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p stat3 s727 49 bd biosciences 624084 152sm p akt s473 d9e standard biotools 3152005a  (fluidigm)


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    fluidigm p stat3 s727 49 bd biosciences 624084 152sm p akt s473 d9e standard biotools 3152005a
    P Stat3 S727 49 Bd Biosciences 624084 152sm P Akt S473 D9e Standard Biotools 3152005a, supplied by fluidigm, used in various techniques. Bioz Stars score: 92/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pakt+s473/Anti-pAkt+%5BS473%5D+(D9E)-152Sm/pm41827061-244-99-109
    Average 92 stars, based on 9 article reviews
    p stat3 s727 49 bd biosciences 624084 152sm p akt s473 d9e standard biotools 3152005a - by Bioz Stars, 2026-09
    92/100 stars

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    Related Articles

    Recombinase Polymerase Amplification:

    Article Title: Dual inhibition of the MEK/ERK and PI3K/AKT pathways prevents pulmonary GVHD suppressing perivenulitis and bronchiolitis.
    Article Snippet: 208 209 Imaging mass cytometry analysis of human lung specimens 210 Formalin-fixed paraffin-embedded slides of human pulmonary GVHD were 211 dewaxed with xylene, hydrated with ethanol, incubated with antigen retrieval buffer 212 (Agilent, Santa Clara, CA), and blocked with 3% BSA. .. Primary antibodies, including 213 anti-human CD4 (EPR6855), CD8a (RPA-T8), CD20 (H1), CD68 (KP1), pAKT S473 214 14 (D9E), and pERK1/2 (D1314.4E) (Fluidigm, South San Francisco, CA) were applied 215 overnight at 4°C. .. Secondary incubation was with the intercalator, iridium (Fluidigm), 216 for 30 min at room temperature.

    Article Title: Dual inhibition of the MEK/ERK and PI3K/AKT pathways prevents pulmonary GVHD suppressing perivenulitis and bronchiolitis
    Article Snippet: Formalin-fixed paraffin-embedded slides of human pulmonary GVHD were dewaxed with xylene, hydrated with ethanol, incubated with antigen retrieval buffer (Agilent, Santa Clara, CA), and blocked with 3% bovine serum albumin. .. Primary antibodies, including anti-human CD4 (EPR6855), CD8a (RPA-T8), CD20 (H1), CD68 (KP1), pAKT S473 (D9E), and pERK1/2 (D1314.4E) (Fluidigm, South San Francisco, CA), were applied overnight at 4°C. .. Secondary incubation was with Cell ID intercalator-Iridium (Fluidigm), for 30 minutes at room temperature.

    other:

    Article Title: High-Dimensional Phospho-CyTOF Characterization of T-Cell Activation Responses in Whole Blood
    Article Snippet: 152 Sm , pAkt (S473) , Standard BioTools , 3152005A , D9E , 36.

    Article Title: Dual Phospho-CyTOF Workflows for Comparative JAK/STAT Signaling Analysis in Human Cryopreserved PBMCs and Whole Blood
    Article Snippet: 152 Sm , pAkt (S473) , Standard BioTools , 3152005A , D9E , 35.



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    Baseline cellular state dictates the impact of mutant KRAS expression. (A) Unsupervised hierarchical clustering of transcriptomic, proteomic, and phosphoproteomic datasets show that clone origin, not KRAS allele, is the major driver of sample segregation, even between clones derived from the same parental line. Color scale denotes row-normalized absolute abundance. (B) UpSet plots showing the overlap of significantly upregulated (top) and downregulated (bottom) genes (transcriptome), proteins (proteome), and phosphosites (phosphoproteome) across all four reconstituted cell lines. A fold change ≥ 1.3 and adjusted p -value ≤ 0.05 threshold were used to determine differential expression of all KRAS MUT relative to KRAS WT for at least two cell lines. Each bar represents the number of shared or unique differentially expressed features between clones. Shared upregulated and downregulated features highlight the limited global convergence of KRAS-dependent molecular responses across cell lines. (C) Quantification of pERK1/2 (T202/Y204) and pAKT (S473) levels relative to total ERK and AKT levels in each cell line. The ratios (geometric means ± geometric SD) of the expression KRAS MUT (n = 7 mutants) relative to KRAS WT (average of n = 3 biologic replicates) for each cell lines are shown. p -values are derived from Brown-Forsythe lognormal ANOVA with Games-Howell’s post-hoc test.

    Journal: bioRxiv

    Article Title: Baseline cellular state dictates the molecular impact of KRAS mutant variants in pancreatic cancer cells

    doi: 10.64898/2026.03.10.710185

    Figure Lengend Snippet: Baseline cellular state dictates the impact of mutant KRAS expression. (A) Unsupervised hierarchical clustering of transcriptomic, proteomic, and phosphoproteomic datasets show that clone origin, not KRAS allele, is the major driver of sample segregation, even between clones derived from the same parental line. Color scale denotes row-normalized absolute abundance. (B) UpSet plots showing the overlap of significantly upregulated (top) and downregulated (bottom) genes (transcriptome), proteins (proteome), and phosphosites (phosphoproteome) across all four reconstituted cell lines. A fold change ≥ 1.3 and adjusted p -value ≤ 0.05 threshold were used to determine differential expression of all KRAS MUT relative to KRAS WT for at least two cell lines. Each bar represents the number of shared or unique differentially expressed features between clones. Shared upregulated and downregulated features highlight the limited global convergence of KRAS-dependent molecular responses across cell lines. (C) Quantification of pERK1/2 (T202/Y204) and pAKT (S473) levels relative to total ERK and AKT levels in each cell line. The ratios (geometric means ± geometric SD) of the expression KRAS MUT (n = 7 mutants) relative to KRAS WT (average of n = 3 biologic replicates) for each cell lines are shown. p -values are derived from Brown-Forsythe lognormal ANOVA with Games-Howell’s post-hoc test.

    Article Snippet: The following antibodies were used for immunoblotting: rabbit anti-HSP90 (Cell Signaling Technologies (CST), 4877, 1:10,000), rabbit anti-pERK1/2 (T202/Y204) (CST, 4370, 1:2000), mouse anti-ERK1/2 (CST, 9107, 1:1000), rabbit anti-pAKT (S473) (CST, 4060, 1:1000), mouse anti-AKT (CST, 2966, 1:2000), mouse anti-KRAS (Sigma-Aldrich, 3B10-2F2, 1:1000).

    Techniques: Mutagenesis, Expressing, Clone Assay, Derivative Assay, Quantitative Proteomics