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phosphorylated smad family member 3  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc phosphorylated smad family member 3
    Phosphorylated Smad Family Member 3, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 3854 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phosphorylated smad family member 3/product/Cell Signaling Technology Inc
    Average 98 stars, based on 3854 article reviews
    phosphorylated smad family member 3 - by Bioz Stars, 2026-02
    98/100 stars

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    Effect of CAPE treatment on EMT markers expression. PANC-1 cells exhibited a weak expression of E-cadherin and strong expression of vimentin by TGF- β stimulation. The downregulation of E-cadherin expression and upregulation of vimentin expression, markers of EMT, were reversed by CAPE treatment, but CAPE treatment did not reduce the expression levels of <t>Smad</t> <t>2/3</t> (at 24 h).
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    Transforming growth factor beta (TGF-β) signaling pathway in REM sleep deprivation with and without lithium treatment. The REM sleep-deprived hearts ( n = 5) had greater expression levels of TGF-β, <t>phosphorylated</t> <t>Smad</t> 2/3, and α-smooth muscle actin (α-SMA) compared with the control ( n = 5) and lithium-treated REM sleep-deprived ( n = 5) hearts. * p < 0.05; ** p < 0.01; *** p < 0.001.
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    Effect of CAPE treatment on EMT markers expression. PANC-1 cells exhibited a weak expression of E-cadherin and strong expression of vimentin by TGF- β stimulation. The downregulation of E-cadherin expression and upregulation of vimentin expression, markers of EMT, were reversed by CAPE treatment, but CAPE treatment did not reduce the expression levels of Smad 2/3 (at 24 h).

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Caffeic Acid Phenethyl Ester Inhibits Epithelial-Mesenchymal Transition of Human Pancreatic Cancer Cells

    doi: 10.1155/2013/270906

    Figure Lengend Snippet: Effect of CAPE treatment on EMT markers expression. PANC-1 cells exhibited a weak expression of E-cadherin and strong expression of vimentin by TGF- β stimulation. The downregulation of E-cadherin expression and upregulation of vimentin expression, markers of EMT, were reversed by CAPE treatment, but CAPE treatment did not reduce the expression levels of Smad 2/3 (at 24 h).

    Article Snippet: The membrane was blocked with 5% defatted milk and then immunoblotted with primary antibodies including E-cadherin, vimentin, Smad 2/3, and phosphorylated Smad 2/3 (BD Transduction Laboratories) at room temperature for 2 hours.

    Techniques: Expressing

    Transforming growth factor beta (TGF-β) signaling pathway in REM sleep deprivation with and without lithium treatment. The REM sleep-deprived hearts ( n = 5) had greater expression levels of TGF-β, phosphorylated Smad 2/3, and α-smooth muscle actin (α-SMA) compared with the control ( n = 5) and lithium-treated REM sleep-deprived ( n = 5) hearts. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Journal: International Journal of Molecular Sciences

    Article Title: Lithium Treatment Improves Cardiac Dysfunction in Rats Deprived of Rapid Eye Movement Sleep

    doi: 10.3390/ijms231911226

    Figure Lengend Snippet: Transforming growth factor beta (TGF-β) signaling pathway in REM sleep deprivation with and without lithium treatment. The REM sleep-deprived hearts ( n = 5) had greater expression levels of TGF-β, phosphorylated Smad 2/3, and α-smooth muscle actin (α-SMA) compared with the control ( n = 5) and lithium-treated REM sleep-deprived ( n = 5) hearts. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Article Snippet: Blots were probed with the following antibodies against regulator proteins involved in cardiac fibrogenesis: TGF-β (1:2000, polyclonal, #3711; Cell Signaling Technology, Beverly, MA, USA), TGF-β RI (1:1000, polyclonal, #sc-398; Santa Cruz Biotechnology, Santa Cruz, CA, USA), total Smad 2/3 (1:2000, monoclonal, #8685; Cell Signaling Technology), phosphorylated Smad 2/3 (1:2000, monoclonal, #8828; Cell Signaling Technology), α-SMA (1:5000, monoclonal, #ab7817; Abcam, Cambridge, UK), AGTR1 (1:2000, polyclonal, #AAR-011; Alomone Labs, Jerusalem, Israel), total NF-κB p65 (1:2000, monoclonal, #8242; Cell Signaling Technology), phosphorylated NF-κB p65 (1:2000, monoclonal, #3033; Cell Signaling Technology), Orai1 (1:2000, polyclonal, #4281; ProSci Incorporated, Poway, CA, USA), STIM1 (1:2000, monoclonal, #610954; BD Transduction Laboratories, San Diego, CA, USA), TRPC 1 channel (1:2000, polyclonal, #ACC-010; Alomone Labs), TRPC3 (1:5000, polyclonal, #ACC-016; Alomone Labs), and TRPC6 (1:2000, polyclonal, #ACC-017; Alomone Labs).

    Techniques: Expressing, Control