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p araf  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p araf
    Aberrant activation of the Raf/ERK signaling pathway in BMPR2-silenced HPAECs. Lysates from control HPAECs and BMPR2-deficient HPAECs were resolved by SDS-PAGE and immunoblotted. pRAF1 (serine 338) and total RAF1 (3 independent experiments in 3 different donors) (A): pARAF (Ser-445) and total <t>ARAF</t> (n = 4) (B), pBRAF (Ser-445) and total BRAF (n = 4) (C), pERK, and total ERK (n = 6) (D), pp38 and total p38 (n = 4) (E), pJNK and total JNK (n = 4) (F), and BIM (BCL2L11; n = 4) (G). Densitometric analyses are normalized to the loading controls and the corresponding siControl condition. Representative blots are shown, and data are presented as means ± SE; *P < 0.05; **P < 0.01. H: schematic diagram of dysregulated Ras/Raf/ERK signaling resulting from BMPR2 loss-of-function. Red (up-regulated) and green (down-regulated) shading indicates the directional changes of significantly regulated transcripts [false discovery rates (FDR) < 0.01; no FC cutoff] by microarray. Black arrows (up or down) indicate experimentally determined directional changes in protein expression and/or activation state.
    P Araf, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p araf/product/Cell Signaling Technology Inc
    Average 93 stars, based on 20 article reviews
    p araf - by Bioz Stars, 2026-05
    93/100 stars

    Images

    1) Product Images from "Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells"

    Article Title: Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    doi: 10.1152/ajplung.00303.2015

    Aberrant activation of the Raf/ERK signaling pathway in BMPR2-silenced HPAECs. Lysates from control HPAECs and BMPR2-deficient HPAECs were resolved by SDS-PAGE and immunoblotted. pRAF1 (serine 338) and total RAF1 (3 independent experiments in 3 different donors) (A): pARAF (Ser-445) and total ARAF (n = 4) (B), pBRAF (Ser-445) and total BRAF (n = 4) (C), pERK, and total ERK (n = 6) (D), pp38 and total p38 (n = 4) (E), pJNK and total JNK (n = 4) (F), and BIM (BCL2L11; n = 4) (G). Densitometric analyses are normalized to the loading controls and the corresponding siControl condition. Representative blots are shown, and data are presented as means ± SE; *P < 0.05; **P < 0.01. H: schematic diagram of dysregulated Ras/Raf/ERK signaling resulting from BMPR2 loss-of-function. Red (up-regulated) and green (down-regulated) shading indicates the directional changes of significantly regulated transcripts [false discovery rates (FDR) < 0.01; no FC cutoff] by microarray. Black arrows (up or down) indicate experimentally determined directional changes in protein expression and/or activation state.
    Figure Legend Snippet: Aberrant activation of the Raf/ERK signaling pathway in BMPR2-silenced HPAECs. Lysates from control HPAECs and BMPR2-deficient HPAECs were resolved by SDS-PAGE and immunoblotted. pRAF1 (serine 338) and total RAF1 (3 independent experiments in 3 different donors) (A): pARAF (Ser-445) and total ARAF (n = 4) (B), pBRAF (Ser-445) and total BRAF (n = 4) (C), pERK, and total ERK (n = 6) (D), pp38 and total p38 (n = 4) (E), pJNK and total JNK (n = 4) (F), and BIM (BCL2L11; n = 4) (G). Densitometric analyses are normalized to the loading controls and the corresponding siControl condition. Representative blots are shown, and data are presented as means ± SE; *P < 0.05; **P < 0.01. H: schematic diagram of dysregulated Ras/Raf/ERK signaling resulting from BMPR2 loss-of-function. Red (up-regulated) and green (down-regulated) shading indicates the directional changes of significantly regulated transcripts [false discovery rates (FDR) < 0.01; no FC cutoff] by microarray. Black arrows (up or down) indicate experimentally determined directional changes in protein expression and/or activation state.

    Techniques Used: Activation Assay, Control, SDS Page, Microarray, Expressing



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    Image Search Results


    Aberrant activation of the Raf/ERK signaling pathway in BMPR2-silenced HPAECs. Lysates from control HPAECs and BMPR2-deficient HPAECs were resolved by SDS-PAGE and immunoblotted. pRAF1 (serine 338) and total RAF1 (3 independent experiments in 3 different donors) (A): pARAF (Ser-445) and total ARAF (n = 4) (B), pBRAF (Ser-445) and total BRAF (n = 4) (C), pERK, and total ERK (n = 6) (D), pp38 and total p38 (n = 4) (E), pJNK and total JNK (n = 4) (F), and BIM (BCL2L11; n = 4) (G). Densitometric analyses are normalized to the loading controls and the corresponding siControl condition. Representative blots are shown, and data are presented as means ± SE; *P < 0.05; **P < 0.01. H: schematic diagram of dysregulated Ras/Raf/ERK signaling resulting from BMPR2 loss-of-function. Red (up-regulated) and green (down-regulated) shading indicates the directional changes of significantly regulated transcripts [false discovery rates (FDR) < 0.01; no FC cutoff] by microarray. Black arrows (up or down) indicate experimentally determined directional changes in protein expression and/or activation state.

    Journal: American Journal of Physiology - Lung Cellular and Molecular Physiology

    Article Title: Raf/ERK drives the proliferative and invasive phenotype of BMPR2-silenced pulmonary artery endothelial cells

    doi: 10.1152/ajplung.00303.2015

    Figure Lengend Snippet: Aberrant activation of the Raf/ERK signaling pathway in BMPR2-silenced HPAECs. Lysates from control HPAECs and BMPR2-deficient HPAECs were resolved by SDS-PAGE and immunoblotted. pRAF1 (serine 338) and total RAF1 (3 independent experiments in 3 different donors) (A): pARAF (Ser-445) and total ARAF (n = 4) (B), pBRAF (Ser-445) and total BRAF (n = 4) (C), pERK, and total ERK (n = 6) (D), pp38 and total p38 (n = 4) (E), pJNK and total JNK (n = 4) (F), and BIM (BCL2L11; n = 4) (G). Densitometric analyses are normalized to the loading controls and the corresponding siControl condition. Representative blots are shown, and data are presented as means ± SE; *P < 0.05; **P < 0.01. H: schematic diagram of dysregulated Ras/Raf/ERK signaling resulting from BMPR2 loss-of-function. Red (up-regulated) and green (down-regulated) shading indicates the directional changes of significantly regulated transcripts [false discovery rates (FDR) < 0.01; no FC cutoff] by microarray. Black arrows (up or down) indicate experimentally determined directional changes in protein expression and/or activation state.

    Article Snippet: Antibodies against p-ERK (no. 9101, 1:1,000), total ERK (no. 9102, 1:1,000), p-p38 (no. 9211, 1:400), total p38 (no. 9212, 1:800), p-JNK (no. 4671, 1:400), total JNK (no. 9258, 1:1,000), p-RAF-1 (no. 9427, 1:1,000), p-ARAF (no. 4431, 1:500), p-BRAF (no. 2696, 1:500), were purchased from Cell Signaling (Danvers, MA).

    Techniques: Activation Assay, Control, SDS Page, Microarray, Expressing