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New England Biolabs
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Cytoskeleton Inc
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Thermo Fisher
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Thermo Fisher
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Journal: bioRxiv
Article Title: Microglial lipid signaling drives glioblastoma invasion and represents a therapeutic vulnerability
doi: 10.64898/2026.04.24.720633
Figure Lengend Snippet: (A) Gene expression of Yap-target genes ( Ankrd1, Ctgf, Cyr61 ) in NSCG (left) and NFpp10 (right) cells upon 24 hours of treatment with BV2 CM, BV2 CM LRA (lipid removal), BV2 CM LRA (lipid removal) LPA 18:1. Relative gene expression to S18. Fold increase. NSCG: n=3, 2way ANOVA, ** p-value<0.0056; *** p-value<0.0003, **** p-value<0.0001; NFpp10: n=3, 2way ANOVA, * p-value<0.0381, ** p-value=0.0012, *** p-value=0.0002, **** p-value<0.0001. (B) Representative immunoblots of Yap nuclear and cytoplasmic levels in NFpp10 cells upon 5 minutes, 10 minutes, 20 minutes of co-culture with BV2 cells and LPA 16:0 treatment. (C) Representative immunoblots of RhoA pulldown and total in NSCG (left) and NFpp10 (right) cells upon 2 minutes, 5 minutes, 10 minutes co-culture with BV2 cells. (D) Representative immunoblots of RhoA pulldown and total in NSCG (left) and NFpp10 (right) cells upon 5 minutes, 10 minutes co-culture with BV2 cells and LPA 18:1 or LPA 16:0 treatment respectively. (E) Invasion assays of NSCG (left) and NFpp10 (right) Scr (control) and YAP/TAZ knock-out cells in the presence or absence of BV2 cells. Fold increase. NSCG: n=3, One-way ANOVA, * p-value=0.0267, *** p-value=0.0001; NFpp10: n=6, One-way ANOVA, * p-value=0.0432, ** p-value=0.0034. (F) Invasion assays of NSCG Scr (control) and YAP knock-out cells in the presence or absence of BV2 cells and LPA 18:1 treatment. Fold increase. NSCG: n=3, One-way ANOVA, ** p-value<0.0022, *** p-value=0.0004, **** p-value<0.0001. (G) Tumor cell number across the 50 distinct TMAs. h. Ratio tumor cell/microglia-macrophages across the selected 15 tumor core and 15 tumor rim TMAs based on tumor cell density. i. Correlation tumor cells/microglia-macrophages across the selected 15 tumor core and 15 tumor rim TMAs. Each dot/number refers to a TMA sample. Correlation index: −0.477. All data represent mean ± SEM.
Article Snippet: Protein extraction was performed using the
Techniques: Gene Expression, Western Blot, Co-Culture Assay, Control, Knock-Out
Journal: bioRxiv
Article Title: NUAK2 is a therapeutically tractable regulator of RNA splicing and tumor progression in neuroendocrine prostate cancer
doi: 10.1101/2025.11.12.687734
Figure Lengend Snippet: (A) Schematic of the experimental strategy integrating label-free phosphoproteomic profiling with miniTurbo-based BioID proximity labeling to investigate NUAK2 function in NEPC. (B, C) Volcano plots showing differential phosphopeptides in NCI-H660 cells treated with the NUAK2 inhibitors HTH-02-006 or G1T-28 compared with DMSO. (D, E) Enrichment analysis of overlapping differentially phosphorylated peptides (DPP) with significantly altered phosphorylation (|log₂FC| ≥ 5) in G1T-28- and HTH-02-006–treated cells relative to DMSO. (F) Bubble plot showing proteins significantly biotinylated by mTb-NUAK2 compared to control(v5-mTb-HcRed). Each bubble represents a distinct protein, with the size of the bubble corresponding to the extent of biotinylation enrichment (number of peptides). (G) Enrichment analysis of proteins identified by NUAK2-dependent biotin labeling reveals significant enrichment of RNA metabolism, RNA splicing, and chromatin remodeling pathways. Enrichment significance determined by hypergeometric test; FDR C Article Snippet: Techniques: Labeling, Phospho-proteomics, Control, Construct, Western Blot, Biomarker Discovery, Expressing, Co-Immunoprecipitation Assay, Generated