-induced HepG2 cells. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. * p < 0.05 compared to the control group, and # p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.
Article Snippet: The
Techniques: Control
Journal: Food Chemistry: Molecular Sciences
Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways
doi: 10.1016/j.fochms.2026.100387
Figure Lengend Snippet: Sangyod rice extract inhibited apoptosis in OA-induced HepG2 cells by suppressing the Bax and caspase-3 pathway. (A) Representative images of nuclei stained with Hoechst 33342. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of apoptotic cells after treatment with Sangyod rice extract in OA-induced HepG2 cells. (C) Western blot analysis of Bax, Bcl-2, procaspase-3, and cleaved caspase-3. (D) Relative expression of Bax and Bcl-2. (E) Relative expression of procaspase 3, and cleaved caspase 3. Results are presented as the mean ± SEM from four independent biological experiments ( n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 compared to the control group, and #p < 0.05 compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.
Article Snippet: The
Techniques: Staining, Western Blot, Expressing, Control
Journal: Food Chemistry: Molecular Sciences
Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways
doi: 10.1016/j.fochms.2026.100387
Figure Lengend Snippet: Sangyod rice extract attenuated inflammation in OA-induced HepG2 cells through inhibition of the NF-κB pathway. (A) TNF-α gene, (B) IL-1β gene, (C) IL-6 gene, (D) IL-10 gene. (E) Western blot analysis of NF-κB. (F) Relative expression of NF-κB protein. Results are presented as the mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.
Article Snippet: The
Techniques: Inhibition, Western Blot, Expressing, Control
Journal: Food Chemistry: Molecular Sciences
Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways
doi: 10.1016/j.fochms.2026.100387
Figure Lengend Snippet: Sangyod rice extract reduced lipid accumulation in OA-induced HepG2 cells. (A) Oil Red O staining was conducted on HepG2 cells, with red fat droplets indicating lipid accumulation. Images shown at ×20 magnification. Scale bar: 50 μm. (B) Percentage of lipid accumulation post Oil Red O extraction. (C) Levels of TG were measured using an assay kit. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.
Article Snippet: The
Techniques: Staining, Extraction, Control
Journal: Food Chemistry: Molecular Sciences
Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways
doi: 10.1016/j.fochms.2026.100387
Figure Lengend Snippet: Effect of Sangyod rice extract on lipid metabolism in OA-induced HepG2 cells. (A) SREBP-1c gene (B) ACC gene, (C) FASN gene (D) CPT-1 A gene, (E) SCD1 gene, (F) MTTP gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.
Article Snippet: The
Techniques: Control
Journal: Food Chemistry: Molecular Sciences
Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways
doi: 10.1016/j.fochms.2026.100387
Figure Lengend Snippet: Effect of Sangyod rice extract on the expression of LPL-1, LPL-2, PGC-1α and PPARα in OA-induced HepG2 cells. (A) LPL-1 gene (B) LPL-2 gene, (C) PPARα gene (D) PGC-1α gene. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.
Article Snippet: The
Techniques: Expressing, Control
Journal: Food Chemistry: Molecular Sciences
Article Title: Sangyod rice extract attenuates oleic acid–induced hepatic steatosis by modulating apoptotic, inflammatory, and lipid metabolic pathways
doi: 10.1016/j.fochms.2026.100387
Figure Lengend Snippet: Sangyod rice extract regulates lipid metabolism through the Akt and MAPK signaling pathways. (A) Western blot analysis of Akt, ERK1/2 amd p38 MAPK, (B) Relative expression of pERK/ERK protein, (C) Relative expression of p-p38/p38 protein, (D) Relative expression of pAkt/Akt protein. The data is displayed as mean ± SEM from four independent biological experiments (n = 4). One-way ANOVA followed by Tukey ' s post hoc test was used to determine statistical significance. *p < 0.05 indicates significance compared to the control group, while #p < 0.05 denotes significance compared to the OA group. Groups: Control (0.1% DMSO); OA (0.4 mM), oleic acid-induced HepG2 cells without treatment; SR 10, OA-induced HepG2 cells +10 μg/mL Sangyod rice extract; SR 50, OA-induced HepG2 cells +50 μg/mL Sangyod rice extract; SR 100, OA-induced HepG2 cells +100 μg/mL Sangyod rice extract.
Article Snippet: The
Techniques: Protein-Protein interactions, Western Blot, Expressing, Control
Journal: Hepatology Communications
Article Title: Molnupiravir is effective against hepatitis E virus infection in an animal model
doi: 10.1097/HC9.0000000000000944
Figure Lengend Snippet: In vitro evaluation of molnupiravir in HEV cell culture models. (A) Cytotoxicity of molnupiravir, ribavirin, and sofosbuvir in PLC/PRF/5 cells and PRH. Three replicates per concentration. Bars represent the mean and SEM. Mean viability at each concentration was compared with the no-drug control group using the Student t test; ** indicates statistically significant difference ( p <0.05). (B) PRH infected with rHEV and treated with either PBS, varying concentrations of molnupiravir, ribavirin, and sofosbuvir, as well as combinations. (C) Immunofluorescence staining for rHEV-infected PRH with/without antivirals: uninfected cells (negative control), rHEV-infected cells treated with either PBS (no drug control), sofosbuvir 10 μM, ribavirin 200 μM, or molnupiravir 100 μM. Cells were stained with polyclonal anti-rHEV sera and counterstained with DAPI. (D) PLC/PRF/5 cells infected with HEV infectious clone Kernow-p6, (E) PLC/PRF/5 cells infected with human-derived HEV. Cells were treated with either PBS, varying concentrations of molnupiravir, ribavirin, and sofosbuvir, as well as combinations. Error bars represent SEM (n=3 replicates per concentration). Mean viral loads at each concentration were compared with the no-drug control group using the Student t test; * indicates statistically significant difference ( p <0.05) from the untreated mean. ** indicates an extremely statistically significant difference ( p <0.01) from the untreated mean. Abbreviations: HEV, hepatitis E virus; PRH, primary rat hepatocytes; SEM, standard error of the mean; PBS, phosphate-buffered saline; rHEV, Rocahepevirus ratti genotype 1; DAPI, 4′,6-diamidino-2-phenylindole.
Article Snippet:
Techniques: In Vitro, Cell Culture, Concentration Assay, Control, Infection, Immunofluorescence, Staining, Negative Control, Derivative Assay, Virus, Saline
Journal: World Journal of Microbiology & Biotechnology
Article Title: Bioproduction, characterization, and evaluation of the biological activities of prodigiosin from Serratia marcescens HMS
doi: 10.1007/s11274-026-04936-8
Figure Lengend Snippet: Inhibitory activity of prodigiosin pigment and cisplatin against viability of HepG2 and MCF-7 cells. Values are presented as mean ± SD ( n = 3). One-way ANOVA showed significant differences in cell viability among treatments ( p < 0.001)
Article Snippet: Cell lines: Human breast adenocarcinoma (MCF-7) and
Techniques: Activity Assay