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pakt s473  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc pakt s473
    Pakt S473, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 17202 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pakt+s473/Phospho-Akt+(Ser473)+XP+Rabbit+mAb/pm41896221-95-51-53
    Average 99 stars, based on 17202 article reviews
    pakt s473 - by Bioz Stars, 2026-09
    99/100 stars

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    Western Blot:

    Article Title: Beta-arrestin 1/2 are essential for embryonic lymphatic vessel development.
    Article Snippet: .. Antibodies used 508 in the WB assay: p-p44/42 MAPK (T202/Y204) (CST, #4370, 1:5,000), p44/42 MAPK (ERK1/2) 509 (CST, #9102, 1:5,000), pAKT(S473) (CST, #4060, 1:5,000), AKT(pan) (CST,#4691, 1:5,000), P-510 CREB(Ser133)(CST, #9198, 1:5,000), CREB(CST,#9197, 1:5,000), VE-Cadherin (R&D, AF1002, 511 1:5,000), β-Catenin (BD, 610153, 1:5,000), GAPDH (Novus Biologicals, #NB300-221, 1:10,000), 512 goat anti-rabbit IR Dye 800 CW (Licor #926-32211, 1:10,000 dilution), goat anti-mouse IR Dye 513 800 CW (Licor #926-32210, 1:10,000 dilution), goat anti-mouse IR Dye 680 CW (Licor #926-514 68020, 1:10,000 dilution). ..

    Article Title: ZFTA-RELA ependymomas make itaconate to epigenetically drive fusion expression.
    Article Snippet: .. The following antibodies were used in the immunoblotting experiments: RELA (Cell Signaling Technology, 8242, 1:1,000); GAPDH (Cell Signaling Technology, 2118, 1:10,000); vinculin (Sigma Aldrich, V9264, 1:40,000); ACOD1-human (Abcam, ab222411, 1:1,000 and Novus Biologicals, NBP3-06244, 1:1,000); ACOD1-mouse (Cell Signaling Technology, 17805, 1:1,000); ZFTA (C11orf95) (VWR, 89379-010, AP11349B, 1:1,000); RFP (Abcam, Ab124754, 1:1,000); MAML3 (Invitrogen, PA5-13678, 1:1,000); SLC1A5 (Cell Signaling Technology, 5345, 1:1,000); GLS-human (Cell Signaling Technology, 49363, 1:1,000); GLS-mouse (Invitrogen, PA5-35365, 1:1,000); MYC (Abcam, 32072, 1:1,000); PTEN (Cell Signaling Technology, 9559, 1:1,000); pAKT (S473) (Cell Signaling Technology, 9271, 1:1,000); AKT (Cell Signaling Technology, 4056, 1:1,000); pS6RP (S235/236) (Cell Signaling Technology, 4858, 1:1,000); S6RP (Cell Signaling Technology, 2217, 1:1,000); pGSK3α/β (Cell Signaling Technology, 9331, 1:1,000); GSK3α/β (Cell Signaling Technology, 5676, 1:1,000); H3K4me3 (Cell Signaling Technology, 9751, 1:1,000); H3K9me3 (Cell Signaling Technology, 13969, 1:1,000); H3K27Ac (Cell Signaling Technology, 8173, 1:1,000); H3K27me3 (EMD Millipore, 07-449, 1:1,000); and total H3 (Cell Signaling Technology, 3638, 1:5,000). ..

    Blocking Assay:

    Article Title: LIN28A-Dependent Kinome and Phosphoproteome Reprogramming Promotes Imatinib Resistance.
    Article Snippet: .. After blocking (TBST + 2% fish gelatin, 45 min), membranes were incubated overnight at 4°C with primary antibodies against: LIN28A (Bio-Techne, AF3757), GAPDH (CST, #97166), PTEN (CST #13866), RICTOR (Bethyl Laboratories, A300‐459A) GSK3-/ (Santa Cruz, sc‐7291), pGSK-/ (CST, #9331), pan-AKT (CST, #2920); pAKT-T308 (CST, #9275), pAKT-S473 (CST, #4060), mTOR (CST, #2972), mTORS2448 (BioLegend, 610302) ERK1/2 (Santa Cruz, sc-514302), pEKR1/2-Y204 (Thermo Fisher, MA515174), PDK1 (CST, #3062), pPDK1-S241 (CST, #3438). .. Following five 5-min TBST washes, blots were incubated (45 min) with fluorescent secondary antibodies: goat anti-mouse StarBright700 (Bio-Rad), donkey anti-goat AlexaFluor680 (Thermo), or donkey anti-rabbit AlexaFluor800 (Thermo).

    Incubation:

    Article Title: LIN28A-Dependent Kinome and Phosphoproteome Reprogramming Promotes Imatinib Resistance.
    Article Snippet: .. After blocking (TBST + 2% fish gelatin, 45 min), membranes were incubated overnight at 4°C with primary antibodies against: LIN28A (Bio-Techne, AF3757), GAPDH (CST, #97166), PTEN (CST #13866), RICTOR (Bethyl Laboratories, A300‐459A) GSK3-/ (Santa Cruz, sc‐7291), pGSK-/ (CST, #9331), pan-AKT (CST, #2920); pAKT-T308 (CST, #9275), pAKT-S473 (CST, #4060), mTOR (CST, #2972), mTORS2448 (BioLegend, 610302) ERK1/2 (Santa Cruz, sc-514302), pEKR1/2-Y204 (Thermo Fisher, MA515174), PDK1 (CST, #3062), pPDK1-S241 (CST, #3438). .. Following five 5-min TBST washes, blots were incubated (45 min) with fluorescent secondary antibodies: goat anti-mouse StarBright700 (Bio-Rad), donkey anti-goat AlexaFluor680 (Thermo), or donkey anti-rabbit AlexaFluor800 (Thermo).

    other:

    Article Title: Growth factors maintain intratumoral heterogeneity and drive therapeutic resistance in triple-negative breast cancer
    Article Snippet: pAKT S473 (clone D9E) , Cell Signaling , Cat#5012; RRID: AB_2224726.



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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 <t>(S473)</t> 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.
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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 <t>(S473)</t> 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.
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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 <t>(S473)</t> 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.
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    Image Search Results


    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