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Cell Signaling Technology Inc donkey anti goat igg
Donkey Anti Goat Igg, supplied by Cell Signaling Technology Inc, 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/donkey anti goat igg/product/Cell Signaling Technology Inc
Average 91 stars, based on 1 article reviews
Price from $9.99 to $1999.99
donkey anti goat igg - by Bioz Stars, 2020-07
91/100 stars

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Article Title: Unraveling the roles of CD44/CD24 and ALDH1 as cancer stem cell markers in tumorigenesis and metastasis
Article Snippet: .. The membranes were blocked with 5% non-fat milk powder (BD Bioscience) in Tris-buffered saline with 0.1% Tween (TBST) for 1 hour at room temperature and then incubated with ALDH1A1 antibody (rabbit mAb, Cell Signal Technology) or CXCR4 antibody (goat mAb, Abcam) overnight at 4 °C, followed by horse-radish-peroxidase conjugated goat anti-rabbit IgG or donkey anti-goat IgG (Cell Signal Technology) respectively for 1 hour at RT in 0.5% non-fat milk powder with TBST. .. Visualization was performed using Image Quant LAS 4000 with an Enhanced Chemiluminescence Kit (Thermo Pierce, Waltham, MA, USA).

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    Cell Signaling Technology Inc anti rat igg h l alexa fluor 488 conjugate
    Pristimerin treatment decreases Shh-induced pericyte motilities of angiogenesis. a Pristimerin suppresses Shh-mediated adhesion ability of endothelial cells. The cells that pre-treated with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) were seeded at 24-well plate. After 1-h culture, the un-attached cells were removed and the attached cells were stained with 0.1% crystal violet. b Pristimerin restrains Shh-induced pericyte migration to newly formed networks in a three-dimensional co-culture system of HUVEC and HBVP. HUVECs (red) were seeded on Matrigel-coated 96-well and cultured for 2 h to allow the formation of tube network. And HBVPs (green) pre-treated with or without pristimerin were added to the endothelial tubes. The recruitment of HBVPs to HUVEC tubes were observed and photographed at 0, 2, and 12 h. Scale bar: 20 μm. c Pristimerin suppresses the nucleus translocation of Gli1in HBVPs. HBVPs were stimulated with Shh (100 ng/mL) and pristimerin for 24 h. After staining with 4% paraformaldehyde, the HBVPs were labeled with Gli1 antibody and <t>Alexa</t> <t>Fluor</t> 488 Donkey anti-Rabbit <t>IgG.</t> DAPI was used to recognize the nucleus, and the images were taken with a laser scanning confocal microscope. d Pristimerin inhibits the distribution of Gli1 in the nucleus. HBVPs were collected and lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit following the manufacturer’s protocol, and then applied for western blotting assay. β-actin and Lamin B were set as loading control. e Pristimerin blocks the downstream of Shh/Gli1 signaling pathway. After being treated with Shh and pristimerin for 24 h, HBVP cells were lysed using RIPA buffer and subjected to western blotting assay. β-actin was set as loading control. The data are presented as mean ± SEM, n = 3. *** P
    Anti Rat Igg H L Alexa Fluor 488 Conjugate, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti rat igg h l alexa fluor 488 conjugate/product/Cell Signaling Technology Inc
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    Cell Signaling Technology Inc alexa fluor 594 donkey anti goat igg
    Pristimerin treatment decreases Shh-induced pericyte motilities of angiogenesis. a Pristimerin suppresses Shh-mediated adhesion ability of endothelial cells. The cells that pre-treated with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) were seeded at 24-well plate. After 1-h culture, the un-attached cells were removed and the attached cells were stained with 0.1% crystal violet. b Pristimerin restrains Shh-induced pericyte migration to newly formed networks in a three-dimensional co-culture system of HUVEC and HBVP. HUVECs (red) were seeded on Matrigel-coated 96-well and cultured for 2 h to allow the formation of tube network. And HBVPs (green) pre-treated with or without pristimerin were added to the endothelial tubes. The recruitment of HBVPs to HUVEC tubes were observed and photographed at 0, 2, and 12 h. Scale bar: 20 μm. c Pristimerin suppresses the nucleus translocation of Gli1in HBVPs. HBVPs were stimulated with Shh (100 ng/mL) and pristimerin for 24 h. After staining with 4% paraformaldehyde, the HBVPs were labeled with Gli1 antibody and <t>Alexa</t> Fluor 488 Donkey anti-Rabbit <t>IgG.</t> DAPI was used to recognize the nucleus, and the images were taken with a laser scanning confocal microscope. d Pristimerin inhibits the distribution of Gli1 in the nucleus. HBVPs were collected and lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit following the manufacturer’s protocol, and then applied for western blotting assay. β-actin and Lamin B were set as loading control. e Pristimerin blocks the downstream of Shh/Gli1 signaling pathway. After being treated with Shh and pristimerin for 24 h, HBVP cells were lysed using RIPA buffer and subjected to western blotting assay. β-actin was set as loading control. The data are presented as mean ± SEM, n = 3. *** P
    Alexa Fluor 594 Donkey Anti Goat Igg, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc donkey anti goat igg horse radish peroxidase conjugated antibodies
    <t>Big-h3</t> was down-regulated in split radiation induced lymphoma tissue samples. (A) The expression of Big-h3 protein in radiation induced thymic lymphoma tissue sample and normal control non irradiated thymus tissue samples detected by western blot assay. (B) The relative expression of Big-h3 protein in radiation induced lymphoma tissue sample and normal control thymus tissue samples by FACS assay. Data are shown the Mean fluorescence intensity from a representative data of at least three independent experiments. The Mean fluorescence intensity of a proper negative control <t>IgG</t> is 5. (C) Statistical analysis of 1A and 1B. T: Tumor, radiation induced lymphoma tissue samples; N: Normal control thymus tissue samples, regarded as 1(100%). *: P
    Donkey Anti Goat Igg Horse Radish Peroxidase Conjugated Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc donkey anti goat igg hrp scbt
    <t>Big-h3</t> was down-regulated in split radiation induced lymphoma tissue samples. (A) The expression of Big-h3 protein in radiation induced thymic lymphoma tissue sample and normal control non irradiated thymus tissue samples detected by western blot assay. (B) The relative expression of Big-h3 protein in radiation induced lymphoma tissue sample and normal control thymus tissue samples by FACS assay. Data are shown the Mean fluorescence intensity from a representative data of at least three independent experiments. The Mean fluorescence intensity of a proper negative control <t>IgG</t> is 5. (C) Statistical analysis of 1A and 1B. T: Tumor, radiation induced lymphoma tissue samples; N: Normal control thymus tissue samples, regarded as 1(100%). *: P
    Donkey Anti Goat Igg Hrp Scbt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Pristimerin treatment decreases Shh-induced pericyte motilities of angiogenesis. a Pristimerin suppresses Shh-mediated adhesion ability of endothelial cells. The cells that pre-treated with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) were seeded at 24-well plate. After 1-h culture, the un-attached cells were removed and the attached cells were stained with 0.1% crystal violet. b Pristimerin restrains Shh-induced pericyte migration to newly formed networks in a three-dimensional co-culture system of HUVEC and HBVP. HUVECs (red) were seeded on Matrigel-coated 96-well and cultured for 2 h to allow the formation of tube network. And HBVPs (green) pre-treated with or without pristimerin were added to the endothelial tubes. The recruitment of HBVPs to HUVEC tubes were observed and photographed at 0, 2, and 12 h. Scale bar: 20 μm. c Pristimerin suppresses the nucleus translocation of Gli1in HBVPs. HBVPs were stimulated with Shh (100 ng/mL) and pristimerin for 24 h. After staining with 4% paraformaldehyde, the HBVPs were labeled with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to recognize the nucleus, and the images were taken with a laser scanning confocal microscope. d Pristimerin inhibits the distribution of Gli1 in the nucleus. HBVPs were collected and lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit following the manufacturer’s protocol, and then applied for western blotting assay. β-actin and Lamin B were set as loading control. e Pristimerin blocks the downstream of Shh/Gli1 signaling pathway. After being treated with Shh and pristimerin for 24 h, HBVP cells were lysed using RIPA buffer and subjected to western blotting assay. β-actin was set as loading control. The data are presented as mean ± SEM, n = 3. *** P

    Journal: Cell Death & Disease

    Article Title: Identification of a novel tumor angiogenesis inhibitor targeting Shh/Gli1 signaling pathway in Non-small cell lung cancer

    doi: 10.1038/s41419-020-2425-0

    Figure Lengend Snippet: Pristimerin treatment decreases Shh-induced pericyte motilities of angiogenesis. a Pristimerin suppresses Shh-mediated adhesion ability of endothelial cells. The cells that pre-treated with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) were seeded at 24-well plate. After 1-h culture, the un-attached cells were removed and the attached cells were stained with 0.1% crystal violet. b Pristimerin restrains Shh-induced pericyte migration to newly formed networks in a three-dimensional co-culture system of HUVEC and HBVP. HUVECs (red) were seeded on Matrigel-coated 96-well and cultured for 2 h to allow the formation of tube network. And HBVPs (green) pre-treated with or without pristimerin were added to the endothelial tubes. The recruitment of HBVPs to HUVEC tubes were observed and photographed at 0, 2, and 12 h. Scale bar: 20 μm. c Pristimerin suppresses the nucleus translocation of Gli1in HBVPs. HBVPs were stimulated with Shh (100 ng/mL) and pristimerin for 24 h. After staining with 4% paraformaldehyde, the HBVPs were labeled with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to recognize the nucleus, and the images were taken with a laser scanning confocal microscope. d Pristimerin inhibits the distribution of Gli1 in the nucleus. HBVPs were collected and lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit following the manufacturer’s protocol, and then applied for western blotting assay. β-actin and Lamin B were set as loading control. e Pristimerin blocks the downstream of Shh/Gli1 signaling pathway. After being treated with Shh and pristimerin for 24 h, HBVP cells were lysed using RIPA buffer and subjected to western blotting assay. β-actin was set as loading control. The data are presented as mean ± SEM, n = 3. *** P

    Article Snippet: Antibodies against α-SMA (19245S), Ki67 (9449T), Akt (4685S), p-AktThr308 (13038S), ERK (4695S), p-ERKThr202/Tyr204 (4370T), PDGFR-β (3174T), p-PDGFR-βTyr857 (3170T), β-actin (4970T), Alexa Fluor 594 Donkey anti-Goat IgG (889S), Alexa Fluor 488 Donkey anti-Rabbit IgG (4416S) and HRP-conjugated anti-rabbit IgG antibody (4412S) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Staining, Migration, Co-Culture Assay, Cell Culture, Translocation Assay, Labeling, Microscopy, Western Blot

    Pristimerin suppresses endothelial cellular motilities required for angiogenesis through inactivating Shh/Gli1 signaling pathway. a Pristimerin suppressed nucleus translocation of Gli1 in endothelial cells. After incubating with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) for 24 h, the HUVECs and HMEC-1 cells were stained with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to label the nucleus. The cells were observed and photographed with a laser scanning confocal microscope. Scale bar: 20 μm. b , c Pristimerin inhibits Gli1 distribution in endothelial cells. The HUVECs and HMEC-1 cells were incubated with Shh and pristimerin for 24 h, and then lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit. After that, proteins were subjected to western blotting assay. β-actin and Lamin B were set as loading control. The quantitative data were presented as ratios of Gli1/β-actin and Gli1/Lamin B. The representative blot and quantitative data were shown in B C, respectively. d , e Pristimerin inactivated Shh/Gli1 and its downstream signaling pathway. The cells were treated with Shh and pristimerin for 24 h and lysed using RIPA buffer. Total proteins were subjected to western blotting assay. The representative blot and quantitative data were shown in d , e , respectively. The data are presented as mean ± SEM, n = 3. *** P

    Journal: Cell Death & Disease

    Article Title: Identification of a novel tumor angiogenesis inhibitor targeting Shh/Gli1 signaling pathway in Non-small cell lung cancer

    doi: 10.1038/s41419-020-2425-0

    Figure Lengend Snippet: Pristimerin suppresses endothelial cellular motilities required for angiogenesis through inactivating Shh/Gli1 signaling pathway. a Pristimerin suppressed nucleus translocation of Gli1 in endothelial cells. After incubating with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) for 24 h, the HUVECs and HMEC-1 cells were stained with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to label the nucleus. The cells were observed and photographed with a laser scanning confocal microscope. Scale bar: 20 μm. b , c Pristimerin inhibits Gli1 distribution in endothelial cells. The HUVECs and HMEC-1 cells were incubated with Shh and pristimerin for 24 h, and then lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit. After that, proteins were subjected to western blotting assay. β-actin and Lamin B were set as loading control. The quantitative data were presented as ratios of Gli1/β-actin and Gli1/Lamin B. The representative blot and quantitative data were shown in B C, respectively. d , e Pristimerin inactivated Shh/Gli1 and its downstream signaling pathway. The cells were treated with Shh and pristimerin for 24 h and lysed using RIPA buffer. Total proteins were subjected to western blotting assay. The representative blot and quantitative data were shown in d , e , respectively. The data are presented as mean ± SEM, n = 3. *** P

    Article Snippet: Antibodies against α-SMA (19245S), Ki67 (9449T), Akt (4685S), p-AktThr308 (13038S), ERK (4695S), p-ERKThr202/Tyr204 (4370T), PDGFR-β (3174T), p-PDGFR-βTyr857 (3170T), β-actin (4970T), Alexa Fluor 594 Donkey anti-Goat IgG (889S), Alexa Fluor 488 Donkey anti-Rabbit IgG (4416S) and HRP-conjugated anti-rabbit IgG antibody (4412S) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Translocation Assay, Staining, Microscopy, Incubation, Western Blot

    Pristimerin treatment decreases Shh-induced pericyte motilities of angiogenesis. a Pristimerin suppresses Shh-mediated adhesion ability of endothelial cells. The cells that pre-treated with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) were seeded at 24-well plate. After 1-h culture, the un-attached cells were removed and the attached cells were stained with 0.1% crystal violet. b Pristimerin restrains Shh-induced pericyte migration to newly formed networks in a three-dimensional co-culture system of HUVEC and HBVP. HUVECs (red) were seeded on Matrigel-coated 96-well and cultured for 2 h to allow the formation of tube network. And HBVPs (green) pre-treated with or without pristimerin were added to the endothelial tubes. The recruitment of HBVPs to HUVEC tubes were observed and photographed at 0, 2, and 12 h. Scale bar: 20 μm. c Pristimerin suppresses the nucleus translocation of Gli1in HBVPs. HBVPs were stimulated with Shh (100 ng/mL) and pristimerin for 24 h. After staining with 4% paraformaldehyde, the HBVPs were labeled with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to recognize the nucleus, and the images were taken with a laser scanning confocal microscope. d Pristimerin inhibits the distribution of Gli1 in the nucleus. HBVPs were collected and lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit following the manufacturer’s protocol, and then applied for western blotting assay. β-actin and Lamin B were set as loading control. e Pristimerin blocks the downstream of Shh/Gli1 signaling pathway. After being treated with Shh and pristimerin for 24 h, HBVP cells were lysed using RIPA buffer and subjected to western blotting assay. β-actin was set as loading control. The data are presented as mean ± SEM, n = 3. *** P

    Journal: Cell Death & Disease

    Article Title: Identification of a novel tumor angiogenesis inhibitor targeting Shh/Gli1 signaling pathway in Non-small cell lung cancer

    doi: 10.1038/s41419-020-2425-0

    Figure Lengend Snippet: Pristimerin treatment decreases Shh-induced pericyte motilities of angiogenesis. a Pristimerin suppresses Shh-mediated adhesion ability of endothelial cells. The cells that pre-treated with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) were seeded at 24-well plate. After 1-h culture, the un-attached cells were removed and the attached cells were stained with 0.1% crystal violet. b Pristimerin restrains Shh-induced pericyte migration to newly formed networks in a three-dimensional co-culture system of HUVEC and HBVP. HUVECs (red) were seeded on Matrigel-coated 96-well and cultured for 2 h to allow the formation of tube network. And HBVPs (green) pre-treated with or without pristimerin were added to the endothelial tubes. The recruitment of HBVPs to HUVEC tubes were observed and photographed at 0, 2, and 12 h. Scale bar: 20 μm. c Pristimerin suppresses the nucleus translocation of Gli1in HBVPs. HBVPs were stimulated with Shh (100 ng/mL) and pristimerin for 24 h. After staining with 4% paraformaldehyde, the HBVPs were labeled with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to recognize the nucleus, and the images were taken with a laser scanning confocal microscope. d Pristimerin inhibits the distribution of Gli1 in the nucleus. HBVPs were collected and lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit following the manufacturer’s protocol, and then applied for western blotting assay. β-actin and Lamin B were set as loading control. e Pristimerin blocks the downstream of Shh/Gli1 signaling pathway. After being treated with Shh and pristimerin for 24 h, HBVP cells were lysed using RIPA buffer and subjected to western blotting assay. β-actin was set as loading control. The data are presented as mean ± SEM, n = 3. *** P

    Article Snippet: Antibodies against α-SMA (19245S), Ki67 (9449T), Akt (4685S), p-AktThr308 (13038S), ERK (4695S), p-ERKThr202/Tyr204 (4370T), PDGFR-β (3174T), p-PDGFR-βTyr857 (3170T), β-actin (4970T), Alexa Fluor 594 Donkey anti-Goat IgG (889S), Alexa Fluor 488 Donkey anti-Rabbit IgG (4416S) and HRP-conjugated anti-rabbit IgG antibody (4412S) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Staining, Migration, Co-Culture Assay, Cell Culture, Translocation Assay, Labeling, Microscopy, Western Blot

    Pristimerin suppresses endothelial cellular motilities required for angiogenesis through inactivating Shh/Gli1 signaling pathway. a Pristimerin suppressed nucleus translocation of Gli1 in endothelial cells. After incubating with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) for 24 h, the HUVECs and HMEC-1 cells were stained with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to label the nucleus. The cells were observed and photographed with a laser scanning confocal microscope. Scale bar: 20 μm. b , c Pristimerin inhibits Gli1 distribution in endothelial cells. The HUVECs and HMEC-1 cells were incubated with Shh and pristimerin for 24 h, and then lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit. After that, proteins were subjected to western blotting assay. β-actin and Lamin B were set as loading control. The quantitative data were presented as ratios of Gli1/β-actin and Gli1/Lamin B. The representative blot and quantitative data were shown in B C, respectively. d , e Pristimerin inactivated Shh/Gli1 and its downstream signaling pathway. The cells were treated with Shh and pristimerin for 24 h and lysed using RIPA buffer. Total proteins were subjected to western blotting assay. The representative blot and quantitative data were shown in d , e , respectively. The data are presented as mean ± SEM, n = 3. *** P

    Journal: Cell Death & Disease

    Article Title: Identification of a novel tumor angiogenesis inhibitor targeting Shh/Gli1 signaling pathway in Non-small cell lung cancer

    doi: 10.1038/s41419-020-2425-0

    Figure Lengend Snippet: Pristimerin suppresses endothelial cellular motilities required for angiogenesis through inactivating Shh/Gli1 signaling pathway. a Pristimerin suppressed nucleus translocation of Gli1 in endothelial cells. After incubating with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) for 24 h, the HUVECs and HMEC-1 cells were stained with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to label the nucleus. The cells were observed and photographed with a laser scanning confocal microscope. Scale bar: 20 μm. b , c Pristimerin inhibits Gli1 distribution in endothelial cells. The HUVECs and HMEC-1 cells were incubated with Shh and pristimerin for 24 h, and then lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit. After that, proteins were subjected to western blotting assay. β-actin and Lamin B were set as loading control. The quantitative data were presented as ratios of Gli1/β-actin and Gli1/Lamin B. The representative blot and quantitative data were shown in B C, respectively. d , e Pristimerin inactivated Shh/Gli1 and its downstream signaling pathway. The cells were treated with Shh and pristimerin for 24 h and lysed using RIPA buffer. Total proteins were subjected to western blotting assay. The representative blot and quantitative data were shown in d , e , respectively. The data are presented as mean ± SEM, n = 3. *** P

    Article Snippet: Antibodies against α-SMA (19245S), Ki67 (9449T), Akt (4685S), p-AktThr308 (13038S), ERK (4695S), p-ERKThr202/Tyr204 (4370T), PDGFR-β (3174T), p-PDGFR-βTyr857 (3170T), β-actin (4970T), Alexa Fluor 594 Donkey anti-Goat IgG (889S), Alexa Fluor 488 Donkey anti-Rabbit IgG (4416S) and HRP-conjugated anti-rabbit IgG antibody (4412S) were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Translocation Assay, Staining, Microscopy, Incubation, Western Blot

    Big-h3 was down-regulated in split radiation induced lymphoma tissue samples. (A) The expression of Big-h3 protein in radiation induced thymic lymphoma tissue sample and normal control non irradiated thymus tissue samples detected by western blot assay. (B) The relative expression of Big-h3 protein in radiation induced lymphoma tissue sample and normal control thymus tissue samples by FACS assay. Data are shown the Mean fluorescence intensity from a representative data of at least three independent experiments. The Mean fluorescence intensity of a proper negative control IgG is 5. (C) Statistical analysis of 1A and 1B. T: Tumor, radiation induced lymphoma tissue samples; N: Normal control thymus tissue samples, regarded as 1(100%). *: P

    Journal: International Journal of Biological Sciences

    Article Title: MiR-21 plays an Important Role in Radiation Induced Carcinogenesis in BALB/c Mice by Directly Targeting the Tumor Suppressor Gene Big-h3

    doi:

    Figure Lengend Snippet: Big-h3 was down-regulated in split radiation induced lymphoma tissue samples. (A) The expression of Big-h3 protein in radiation induced thymic lymphoma tissue sample and normal control non irradiated thymus tissue samples detected by western blot assay. (B) The relative expression of Big-h3 protein in radiation induced lymphoma tissue sample and normal control thymus tissue samples by FACS assay. Data are shown the Mean fluorescence intensity from a representative data of at least three independent experiments. The Mean fluorescence intensity of a proper negative control IgG is 5. (C) Statistical analysis of 1A and 1B. T: Tumor, radiation induced lymphoma tissue samples; N: Normal control thymus tissue samples, regarded as 1(100%). *: P

    Article Snippet: Blots were probed with antibodies specific for murine Big-h3 (sc-14742, Santa Cruz) with appropriate donkey anti-goat IgG-horse radish peroxidase-conjugated antibodies as secondary antibodies (Cell Signaling).

    Techniques: Expressing, Irradiation, Western Blot, FACS, Fluorescence, Negative Control