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MedChemExpress
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TargetMol
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Selleck Chemicals
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Cell Signaling Technology Inc
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Tocris
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Tocris
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Santa Cruz Biotechnology
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Toronto Research Chemicals
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InvivoGen
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BioMarin Inc
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Cayman Chemical
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LC Laboratories
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Image Search Results
Journal: bioRxiv
Article Title: Intrinsically disordered SERBP1 regulates translation through topology-driven G-quadruplex recognition
doi: 10.64898/2026.03.03.709370
Figure Lengend Snippet: ( A , B ) Western blot showing mTOR and SERBP1 expression levels in control and SERBP1 knockdown U251 and U343 cells. ( C ) Sequence of mTOR 5’ UTR highlighting predicted and experimentally validated G4s, and deleted region (mTOR ΔG4). ( D ) Expression levels of wild-type mTOR 5’UTR or mTOR 5’UTR with deletion of the mTOR 23 G4 region (ΔG4) upon SERBP1 knockdown, measured in reporter constructs by normalized luciferase activity. ns, not significant; **, P ≤ 0.01. ( E-H ) Confluence of U251 and U343 glioblastoma cell lines upon SERBP1 knockdown in the presence or absence of Torin 1. Data are shown as means ± standard error; ns, not significant; ****, P ≤ 0.0001 (one-way ANOVA). Combination Index (CI) <1 indicates a synergistic effect of the combination treatment.
Article Snippet: Four conditions were tested in triplicate: siCTRL + vehicle, siSERBP1 + vehicle,
Techniques: Western Blot, Expressing, Control, Knockdown, Sequencing, Construct, Luciferase, Activity Assay
Journal: Antioxidants (Basel, Switzerland)
Article Title: The PERK-eIF2α-ATF4 Axis Is Involved in Mediating ER-Stress-Induced Ferroptosis via DDIT4-mTORC1 Inhibition and Acetaminophen-Induced Hepatotoxicity.
doi: 10.3390/antiox14030307
Figure Lengend Snippet: Figure 4. ATF4-induced DDIT4 and subsequent mTORC1 inhibition trigger ferroptotic signaling. (A) Western blot analysis of indicated proteins in AML12 cells after Torin1 treatment (0, 0.5, 1, and 2 µM) for 24 h. (B–D) AML12 cells were treated with erastin (5 µM) or Torin1 (0.5 µM) in the presence or absence of Fer-1 (10 µM) for 16 h. (B) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. (C) Cell viability assessed by MTT. (D) Quantification of mRNA level of Ptgs2. (E) Western blot analysis of indicated proteins in AML12 after treatment with erastin (10 µM) at indicated times. (F–I) For knockdown Ddit4, AML12 cells were transfected with control siRNA (scRNA) or siDdit4 for 36 h. (F) Western blot analysis of indicated proteins after erastin (10 µM) treatment for 24 h. (G) Quantification of mRNA level of indicated genes. (H) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. (I) Cell viability assessed by MTT assay after erastin treatment (0, 1.25, 2.5, 5, 10, and 20 µM) for 24 h. (J) Atf4−/−cells were infected with Ad-GFP or Ad-ATF4 and then treated with erastin (10 µM) for 24 h. Western blot analysis of indicated proteins. (K–L) Ad-GFP and Ad-ATF4 were infected in scRNA or siDdit4-transfected AML12 cells followed by erastin (10 µM) treatment for 24 h. (K) Western blot analysis of indicated proteins. (L) Lipid ROS was stained with BODIPY™581/591 C11 and measured by flow cytometry. Data are mean ± SD (n = 3); * p < 0.05, ** p < 0.01, *** p < 0.001, and NS, not significant.
Article Snippet:
Techniques: Inhibition, Western Blot, Staining, Flow Cytometry, Knockdown, Transfection, Control, MTT Assay, Infection