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mouse m alk1 fc  (R&D Systems)


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    Structured Review

    R&D Systems mouse m alk1 fc
    TGFβR1 mediates TGFβ-induced Smad1/5 phosphorylation in mPASMC. SB505124 (SB), an ALK4/5/7 inhibitor, prevented TGFβ-induced Smad1/5 phosphorylation, while dorsomorphin (DM), an <t>ALK1/2/3/6</t> inhibitor, partly decreased TGFβ-induced Smad1/5 phosphorylation. Serum-starved cells were treated with 1 μM SB, 10 μM DM, or DMSO vehicle for 1 h before additional treatment with 2.5 ng/ml TGFβ1 or 20 ng/ml BMP4 for 1 h. Cell lysates were collected, and the protein expression level of the indicated Smads and GAPDH were detected using immunoblotting. Immunoblot images shown are representative of at least three independent experiments. For the densitometry analysis, n = 4 in each group; *P < 0.05.
    Mouse M Alk1 Fc, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse m alk1 fc/product/R&D Systems
    Average 91 stars, based on 14 article reviews
    mouse m alk1 fc - by Bioz Stars, 2026-03
    91/100 stars

    Images

    1) Product Images from "Transforming growth factor-β stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1"

    Article Title: Transforming growth factor-β stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1

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

    doi: 10.1152/ajplung.00079.2017

    TGFβR1 mediates TGFβ-induced Smad1/5 phosphorylation in mPASMC. SB505124 (SB), an ALK4/5/7 inhibitor, prevented TGFβ-induced Smad1/5 phosphorylation, while dorsomorphin (DM), an ALK1/2/3/6 inhibitor, partly decreased TGFβ-induced Smad1/5 phosphorylation. Serum-starved cells were treated with 1 μM SB, 10 μM DM, or DMSO vehicle for 1 h before additional treatment with 2.5 ng/ml TGFβ1 or 20 ng/ml BMP4 for 1 h. Cell lysates were collected, and the protein expression level of the indicated Smads and GAPDH were detected using immunoblotting. Immunoblot images shown are representative of at least three independent experiments. For the densitometry analysis, n = 4 in each group; *P < 0.05.
    Figure Legend Snippet: TGFβR1 mediates TGFβ-induced Smad1/5 phosphorylation in mPASMC. SB505124 (SB), an ALK4/5/7 inhibitor, prevented TGFβ-induced Smad1/5 phosphorylation, while dorsomorphin (DM), an ALK1/2/3/6 inhibitor, partly decreased TGFβ-induced Smad1/5 phosphorylation. Serum-starved cells were treated with 1 μM SB, 10 μM DM, or DMSO vehicle for 1 h before additional treatment with 2.5 ng/ml TGFβ1 or 20 ng/ml BMP4 for 1 h. Cell lysates were collected, and the protein expression level of the indicated Smads and GAPDH were detected using immunoblotting. Immunoblot images shown are representative of at least three independent experiments. For the densitometry analysis, n = 4 in each group; *P < 0.05.

    Techniques Used: Expressing, Western Blot

    ALK1 is expressed in mPASMC, mFibroblasts, and the mouse pup lung. A: ALK1 mRNA expression in the indicated adult and P10 mouse tissues and cells detected using RT-PCR. B: ALK1 protein expression in the indicated tissues and cell lysates detected using immunoblotting. Equal amounts of proteins were resolved using PAGE; effective protein transfer to the immunoblot membrane was demonstrated using Ponceau S staining. ALK1 protein expression data shown are representative of at least three independent experiments. C: ALK1 immunoreactivity (red) was detected in smooth muscle cells in pulmonary arteries (arrows), epithelial cells (arrowheads), interstitial cells (double arrows), and macrophages (*) in P10 mouse pup lungs, counterstained with hematoxylin. Representative images from three pups; scale bar is 25 µm long.
    Figure Legend Snippet: ALK1 is expressed in mPASMC, mFibroblasts, and the mouse pup lung. A: ALK1 mRNA expression in the indicated adult and P10 mouse tissues and cells detected using RT-PCR. B: ALK1 protein expression in the indicated tissues and cell lysates detected using immunoblotting. Equal amounts of proteins were resolved using PAGE; effective protein transfer to the immunoblot membrane was demonstrated using Ponceau S staining. ALK1 protein expression data shown are representative of at least three independent experiments. C: ALK1 immunoreactivity (red) was detected in smooth muscle cells in pulmonary arteries (arrows), epithelial cells (arrowheads), interstitial cells (double arrows), and macrophages (*) in P10 mouse pup lungs, counterstained with hematoxylin. Representative images from three pups; scale bar is 25 µm long.

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Membrane, Staining

    ALK1 regulates TGFβ-stimulated pSmad1/5 nuclear localization in mPASMC. A: ALK1 immunoreactivity is detected on the surface of mPASMC unless the antibody is preadsorbed with solubilized extracellular ALK1 domain (mALK1-Fc). Live cells were reacted with an anti-mALK1 antibody, an IgG2b monoclonal rat antibody that was generated against an extracellular fragment of mouse ALK1, without and with previous exposure to mALK1-Fc, or rat IgG2b, washed, fixed, and then reacted with a fluorescently labeled secondary antibody and DAPI. Subsequently, epifluorescence microscopy was performed. Typical images of two or three independent studies are shown. B: pretreatment with an anti-mALK1 antibody inhibits TGFβ-mediated BMP R-Smad phosphorylation. Cells were treated with 0 or 15 µg/ml anti-mALK1 and then incubated with 0 or 2.5 ng/ml TGFβ1 for 1 h. Subsequently, the cells were fixed and pSmad1/5 immunoreactivity, and DAPI reactivity was assessed. In additional immunoreactivity control studies, the cells were reacted with an isotype control instead of the anti-pSmad1/5 antibody. The nuclear immunoreactivity intensity signal in a region of interest identified by the DAPI reactivity was quantified and normalized with the mean level detected in the control cells. n = 45 per group; *P < 0.05. Scale bars = 50 µm.
    Figure Legend Snippet: ALK1 regulates TGFβ-stimulated pSmad1/5 nuclear localization in mPASMC. A: ALK1 immunoreactivity is detected on the surface of mPASMC unless the antibody is preadsorbed with solubilized extracellular ALK1 domain (mALK1-Fc). Live cells were reacted with an anti-mALK1 antibody, an IgG2b monoclonal rat antibody that was generated against an extracellular fragment of mouse ALK1, without and with previous exposure to mALK1-Fc, or rat IgG2b, washed, fixed, and then reacted with a fluorescently labeled secondary antibody and DAPI. Subsequently, epifluorescence microscopy was performed. Typical images of two or three independent studies are shown. B: pretreatment with an anti-mALK1 antibody inhibits TGFβ-mediated BMP R-Smad phosphorylation. Cells were treated with 0 or 15 µg/ml anti-mALK1 and then incubated with 0 or 2.5 ng/ml TGFβ1 for 1 h. Subsequently, the cells were fixed and pSmad1/5 immunoreactivity, and DAPI reactivity was assessed. In additional immunoreactivity control studies, the cells were reacted with an isotype control instead of the anti-pSmad1/5 antibody. The nuclear immunoreactivity intensity signal in a region of interest identified by the DAPI reactivity was quantified and normalized with the mean level detected in the control cells. n = 45 per group; *P < 0.05. Scale bars = 50 µm.

    Techniques Used: Generated, Labeling, Epifluorescence Microscopy, Incubation



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    mouse m alk1 fc  (R&D Systems)
    91
    R&D Systems mouse m alk1 fc
    TGFβR1 mediates TGFβ-induced Smad1/5 phosphorylation in mPASMC. SB505124 (SB), an ALK4/5/7 inhibitor, prevented TGFβ-induced Smad1/5 phosphorylation, while dorsomorphin (DM), an <t>ALK1/2/3/6</t> inhibitor, partly decreased TGFβ-induced Smad1/5 phosphorylation. Serum-starved cells were treated with 1 μM SB, 10 μM DM, or DMSO vehicle for 1 h before additional treatment with 2.5 ng/ml TGFβ1 or 20 ng/ml BMP4 for 1 h. Cell lysates were collected, and the protein expression level of the indicated Smads and GAPDH were detected using immunoblotting. Immunoblot images shown are representative of at least three independent experiments. For the densitometry analysis, n = 4 in each group; *P < 0.05.
    Mouse M Alk1 Fc, supplied by R&D Systems, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mouse m alk1 fc/product/R&D Systems
    Average 91 stars, based on 1 article reviews
    mouse m alk1 fc - by Bioz Stars, 2026-03
    91/100 stars
    		  Buy from Supplier

    Image Search Results


    TGFβR1 mediates TGFβ-induced Smad1/5 phosphorylation in mPASMC. SB505124 (SB), an ALK4/5/7 inhibitor, prevented TGFβ-induced Smad1/5 phosphorylation, while dorsomorphin (DM), an ALK1/2/3/6 inhibitor, partly decreased TGFβ-induced Smad1/5 phosphorylation. Serum-starved cells were treated with 1 μM SB, 10 μM DM, or DMSO vehicle for 1 h before additional treatment with 2.5 ng/ml TGFβ1 or 20 ng/ml BMP4 for 1 h. Cell lysates were collected, and the protein expression level of the indicated Smads and GAPDH were detected using immunoblotting. Immunoblot images shown are representative of at least three independent experiments. For the densitometry analysis, n = 4 in each group; *P < 0.05.

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

    Article Title: Transforming growth factor-β stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1

    doi: 10.1152/ajplung.00079.2017

    Figure Lengend Snippet: TGFβR1 mediates TGFβ-induced Smad1/5 phosphorylation in mPASMC. SB505124 (SB), an ALK4/5/7 inhibitor, prevented TGFβ-induced Smad1/5 phosphorylation, while dorsomorphin (DM), an ALK1/2/3/6 inhibitor, partly decreased TGFβ-induced Smad1/5 phosphorylation. Serum-starved cells were treated with 1 μM SB, 10 μM DM, or DMSO vehicle for 1 h before additional treatment with 2.5 ng/ml TGFβ1 or 20 ng/ml BMP4 for 1 h. Cell lysates were collected, and the protein expression level of the indicated Smads and GAPDH were detected using immunoblotting. Immunoblot images shown are representative of at least three independent experiments. For the densitometry analysis, n = 4 in each group; *P < 0.05.

    Article Snippet: Recombinant human TGF-β1 and BMP4, mouse (m)ALK1-Fc (all obtained from R&D Systems), and the kinase inhibitors SB505124 (S4696; Sigma) dorsomorphin (ab144821; Abcam) and LDN212854 (SML0965; Sigma) were also used.

    Techniques: Expressing, Western Blot

    ALK1 is expressed in mPASMC, mFibroblasts, and the mouse pup lung. A: ALK1 mRNA expression in the indicated adult and P10 mouse tissues and cells detected using RT-PCR. B: ALK1 protein expression in the indicated tissues and cell lysates detected using immunoblotting. Equal amounts of proteins were resolved using PAGE; effective protein transfer to the immunoblot membrane was demonstrated using Ponceau S staining. ALK1 protein expression data shown are representative of at least three independent experiments. C: ALK1 immunoreactivity (red) was detected in smooth muscle cells in pulmonary arteries (arrows), epithelial cells (arrowheads), interstitial cells (double arrows), and macrophages (*) in P10 mouse pup lungs, counterstained with hematoxylin. Representative images from three pups; scale bar is 25 µm long.

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

    Article Title: Transforming growth factor-β stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1

    doi: 10.1152/ajplung.00079.2017

    Figure Lengend Snippet: ALK1 is expressed in mPASMC, mFibroblasts, and the mouse pup lung. A: ALK1 mRNA expression in the indicated adult and P10 mouse tissues and cells detected using RT-PCR. B: ALK1 protein expression in the indicated tissues and cell lysates detected using immunoblotting. Equal amounts of proteins were resolved using PAGE; effective protein transfer to the immunoblot membrane was demonstrated using Ponceau S staining. ALK1 protein expression data shown are representative of at least three independent experiments. C: ALK1 immunoreactivity (red) was detected in smooth muscle cells in pulmonary arteries (arrows), epithelial cells (arrowheads), interstitial cells (double arrows), and macrophages (*) in P10 mouse pup lungs, counterstained with hematoxylin. Representative images from three pups; scale bar is 25 µm long.

    Article Snippet: Recombinant human TGF-β1 and BMP4, mouse (m)ALK1-Fc (all obtained from R&D Systems), and the kinase inhibitors SB505124 (S4696; Sigma) dorsomorphin (ab144821; Abcam) and LDN212854 (SML0965; Sigma) were also used.

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Membrane, Staining

    ALK1 regulates TGFβ-stimulated pSmad1/5 nuclear localization in mPASMC. A: ALK1 immunoreactivity is detected on the surface of mPASMC unless the antibody is preadsorbed with solubilized extracellular ALK1 domain (mALK1-Fc). Live cells were reacted with an anti-mALK1 antibody, an IgG2b monoclonal rat antibody that was generated against an extracellular fragment of mouse ALK1, without and with previous exposure to mALK1-Fc, or rat IgG2b, washed, fixed, and then reacted with a fluorescently labeled secondary antibody and DAPI. Subsequently, epifluorescence microscopy was performed. Typical images of two or three independent studies are shown. B: pretreatment with an anti-mALK1 antibody inhibits TGFβ-mediated BMP R-Smad phosphorylation. Cells were treated with 0 or 15 µg/ml anti-mALK1 and then incubated with 0 or 2.5 ng/ml TGFβ1 for 1 h. Subsequently, the cells were fixed and pSmad1/5 immunoreactivity, and DAPI reactivity was assessed. In additional immunoreactivity control studies, the cells were reacted with an isotype control instead of the anti-pSmad1/5 antibody. The nuclear immunoreactivity intensity signal in a region of interest identified by the DAPI reactivity was quantified and normalized with the mean level detected in the control cells. n = 45 per group; *P < 0.05. Scale bars = 50 µm.

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

    Article Title: Transforming growth factor-β stimulates Smad1/5 signaling in pulmonary artery smooth muscle cells and fibroblasts of the newborn mouse through ALK1

    doi: 10.1152/ajplung.00079.2017

    Figure Lengend Snippet: ALK1 regulates TGFβ-stimulated pSmad1/5 nuclear localization in mPASMC. A: ALK1 immunoreactivity is detected on the surface of mPASMC unless the antibody is preadsorbed with solubilized extracellular ALK1 domain (mALK1-Fc). Live cells were reacted with an anti-mALK1 antibody, an IgG2b monoclonal rat antibody that was generated against an extracellular fragment of mouse ALK1, without and with previous exposure to mALK1-Fc, or rat IgG2b, washed, fixed, and then reacted with a fluorescently labeled secondary antibody and DAPI. Subsequently, epifluorescence microscopy was performed. Typical images of two or three independent studies are shown. B: pretreatment with an anti-mALK1 antibody inhibits TGFβ-mediated BMP R-Smad phosphorylation. Cells were treated with 0 or 15 µg/ml anti-mALK1 and then incubated with 0 or 2.5 ng/ml TGFβ1 for 1 h. Subsequently, the cells were fixed and pSmad1/5 immunoreactivity, and DAPI reactivity was assessed. In additional immunoreactivity control studies, the cells were reacted with an isotype control instead of the anti-pSmad1/5 antibody. The nuclear immunoreactivity intensity signal in a region of interest identified by the DAPI reactivity was quantified and normalized with the mean level detected in the control cells. n = 45 per group; *P < 0.05. Scale bars = 50 µm.

    Article Snippet: Recombinant human TGF-β1 and BMP4, mouse (m)ALK1-Fc (all obtained from R&D Systems), and the kinase inhibitors SB505124 (S4696; Sigma) dorsomorphin (ab144821; Abcam) and LDN212854 (SML0965; Sigma) were also used.

    Techniques: Generated, Labeling, Epifluorescence Microscopy, Incubation