phospho p70s6kinase  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho p70s6kinase
    Phospho P70s6kinase, 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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    phospho p70s6kinase  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho p70s6kinase
    Phospho P70s6kinase, 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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    anti src 3 antibodies  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti src 3 antibodies
    <t>SRC-3</t> +/+ ApoE -/- mice exhibit more severe atherosclerosis. (A) SRC-3 was highly expressed in human atherosclerotic plaques. N represents plaque-adjacent vasculature in the lower limb aorta. AS represents atherosclerotic plaques in the lower limb aorta. (B) SRC-3 expression was upregulated in the aortas of ApoE -/- mice after the mice were fed a WD for 12 weeks. (C) SRC-3 was expressed in the endothelial cells and vascular smooth muscle cells of chow-fed SRC-3 -/- ApoE -/- mice and was further increased after the mice were fed a WD for 12 weeks. Sections of frozen aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to X-gal staining. Arrows indicate positively stained cells (blue). Scale bar, 100 µm. (D) SRC-3 promoted atherosclerotic plaque formation. Representative images of en face Oil Red O-stained aortas from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice (left panel). Quantification of the plaque areas in aortas (right panel). (E-K) Cross-sections of the aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to (E-F) H&E staining (scale bar, 500 µm (E); scale bar, 200 µm (F)), (G) α-SMA staining (scale bar, 200 µm), (H-I) Masson staining (scale bar, 200 µm (H); scale bar, 200 µm (I)), (J) Oil Red O staining (scale bar, 500 µm), and (K) F4/80 staining (scale bar, 200 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. “×” indicates necrotic area. (L) Plaque stability was significantly increased in SRC-3 -/- ApoE -/- mice. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; ** P <0.01.
    Anti Src 3 Antibodies, 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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    1) Product Images from "SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment"

    Article Title: SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment

    Journal: International Journal of Biological Sciences

    doi: 10.7150/ijbs.74864

    SRC-3 +/+ ApoE -/- mice exhibit more severe atherosclerosis. (A) SRC-3 was highly expressed in human atherosclerotic plaques. N represents plaque-adjacent vasculature in the lower limb aorta. AS represents atherosclerotic plaques in the lower limb aorta. (B) SRC-3 expression was upregulated in the aortas of ApoE -/- mice after the mice were fed a WD for 12 weeks. (C) SRC-3 was expressed in the endothelial cells and vascular smooth muscle cells of chow-fed SRC-3 -/- ApoE -/- mice and was further increased after the mice were fed a WD for 12 weeks. Sections of frozen aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to X-gal staining. Arrows indicate positively stained cells (blue). Scale bar, 100 µm. (D) SRC-3 promoted atherosclerotic plaque formation. Representative images of en face Oil Red O-stained aortas from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice (left panel). Quantification of the plaque areas in aortas (right panel). (E-K) Cross-sections of the aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to (E-F) H&E staining (scale bar, 500 µm (E); scale bar, 200 µm (F)), (G) α-SMA staining (scale bar, 200 µm), (H-I) Masson staining (scale bar, 200 µm (H); scale bar, 200 µm (I)), (J) Oil Red O staining (scale bar, 500 µm), and (K) F4/80 staining (scale bar, 200 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. “×” indicates necrotic area. (L) Plaque stability was significantly increased in SRC-3 -/- ApoE -/- mice. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; ** P <0.01.
    Figure Legend Snippet: SRC-3 +/+ ApoE -/- mice exhibit more severe atherosclerosis. (A) SRC-3 was highly expressed in human atherosclerotic plaques. N represents plaque-adjacent vasculature in the lower limb aorta. AS represents atherosclerotic plaques in the lower limb aorta. (B) SRC-3 expression was upregulated in the aortas of ApoE -/- mice after the mice were fed a WD for 12 weeks. (C) SRC-3 was expressed in the endothelial cells and vascular smooth muscle cells of chow-fed SRC-3 -/- ApoE -/- mice and was further increased after the mice were fed a WD for 12 weeks. Sections of frozen aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to X-gal staining. Arrows indicate positively stained cells (blue). Scale bar, 100 µm. (D) SRC-3 promoted atherosclerotic plaque formation. Representative images of en face Oil Red O-stained aortas from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice (left panel). Quantification of the plaque areas in aortas (right panel). (E-K) Cross-sections of the aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to (E-F) H&E staining (scale bar, 500 µm (E); scale bar, 200 µm (F)), (G) α-SMA staining (scale bar, 200 µm), (H-I) Masson staining (scale bar, 200 µm (H); scale bar, 200 µm (I)), (J) Oil Red O staining (scale bar, 500 µm), and (K) F4/80 staining (scale bar, 200 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. “×” indicates necrotic area. (L) Plaque stability was significantly increased in SRC-3 -/- ApoE -/- mice. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; ** P <0.01.

    Techniques Used: Expressing, Staining, Two Tailed Test

    SRC-3 in endothelial cells contributes to the development of atherosclerosis. (A) Western blot showing that AAV-mediated SRC-3 shRNA decreased SRC-3 expression levels in the aortas of ApoE -/- mice. (B) SRC-3 knockdown reduced WD-induced atherosclerotic plaque formation in ApoE -/- mice. Representative images of en face Oil Red O-stained aortas from ApoE -/- mice injected with AAV-mediated SRC-3 shRNA and scramble shRNA (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (C-F) Cross-sections of the aortic roots of ApoE -/- mice injected with AAV-mediated SRC-3 shRNA and scramble shRNA were subjected to (C) H&E staining (scale bar, 100 µm), (D) Masson staining (scale bar, 500 µm), (E) Oil Red O staining (scale bar, 100 µm), (F) F4/80 staining (scale bar, 100 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01; ***, P <0.001.
    Figure Legend Snippet: SRC-3 in endothelial cells contributes to the development of atherosclerosis. (A) Western blot showing that AAV-mediated SRC-3 shRNA decreased SRC-3 expression levels in the aortas of ApoE -/- mice. (B) SRC-3 knockdown reduced WD-induced atherosclerotic plaque formation in ApoE -/- mice. Representative images of en face Oil Red O-stained aortas from ApoE -/- mice injected with AAV-mediated SRC-3 shRNA and scramble shRNA (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (C-F) Cross-sections of the aortic roots of ApoE -/- mice injected with AAV-mediated SRC-3 shRNA and scramble shRNA were subjected to (C) H&E staining (scale bar, 100 µm), (D) Masson staining (scale bar, 500 µm), (E) Oil Red O staining (scale bar, 100 µm), (F) F4/80 staining (scale bar, 100 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01; ***, P <0.001.

    Techniques Used: Western Blot, shRNA, Expressing, Staining, Injection, Two Tailed Test

    SRC-3 increases ICAM-1 expression during atherosclerosis development. (A) KEGG enrichment pathway analysis and (B) Gene Ontology (GO) biological process analysis of mRNA profiles in the aortas of SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice after WD feeding for 12 weeks. (C) Selected genes involved in leukocyte recruitment and proinflammatory markers are shown as a heat map. (D) The mRNA level of ICAM-1 in the aortas of SRC-3 -/- ApoE -/- mice was significantly decreased after WD feeding for 12 weeks. (E) The protein level of ICAM-1 in the aortas of SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice after WD feeding for 12 weeks. Each lane represents a pooled sample of three representative mice. (F) Western blot analysis of SRC-3 and ICAM-1 in 16 atherosclerotic plaques and plaque-adjacent vasculature in the lower limb aorta of accident patients. N represents plaque-adjacent vasculature in the lower limb aorta; AS represents atherosclerotic plaques in the lower limb aorta. (G) Correlation between SRC-3 and ICAM-1 protein levels in 16 atherosclerotic plaques and plaque-adjacent vasculature in the lower limb aorta. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05.
    Figure Legend Snippet: SRC-3 increases ICAM-1 expression during atherosclerosis development. (A) KEGG enrichment pathway analysis and (B) Gene Ontology (GO) biological process analysis of mRNA profiles in the aortas of SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice after WD feeding for 12 weeks. (C) Selected genes involved in leukocyte recruitment and proinflammatory markers are shown as a heat map. (D) The mRNA level of ICAM-1 in the aortas of SRC-3 -/- ApoE -/- mice was significantly decreased after WD feeding for 12 weeks. (E) The protein level of ICAM-1 in the aortas of SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice after WD feeding for 12 weeks. Each lane represents a pooled sample of three representative mice. (F) Western blot analysis of SRC-3 and ICAM-1 in 16 atherosclerotic plaques and plaque-adjacent vasculature in the lower limb aorta of accident patients. N represents plaque-adjacent vasculature in the lower limb aorta; AS represents atherosclerotic plaques in the lower limb aorta. (G) Correlation between SRC-3 and ICAM-1 protein levels in 16 atherosclerotic plaques and plaque-adjacent vasculature in the lower limb aorta. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05.

    Techniques Used: Expressing, Western Blot, Two Tailed Test

    SRC-3 regulates ICAM-1 expression via enhancing NF-κB signaling. (A) The protein levels of SRC-3 and ICAM-1 in SRC-3 siRNA-transfected HUVECs were significantly reduced compared with those in scrambled siRNA-transfected HUVECs after TNFα or IL-1β treatment. (B) The mRNA level of ICAM-1 in the SRC-3 siRNA-transfected HUVECs was markedly decreased after TNFα or IL-1β treatment. (C) ICAM-1 promoter activity was reduced in SRC-3 siRNA-transfected HUVECs after TNFα or IL-1β treatment. (D) SRC-3 cooperated with p65 to enhance the activity of the NF-κB reporter (upper panel) and ICAM-1 promoter (lower panel). (E) NF-κB binding site mutation abolished NF-κB-mediated ICAM-1 promoter activity. (F) The recruitment of SRC-3 and p65 was significantly reduced in SRC-3 siRNA-transfected HUVECs after TNFα or IL-1β treatment (right panel). Position of the subfragments detected by ChIP assays (left panel). (G) The SRC-3 siRNA-transfected HUVECs monolayer exhibited a significantly decreased number of adhered (upper panel) and transmigrated (lower panel) THP-1 cells after TNFα or IL-1β treatment. (H) Western blot showing ICAM-1 overexpression in SRC-3 siRNA-transfected HUVECs. (I) ICAM-1 overexpression in SRC-3 siRNA-transfected HUVECs rescued monocyte attachment to HUVECs and monocyte transendothelial migration after TNFα or IL-1β treatment. The data represent the mean ± SEM of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01;***, P <0.001.
    Figure Legend Snippet: SRC-3 regulates ICAM-1 expression via enhancing NF-κB signaling. (A) The protein levels of SRC-3 and ICAM-1 in SRC-3 siRNA-transfected HUVECs were significantly reduced compared with those in scrambled siRNA-transfected HUVECs after TNFα or IL-1β treatment. (B) The mRNA level of ICAM-1 in the SRC-3 siRNA-transfected HUVECs was markedly decreased after TNFα or IL-1β treatment. (C) ICAM-1 promoter activity was reduced in SRC-3 siRNA-transfected HUVECs after TNFα or IL-1β treatment. (D) SRC-3 cooperated with p65 to enhance the activity of the NF-κB reporter (upper panel) and ICAM-1 promoter (lower panel). (E) NF-κB binding site mutation abolished NF-κB-mediated ICAM-1 promoter activity. (F) The recruitment of SRC-3 and p65 was significantly reduced in SRC-3 siRNA-transfected HUVECs after TNFα or IL-1β treatment (right panel). Position of the subfragments detected by ChIP assays (left panel). (G) The SRC-3 siRNA-transfected HUVECs monolayer exhibited a significantly decreased number of adhered (upper panel) and transmigrated (lower panel) THP-1 cells after TNFα or IL-1β treatment. (H) Western blot showing ICAM-1 overexpression in SRC-3 siRNA-transfected HUVECs. (I) ICAM-1 overexpression in SRC-3 siRNA-transfected HUVECs rescued monocyte attachment to HUVECs and monocyte transendothelial migration after TNFα or IL-1β treatment. The data represent the mean ± SEM of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01;***, P <0.001.

    Techniques Used: Expressing, Transfection, Activity Assay, Binding Assay, Mutagenesis, Western Blot, Over Expression, Migration, Two Tailed Test

    Pharmacological inhibition of SRC-3 reduces atherosclerosis. (A) The protein levels of SRC-3, ICAM-1 and p-p65 in bufalin-treated HUVECs were significantly reduced compared with those in vehicle-treated HUVECs after TNFα or IL-1β treatment. The bufalin-treated HUVECs monolayer resulted in a dramatically decreased number of adhered (upper panel) and transmigrated (lower panel) THP-1 cells after TNFα or IL-1β treatment. (B-C) ApoE -/- mice were administered vehicle or bufalin (1.0 mg/kg, six times a week) by intraperitoneal injection for 13 weeks concomitant with WD feeding. (B) Dosing regimen (ApoE -/- prevention model). (C) Representative images of en face Oil Red O-stained aortas from ApoE -/- mice treated with vehicle or bufalin (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (D) The protein levels of SRC-3 and ICAM-1 in the aortas of ApoE -/- mice treated with bufalin were significantly reduced in the ApoE -/- prevention model. (E-F) ApoE -/- mice were fed a WD for 10 weeks and then treated with vehicle or bufalin (1.0 mg/kg, six times a week) by intraperitoneal injection for 13 weeks concomitant with WD feeding. (E) Dosing regimen (ApoE -/- regression model). (F) Representative images of en face Oil Red O-stained aortas from ApoE -/- mice treated with vehicle or bufalin (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (G) The protein levels of SRC-3 and ICAM-1 in the aortas of ApoE -/- mice treated with bufalin were significantly reduced in the ApoE -/- regression model. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01;***, P <0.001.
    Figure Legend Snippet: Pharmacological inhibition of SRC-3 reduces atherosclerosis. (A) The protein levels of SRC-3, ICAM-1 and p-p65 in bufalin-treated HUVECs were significantly reduced compared with those in vehicle-treated HUVECs after TNFα or IL-1β treatment. The bufalin-treated HUVECs monolayer resulted in a dramatically decreased number of adhered (upper panel) and transmigrated (lower panel) THP-1 cells after TNFα or IL-1β treatment. (B-C) ApoE -/- mice were administered vehicle or bufalin (1.0 mg/kg, six times a week) by intraperitoneal injection for 13 weeks concomitant with WD feeding. (B) Dosing regimen (ApoE -/- prevention model). (C) Representative images of en face Oil Red O-stained aortas from ApoE -/- mice treated with vehicle or bufalin (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (D) The protein levels of SRC-3 and ICAM-1 in the aortas of ApoE -/- mice treated with bufalin were significantly reduced in the ApoE -/- prevention model. (E-F) ApoE -/- mice were fed a WD for 10 weeks and then treated with vehicle or bufalin (1.0 mg/kg, six times a week) by intraperitoneal injection for 13 weeks concomitant with WD feeding. (E) Dosing regimen (ApoE -/- regression model). (F) Representative images of en face Oil Red O-stained aortas from ApoE -/- mice treated with vehicle or bufalin (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (G) The protein levels of SRC-3 and ICAM-1 in the aortas of ApoE -/- mice treated with bufalin were significantly reduced in the ApoE -/- regression model. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01;***, P <0.001.

    Techniques Used: Inhibition, Injection, Staining, Two Tailed Test

    Schematic model of the mechanism by which SRC-3 accelerates atherosclerosis development. SRC-3 promotes atherosclerosis development by increasing ICAM-1 transcription by enhancing the function of NF-κB in endothelial cells to promote macrophage recruitment. SRC-3 depletion or pharmacological inhibition of SRC-3 by bufalin ameliorates atherosclerosis development through decreasing endothelial ICAM-1 expression and macrophage recruitment via reduction of NF-κB function.
    Figure Legend Snippet: Schematic model of the mechanism by which SRC-3 accelerates atherosclerosis development. SRC-3 promotes atherosclerosis development by increasing ICAM-1 transcription by enhancing the function of NF-κB in endothelial cells to promote macrophage recruitment. SRC-3 depletion or pharmacological inhibition of SRC-3 by bufalin ameliorates atherosclerosis development through decreasing endothelial ICAM-1 expression and macrophage recruitment via reduction of NF-κB function.

    Techniques Used: Inhibition, Expressing

    p 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4e bp1
    P 4e Bp1, 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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    p 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4e bp1
    Intracellular concentrations <t>of</t> <t>phosphorylated-4E-BP1</t> <t>(p-4E-BP1),</t> evaluated by Western blot (absorbance units) . *p < 0.05 vs. Controls.
    P 4e Bp1, 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
    https://www.bioz.com/result/p 4e bp1/product/Cell Signaling Technology Inc
    Average 94 stars, based on 1 article reviews
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    1) Product Images from "Intracellular molecular effects of insulin resistance in patients with metabolic syndrome"

    Article Title: Intracellular molecular effects of insulin resistance in patients with metabolic syndrome

    Journal: Cardiovascular Diabetology

    doi: 10.1186/1475-2840-9-46

    Intracellular concentrations of phosphorylated-4E-BP1 (p-4E-BP1), evaluated by Western blot (absorbance units) . *p < 0.05 vs. Controls.
    Figure Legend Snippet: Intracellular concentrations of phosphorylated-4E-BP1 (p-4E-BP1), evaluated by Western blot (absorbance units) . *p < 0.05 vs. Controls.

    Techniques Used: Western Blot

    thr70p 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc thr70p 4e bp1
    Histology and immunohistochemistry (IHC) of ALCL tumor samples. (A, B) Histology of ALCL tumor samples (HE staining). (A) The classic type of ALCL. The tumor cells are large with abundant cytoplasm and manifest prominent nucleoli with an eccentrically located and pleomorphic nucleus of kidney-shape. (B) ALCL of small cell type. The tumor cells are small in size, with abundant cytoplasm and prominent nucleoli. (C to H) IHC staining of ALCL tumor samples (EnVision staining). Expression of ALK, p-AKT, <t>p-mTOR,</t> <t>p-4E-BP1,</t> and p-p70S6K eIF4E was assessed. (C, D) IHC staining with ALK1 antibody. (C) The tumor cells show cytoplasmic and nuclear staining. (D) The tumor cells manifest cytoplasmic staining only. (E) IHC staining with Thr308p-AKT antibody. The tumor cells show cytoplasmic and nuclear staining. (F) IHC staining with Ser2448p-mTOR antibody. The tumor cells show cytoplasmic staining. (G) IHC staining with <t>Thr70p-4E-BP1</t> antibody. The tumor cells show cytoplasmic staining. (H) IHC staining with Thr421p-p70S6K antibody. The tumor cells show cytoplasmic staining. All images were captured at 400× magnification.
    Thr70p 4e Bp1, 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
    https://www.bioz.com/result/thr70p 4e bp1/product/Cell Signaling Technology Inc
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    Images

    1) Product Images from "Prognostic significance and therapeutic potential of the activation of anaplastic lymphoma kinase/protein kinase B/mammalian target of rapamycin signaling pathway in anaplastic large cell lymphoma"

    Article Title: Prognostic significance and therapeutic potential of the activation of anaplastic lymphoma kinase/protein kinase B/mammalian target of rapamycin signaling pathway in anaplastic large cell lymphoma

    Journal: BMC Cancer

    doi: 10.1186/1471-2407-13-471

    Histology and immunohistochemistry (IHC) of ALCL tumor samples. (A, B) Histology of ALCL tumor samples (HE staining). (A) The classic type of ALCL. The tumor cells are large with abundant cytoplasm and manifest prominent nucleoli with an eccentrically located and pleomorphic nucleus of kidney-shape. (B) ALCL of small cell type. The tumor cells are small in size, with abundant cytoplasm and prominent nucleoli. (C to H) IHC staining of ALCL tumor samples (EnVision staining). Expression of ALK, p-AKT, p-mTOR, p-4E-BP1, and p-p70S6K eIF4E was assessed. (C, D) IHC staining with ALK1 antibody. (C) The tumor cells show cytoplasmic and nuclear staining. (D) The tumor cells manifest cytoplasmic staining only. (E) IHC staining with Thr308p-AKT antibody. The tumor cells show cytoplasmic and nuclear staining. (F) IHC staining with Ser2448p-mTOR antibody. The tumor cells show cytoplasmic staining. (G) IHC staining with Thr70p-4E-BP1 antibody. The tumor cells show cytoplasmic staining. (H) IHC staining with Thr421p-p70S6K antibody. The tumor cells show cytoplasmic staining. All images were captured at 400× magnification.
    Figure Legend Snippet: Histology and immunohistochemistry (IHC) of ALCL tumor samples. (A, B) Histology of ALCL tumor samples (HE staining). (A) The classic type of ALCL. The tumor cells are large with abundant cytoplasm and manifest prominent nucleoli with an eccentrically located and pleomorphic nucleus of kidney-shape. (B) ALCL of small cell type. The tumor cells are small in size, with abundant cytoplasm and prominent nucleoli. (C to H) IHC staining of ALCL tumor samples (EnVision staining). Expression of ALK, p-AKT, p-mTOR, p-4E-BP1, and p-p70S6K eIF4E was assessed. (C, D) IHC staining with ALK1 antibody. (C) The tumor cells show cytoplasmic and nuclear staining. (D) The tumor cells manifest cytoplasmic staining only. (E) IHC staining with Thr308p-AKT antibody. The tumor cells show cytoplasmic and nuclear staining. (F) IHC staining with Ser2448p-mTOR antibody. The tumor cells show cytoplasmic staining. (G) IHC staining with Thr70p-4E-BP1 antibody. The tumor cells show cytoplasmic staining. (H) IHC staining with Thr421p-p70S6K antibody. The tumor cells show cytoplasmic staining. All images were captured at 400× magnification.

    Techniques Used: Immunohistochemistry, Staining, Expressing

    Relationship between expression of  p-4E-BP1  and p-p70S6K and activation of ALK, AKT, and mTOR
    Figure Legend Snippet: Relationship between expression of p-4E-BP1 and p-p70S6K and activation of ALK, AKT, and mTOR

    Techniques Used: Expressing, Activation Assay, Significance Assay

    Overexpression of NPM-ALK activated the AKT/mTOR pathway. Overexpression of NPM-ALK in BaF3 cells induced hyper-activation of the AKT/mTOR pathway, as demonstrated by hyperphosphorylation of AKT and downstream molecules of mTOR: 4E-BP1 and p70SK6.
    Figure Legend Snippet: Overexpression of NPM-ALK activated the AKT/mTOR pathway. Overexpression of NPM-ALK in BaF3 cells induced hyper-activation of the AKT/mTOR pathway, as demonstrated by hyperphosphorylation of AKT and downstream molecules of mTOR: 4E-BP1 and p70SK6.

    Techniques Used: Over Expression, Activation Assay

    p 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4e bp1
    mTOR activity was not altered in trehalose-treated podocytes. Podocytes were treated with trehalose (50 mM) for 0, 12, 24, 36, 48 and 60 h. The phosphorylation level of p-mTOR ( A ) and its substrates p-p70S6K ( B ) <t>and</t> <t>p-4E-BP1</t> ( C ) were measured by Western blotting, n = 5, 5 and 6 respectively. However, no significant changes were observed. The representative immunoblot was shown along with the statistical results.
    P 4e Bp1, 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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    1) Product Images from "Trehalose, an mTOR Independent Autophagy Inducer, Alleviates Human Podocyte Injury after Puromycin Aminonucleoside Treatment"

    Article Title: Trehalose, an mTOR Independent Autophagy Inducer, Alleviates Human Podocyte Injury after Puromycin Aminonucleoside Treatment

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0113520

    mTOR activity was not altered in trehalose-treated podocytes. Podocytes were treated with trehalose (50 mM) for 0, 12, 24, 36, 48 and 60 h. The phosphorylation level of p-mTOR ( A ) and its substrates p-p70S6K ( B ) and p-4E-BP1 ( C ) were measured by Western blotting, n = 5, 5 and 6 respectively. However, no significant changes were observed. The representative immunoblot was shown along with the statistical results.
    Figure Legend Snippet: mTOR activity was not altered in trehalose-treated podocytes. Podocytes were treated with trehalose (50 mM) for 0, 12, 24, 36, 48 and 60 h. The phosphorylation level of p-mTOR ( A ) and its substrates p-p70S6K ( B ) and p-4E-BP1 ( C ) were measured by Western blotting, n = 5, 5 and 6 respectively. However, no significant changes were observed. The representative immunoblot was shown along with the statistical results.

    Techniques Used: Activity Assay, Western Blot

    phospho 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho 4e bp1
    Schematic presentation of mechanisms of gartanin’s action in induction of autophagy and apoptosis. (1) Gartanin activates AMPK α and inhibits AKT activation, which causes down-regulation of p70S6 <t>and</t> <t>4E-BP1</t> leading to autophagy; (2) Gartanin down-regulates Bcl-2 and up-regulates p53, PUMA and Bax, which results in activation of Caspase-3 and PARP cleavages to induce apoptosis.
    Phospho 4e Bp1, 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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    1) Product Images from "The effect of gartanin, a naturally- occurring xanthone in mangosteen juice, on the mTOR pathway, autophagy, apoptosis and the growth of human urinary bladder cancer cell Lines"

    Article Title: The effect of gartanin, a naturally- occurring xanthone in mangosteen juice, on the mTOR pathway, autophagy, apoptosis and the growth of human urinary bladder cancer cell Lines

    Journal: Nutrition and cancer

    doi: 10.1080/01635581.2013.785011

    Schematic presentation of mechanisms of gartanin’s action in induction of autophagy and apoptosis. (1) Gartanin activates AMPK α and inhibits AKT activation, which causes down-regulation of p70S6 and 4E-BP1 leading to autophagy; (2) Gartanin down-regulates Bcl-2 and up-regulates p53, PUMA and Bax, which results in activation of Caspase-3 and PARP cleavages to induce apoptosis.
    Figure Legend Snippet: Schematic presentation of mechanisms of gartanin’s action in induction of autophagy and apoptosis. (1) Gartanin activates AMPK α and inhibits AKT activation, which causes down-regulation of p70S6 and 4E-BP1 leading to autophagy; (2) Gartanin down-regulates Bcl-2 and up-regulates p53, PUMA and Bax, which results in activation of Caspase-3 and PARP cleavages to induce apoptosis.

    Techniques Used: Activation Assay

    4e bp1 phosphothr70  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 4e bp1 phosphothr70
    Selected antibodies, fluorescence intensities and Log 2 FC in protein & phosphoprotein quantities in T15 and JIMT-1 relative to SKBR3.
    4e Bp1 Phosphothr70, 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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    1) Product Images from "PKC-mediated phosphorylation and activation of the MEK/ERK pathway as a mechanism of acquired trastuzumab resistance in HER2-positive breast cancer"

    Article Title: PKC-mediated phosphorylation and activation of the MEK/ERK pathway as a mechanism of acquired trastuzumab resistance in HER2-positive breast cancer

    Journal: Frontiers in Endocrinology

    doi: 10.3389/fendo.2022.1010092

    Selected antibodies, fluorescence intensities and Log 2 FC in protein & phosphoprotein quantities in T15 and JIMT-1 relative to SKBR3.
    Figure Legend Snippet: Selected antibodies, fluorescence intensities and Log 2 FC in protein & phosphoprotein quantities in T15 and JIMT-1 relative to SKBR3.

    Techniques Used: Fluorescence

    phospho  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho
    Phospho, 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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    phospho 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho 4e bp1
    (A) Over-activation of TOR signalling in nephrocytes caused a significant hypertrophy phenotype. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR OA: w; sns -Gal4/UAS- rheb ;UAS- dicer2 /UAS- tor-wild type . t test: *** P < 0.001. (B) Hyperactivation of Yorkie (Yap/Taz) in nephrocytes revealed a hypertrophy effect as well. Control: w; sns -Gal4/+; UAS- dicer2 /+; Yki OA: w; sns -Gal4/+; UAS- dicer2 /UAS- yki.S111A.S168A.S250A.V5 . t test: **** P < 0.0001. (C) Expression of constitutively active Armadillo (β-Catenin) resulted in a significant size increase in nephrocytes. Control: w; sns -Gal4/+; UAS- dicer2 /+; WNT OA: UAS- arm.S10/ w; sns -Gal4/+; UAS- dicer2 /+. t test: *** P < 0.001. (D) Quantification of the cell size based on GFP-tags to the Cheerio constructs revealed a significant size increase of Cher Active when compared with Cher Inactive cells. This increase was completely reversed when TOR signalling was inhibited with a dominant negative TOR variant (TOR DN). Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; TOR DN: w; sns -Gal4/+; UAS- cher active /UAS- tor-dominant-negative . One-way ANOVA plus Tukey’s multiple comparisons test: * P < 0.05. (E) Combination of Cher Active with Hippo, which results in the inhibition of Yorkie (Yap/Taz) caused a significant reduction of nephrocyte size, even below the cell size of Cher Inactive nephrocytes. Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; HIPPO: w; sns -Gal4/+; UAS- cher active /UAS- hippo(dMST).flag . One-way ANOVA plus Tukey’s multiple comparisons test: ** P < 0.01; **** P < 0.0001. (F) FITC Albumin assays revealed a significant size decrease when dominant negative TOR is expressed exclusively. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR DN: w; sns -Gal4/+; UAS- dicer2 /UAS- tor-dominant-negative . t test: **** P < 0.0001. (G) Expression of Hippo also resulted in a significant size decrease as assessed with FITC Albumin assays. Control: w; sns -Gal4/+; UAS- dicer2 /+; HIPPO: w; sns -Gal4/+; UAS- dicer2 /UAS- hippo(dMST).flag . t test: *** P < 0.001. (H) Quantification of the mean intensity of <t>phosphorylated</t> <t>4E-BP1</t> based on immunofluorescence staining did not reveal any significant differences in nephrocytes expressing active or inactive Cheerio in comparison with control cells. (I) Quantification of immunofluorescence staining using an antibody against Yorkie revealed a significantly higher mean nuclear intensity in nephrocytes expressing active Cheerio when compared with control cells. One-way ANOVA plus Tukey’s multiple comparisons test: **** P < 0.0001. (J) Nephrocyte size was significantly increased when combining active Cheerio with over-active TOR, whereas the combination of active Cheerio with over-active Yorkie did not cause a significant size increase. One-way ANOVA plus Tukey’s multiple comparisons test: ** P < 0.01.
    Phospho 4e Bp1, 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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    Images

    1) Product Images from "A protective role for Drosophila Filamin in nephrocytes via Yorkie mediated hypertrophy"

    Article Title: A protective role for Drosophila Filamin in nephrocytes via Yorkie mediated hypertrophy

    Journal: Life Science Alliance

    doi: 10.26508/lsa.202101281

    (A) Over-activation of TOR signalling in nephrocytes caused a significant hypertrophy phenotype. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR OA: w; sns -Gal4/UAS- rheb ;UAS- dicer2 /UAS- tor-wild type . t test: *** P < 0.001. (B) Hyperactivation of Yorkie (Yap/Taz) in nephrocytes revealed a hypertrophy effect as well. Control: w; sns -Gal4/+; UAS- dicer2 /+; Yki OA: w; sns -Gal4/+; UAS- dicer2 /UAS- yki.S111A.S168A.S250A.V5 . t test: **** P < 0.0001. (C) Expression of constitutively active Armadillo (β-Catenin) resulted in a significant size increase in nephrocytes. Control: w; sns -Gal4/+; UAS- dicer2 /+; WNT OA: UAS- arm.S10/ w; sns -Gal4/+; UAS- dicer2 /+. t test: *** P < 0.001. (D) Quantification of the cell size based on GFP-tags to the Cheerio constructs revealed a significant size increase of Cher Active when compared with Cher Inactive cells. This increase was completely reversed when TOR signalling was inhibited with a dominant negative TOR variant (TOR DN). Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; TOR DN: w; sns -Gal4/+; UAS- cher active /UAS- tor-dominant-negative . One-way ANOVA plus Tukey’s multiple comparisons test: * P < 0.05. (E) Combination of Cher Active with Hippo, which results in the inhibition of Yorkie (Yap/Taz) caused a significant reduction of nephrocyte size, even below the cell size of Cher Inactive nephrocytes. Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; HIPPO: w; sns -Gal4/+; UAS- cher active /UAS- hippo(dMST).flag . One-way ANOVA plus Tukey’s multiple comparisons test: ** P < 0.01; **** P < 0.0001. (F) FITC Albumin assays revealed a significant size decrease when dominant negative TOR is expressed exclusively. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR DN: w; sns -Gal4/+; UAS- dicer2 /UAS- tor-dominant-negative . t test: **** P < 0.0001. (G) Expression of Hippo also resulted in a significant size decrease as assessed with FITC Albumin assays. Control: w; sns -Gal4/+; UAS- dicer2 /+; HIPPO: w; sns -Gal4/+; UAS- dicer2 /UAS- hippo(dMST).flag . t test: *** P < 0.001. (H) Quantification of the mean intensity of phosphorylated 4E-BP1 based on immunofluorescence staining did not reveal any significant differences in nephrocytes expressing active or inactive Cheerio in comparison with control cells. (I) Quantification of immunofluorescence staining using an antibody against Yorkie revealed a significantly higher mean nuclear intensity in nephrocytes expressing active Cheerio when compared with control cells. One-way ANOVA plus Tukey’s multiple comparisons test: **** P < 0.0001. (J) Nephrocyte size was significantly increased when combining active Cheerio with over-active TOR, whereas the combination of active Cheerio with over-active Yorkie did not cause a significant size increase. One-way ANOVA plus Tukey’s multiple comparisons test: ** P < 0.01.
    Figure Legend Snippet: (A) Over-activation of TOR signalling in nephrocytes caused a significant hypertrophy phenotype. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR OA: w; sns -Gal4/UAS- rheb ;UAS- dicer2 /UAS- tor-wild type . t test: *** P < 0.001. (B) Hyperactivation of Yorkie (Yap/Taz) in nephrocytes revealed a hypertrophy effect as well. Control: w; sns -Gal4/+; UAS- dicer2 /+; Yki OA: w; sns -Gal4/+; UAS- dicer2 /UAS- yki.S111A.S168A.S250A.V5 . t test: **** P < 0.0001. (C) Expression of constitutively active Armadillo (β-Catenin) resulted in a significant size increase in nephrocytes. Control: w; sns -Gal4/+; UAS- dicer2 /+; WNT OA: UAS- arm.S10/ w; sns -Gal4/+; UAS- dicer2 /+. t test: *** P < 0.001. (D) Quantification of the cell size based on GFP-tags to the Cheerio constructs revealed a significant size increase of Cher Active when compared with Cher Inactive cells. This increase was completely reversed when TOR signalling was inhibited with a dominant negative TOR variant (TOR DN). Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; TOR DN: w; sns -Gal4/+; UAS- cher active /UAS- tor-dominant-negative . One-way ANOVA plus Tukey’s multiple comparisons test: * P < 0.05. (E) Combination of Cher Active with Hippo, which results in the inhibition of Yorkie (Yap/Taz) caused a significant reduction of nephrocyte size, even below the cell size of Cher Inactive nephrocytes. Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; HIPPO: w; sns -Gal4/+; UAS- cher active /UAS- hippo(dMST).flag . One-way ANOVA plus Tukey’s multiple comparisons test: ** P < 0.01; **** P < 0.0001. (F) FITC Albumin assays revealed a significant size decrease when dominant negative TOR is expressed exclusively. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR DN: w; sns -Gal4/+; UAS- dicer2 /UAS- tor-dominant-negative . t test: **** P < 0.0001. (G) Expression of Hippo also resulted in a significant size decrease as assessed with FITC Albumin assays. Control: w; sns -Gal4/+; UAS- dicer2 /+; HIPPO: w; sns -Gal4/+; UAS- dicer2 /UAS- hippo(dMST).flag . t test: *** P < 0.001. (H) Quantification of the mean intensity of phosphorylated 4E-BP1 based on immunofluorescence staining did not reveal any significant differences in nephrocytes expressing active or inactive Cheerio in comparison with control cells. (I) Quantification of immunofluorescence staining using an antibody against Yorkie revealed a significantly higher mean nuclear intensity in nephrocytes expressing active Cheerio when compared with control cells. One-way ANOVA plus Tukey’s multiple comparisons test: **** P < 0.0001. (J) Nephrocyte size was significantly increased when combining active Cheerio with over-active TOR, whereas the combination of active Cheerio with over-active Yorkie did not cause a significant size increase. One-way ANOVA plus Tukey’s multiple comparisons test: ** P < 0.01.

    Techniques Used: Activation Assay, Expressing, Construct, Dominant Negative Mutation, Variant Assay, Inhibition, Immunofluorescence, Staining

    (A) Over-activation of TOR signalling in nephrocytes caused a hypertrophy phenotype revealed by FITC-Albumin uptake assay. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR OA: w; sns -Gal4/UAS- rheb ;UAS- dicer2 /UAS- tor-wildtype . (B) Hyperactivation of Yorkie (Yap/Taz) in nephrocytes revealed a hypertrophy effect as well. Control: w; sns -Gal4/+; UAS- dicer2 /+; Yki OA: w; sns -Gal4/+; UAS- dicer2 /UAS- yki.S111A.S168A.S250A.V5 . (C) Expression of constitutively active Armadillo (β-Catenin) resulted in a size increase in nephrocytes. Control: w; sns -Gal4/+; UAS- dicer2 /+; WNT OA: UAS- arm.S10/ w; sns -Gal4/+; UAS- dicer2 /+. (D) Blocking of WNT signalling by expression of a TCF repressor (WNT DN) resulted in the absence of nephrocytes as shown by FITC-Albumin assays. (E) Nephrocytes expressing active Cheerio present with a hypertrophy phenotype when compared with Cher Inactive cells, which was reversed by expressing dominant-negative TOR simultaneously. Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; TOR DN: w; sns -Gal4/+; UAS- cher active /UAS- tor-dominant-negative . (F) Combination of Cher Active with Hippo, which results in the inhibition of Yorkie (Yap/Taz) caused a reduction of nephrocyte size, even below the cell size of Cher Inactive nephrocytes. Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; HIPPO: w; sns -Gal4/+; UAS- cher active /UAS- hippo(dMST).flag . (G) FITC Albumin assays revealed a size decrease when dominant negative TOR is expressed exclusively. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR DN: w; sns -Gal4/+; UAS- dicer2 /UAS- tor-dominant-negative . (H) Expression of Hippo also resulted in a size decrease as assessed with FITC Albumin assays. Control: w; sns -Gal4/+; UAS- dicer2 /+; HIPPO: w; sns -Gal4/+; UAS- dicer2 /UAS- hippo(dMST).flag . (I) Immunofluorescence staining using an antibody against phosphorylated 4E-BP1 did not reveal any differences in control cells and nephrocytes expressing inactive or active Cheerio. Scale bar = 25 μm. (J) Immunofluorescence imaging using a Yorkie antibody revealed a significant increase in nuclear Yorkie upon expression of active Cheerio, whereas expressing inactive Cheerio did not change nuclear Yorkie. Yorkie: cyan, DAPI: blue. Scale bar = 25 μm.
    Figure Legend Snippet: (A) Over-activation of TOR signalling in nephrocytes caused a hypertrophy phenotype revealed by FITC-Albumin uptake assay. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR OA: w; sns -Gal4/UAS- rheb ;UAS- dicer2 /UAS- tor-wildtype . (B) Hyperactivation of Yorkie (Yap/Taz) in nephrocytes revealed a hypertrophy effect as well. Control: w; sns -Gal4/+; UAS- dicer2 /+; Yki OA: w; sns -Gal4/+; UAS- dicer2 /UAS- yki.S111A.S168A.S250A.V5 . (C) Expression of constitutively active Armadillo (β-Catenin) resulted in a size increase in nephrocytes. Control: w; sns -Gal4/+; UAS- dicer2 /+; WNT OA: UAS- arm.S10/ w; sns -Gal4/+; UAS- dicer2 /+. (D) Blocking of WNT signalling by expression of a TCF repressor (WNT DN) resulted in the absence of nephrocytes as shown by FITC-Albumin assays. (E) Nephrocytes expressing active Cheerio present with a hypertrophy phenotype when compared with Cher Inactive cells, which was reversed by expressing dominant-negative TOR simultaneously. Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; TOR DN: w; sns -Gal4/+; UAS- cher active /UAS- tor-dominant-negative . (F) Combination of Cher Active with Hippo, which results in the inhibition of Yorkie (Yap/Taz) caused a reduction of nephrocyte size, even below the cell size of Cher Inactive nephrocytes. Cher Inactive: w; sns -Gal4/+; UAS- cher Inactive /+; Cher Active: w; sns -Gal4/+; UAS- cher active /+; Cher Active; HIPPO: w; sns -Gal4/+; UAS- cher active /UAS- hippo(dMST).flag . (G) FITC Albumin assays revealed a size decrease when dominant negative TOR is expressed exclusively. Control: w; sns -Gal4/+; UAS- dicer2 /+; TOR DN: w; sns -Gal4/+; UAS- dicer2 /UAS- tor-dominant-negative . (H) Expression of Hippo also resulted in a size decrease as assessed with FITC Albumin assays. Control: w; sns -Gal4/+; UAS- dicer2 /+; HIPPO: w; sns -Gal4/+; UAS- dicer2 /UAS- hippo(dMST).flag . (I) Immunofluorescence staining using an antibody against phosphorylated 4E-BP1 did not reveal any differences in control cells and nephrocytes expressing inactive or active Cheerio. Scale bar = 25 μm. (J) Immunofluorescence imaging using a Yorkie antibody revealed a significant increase in nuclear Yorkie upon expression of active Cheerio, whereas expressing inactive Cheerio did not change nuclear Yorkie. Yorkie: cyan, DAPI: blue. Scale bar = 25 μm.

    Techniques Used: Activation Assay, Expressing, Blocking Assay, Dominant Negative Mutation, Inhibition, Immunofluorescence, Staining, Imaging

    List of antibodies.
    Figure Legend Snippet: List of antibodies.

    Techniques Used:

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    <t>SRC-3</t> +/+ ApoE -/- mice exhibit more severe atherosclerosis. (A) SRC-3 was highly expressed in human atherosclerotic plaques. N represents plaque-adjacent vasculature in the lower limb aorta. AS represents atherosclerotic plaques in the lower limb aorta. (B) SRC-3 expression was upregulated in the aortas of ApoE -/- mice after the mice were fed a WD for 12 weeks. (C) SRC-3 was expressed in the endothelial cells and vascular smooth muscle cells of chow-fed SRC-3 -/- ApoE -/- mice and was further increased after the mice were fed a WD for 12 weeks. Sections of frozen aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to X-gal staining. Arrows indicate positively stained cells (blue). Scale bar, 100 µm. (D) SRC-3 promoted atherosclerotic plaque formation. Representative images of en face Oil Red O-stained aortas from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice (left panel). Quantification of the plaque areas in aortas (right panel). (E-K) Cross-sections of the aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to (E-F) H&E staining (scale bar, 500 µm (E); scale bar, 200 µm (F)), (G) α-SMA staining (scale bar, 200 µm), (H-I) Masson staining (scale bar, 200 µm (H); scale bar, 200 µm (I)), (J) Oil Red O staining (scale bar, 500 µm), and (K) F4/80 staining (scale bar, 200 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. “×” indicates necrotic area. (L) Plaque stability was significantly increased in SRC-3 -/- ApoE -/- mice. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; ** P <0.01.
    P 4e Bp1, 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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    Image Search Results


    SRC-3 +/+ ApoE -/- mice exhibit more severe atherosclerosis. (A) SRC-3 was highly expressed in human atherosclerotic plaques. N represents plaque-adjacent vasculature in the lower limb aorta. AS represents atherosclerotic plaques in the lower limb aorta. (B) SRC-3 expression was upregulated in the aortas of ApoE -/- mice after the mice were fed a WD for 12 weeks. (C) SRC-3 was expressed in the endothelial cells and vascular smooth muscle cells of chow-fed SRC-3 -/- ApoE -/- mice and was further increased after the mice were fed a WD for 12 weeks. Sections of frozen aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to X-gal staining. Arrows indicate positively stained cells (blue). Scale bar, 100 µm. (D) SRC-3 promoted atherosclerotic plaque formation. Representative images of en face Oil Red O-stained aortas from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice (left panel). Quantification of the plaque areas in aortas (right panel). (E-K) Cross-sections of the aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to (E-F) H&E staining (scale bar, 500 µm (E); scale bar, 200 µm (F)), (G) α-SMA staining (scale bar, 200 µm), (H-I) Masson staining (scale bar, 200 µm (H); scale bar, 200 µm (I)), (J) Oil Red O staining (scale bar, 500 µm), and (K) F4/80 staining (scale bar, 200 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. “×” indicates necrotic area. (L) Plaque stability was significantly increased in SRC-3 -/- ApoE -/- mice. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; ** P <0.01.

    Journal: International Journal of Biological Sciences

    Article Title: SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment

    doi: 10.7150/ijbs.74864

    Figure Lengend Snippet: SRC-3 +/+ ApoE -/- mice exhibit more severe atherosclerosis. (A) SRC-3 was highly expressed in human atherosclerotic plaques. N represents plaque-adjacent vasculature in the lower limb aorta. AS represents atherosclerotic plaques in the lower limb aorta. (B) SRC-3 expression was upregulated in the aortas of ApoE -/- mice after the mice were fed a WD for 12 weeks. (C) SRC-3 was expressed in the endothelial cells and vascular smooth muscle cells of chow-fed SRC-3 -/- ApoE -/- mice and was further increased after the mice were fed a WD for 12 weeks. Sections of frozen aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to X-gal staining. Arrows indicate positively stained cells (blue). Scale bar, 100 µm. (D) SRC-3 promoted atherosclerotic plaque formation. Representative images of en face Oil Red O-stained aortas from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice (left panel). Quantification of the plaque areas in aortas (right panel). (E-K) Cross-sections of the aortic roots from SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice were subjected to (E-F) H&E staining (scale bar, 500 µm (E); scale bar, 200 µm (F)), (G) α-SMA staining (scale bar, 200 µm), (H-I) Masson staining (scale bar, 200 µm (H); scale bar, 200 µm (I)), (J) Oil Red O staining (scale bar, 500 µm), and (K) F4/80 staining (scale bar, 200 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. “×” indicates necrotic area. (L) Plaque stability was significantly increased in SRC-3 -/- ApoE -/- mice. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; ** P <0.01.

    Article Snippet: Anti-SRC-3 antibodies (C-20, sc-7216) and anti-p65 (D14E12, #8284) antibodies were purchased from Santa Cruz Biotechnology and Cell Signaling Technology, respectively.

    Techniques: Expressing, Staining, Two Tailed Test

    SRC-3 in endothelial cells contributes to the development of atherosclerosis. (A) Western blot showing that AAV-mediated SRC-3 shRNA decreased SRC-3 expression levels in the aortas of ApoE -/- mice. (B) SRC-3 knockdown reduced WD-induced atherosclerotic plaque formation in ApoE -/- mice. Representative images of en face Oil Red O-stained aortas from ApoE -/- mice injected with AAV-mediated SRC-3 shRNA and scramble shRNA (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (C-F) Cross-sections of the aortic roots of ApoE -/- mice injected with AAV-mediated SRC-3 shRNA and scramble shRNA were subjected to (C) H&E staining (scale bar, 100 µm), (D) Masson staining (scale bar, 500 µm), (E) Oil Red O staining (scale bar, 100 µm), (F) F4/80 staining (scale bar, 100 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01; ***, P <0.001.

    Journal: International Journal of Biological Sciences

    Article Title: SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment

    doi: 10.7150/ijbs.74864

    Figure Lengend Snippet: SRC-3 in endothelial cells contributes to the development of atherosclerosis. (A) Western blot showing that AAV-mediated SRC-3 shRNA decreased SRC-3 expression levels in the aortas of ApoE -/- mice. (B) SRC-3 knockdown reduced WD-induced atherosclerotic plaque formation in ApoE -/- mice. Representative images of en face Oil Red O-stained aortas from ApoE -/- mice injected with AAV-mediated SRC-3 shRNA and scramble shRNA (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (C-F) Cross-sections of the aortic roots of ApoE -/- mice injected with AAV-mediated SRC-3 shRNA and scramble shRNA were subjected to (C) H&E staining (scale bar, 100 µm), (D) Masson staining (scale bar, 500 µm), (E) Oil Red O staining (scale bar, 100 µm), (F) F4/80 staining (scale bar, 100 µm). Left panels, representative images. Right panels, quantification of stained area or a percentage of lesion area. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01; ***, P <0.001.

    Article Snippet: Anti-SRC-3 antibodies (C-20, sc-7216) and anti-p65 (D14E12, #8284) antibodies were purchased from Santa Cruz Biotechnology and Cell Signaling Technology, respectively.

    Techniques: Western Blot, shRNA, Expressing, Staining, Injection, Two Tailed Test

    SRC-3 increases ICAM-1 expression during atherosclerosis development. (A) KEGG enrichment pathway analysis and (B) Gene Ontology (GO) biological process analysis of mRNA profiles in the aortas of SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice after WD feeding for 12 weeks. (C) Selected genes involved in leukocyte recruitment and proinflammatory markers are shown as a heat map. (D) The mRNA level of ICAM-1 in the aortas of SRC-3 -/- ApoE -/- mice was significantly decreased after WD feeding for 12 weeks. (E) The protein level of ICAM-1 in the aortas of SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice after WD feeding for 12 weeks. Each lane represents a pooled sample of three representative mice. (F) Western blot analysis of SRC-3 and ICAM-1 in 16 atherosclerotic plaques and plaque-adjacent vasculature in the lower limb aorta of accident patients. N represents plaque-adjacent vasculature in the lower limb aorta; AS represents atherosclerotic plaques in the lower limb aorta. (G) Correlation between SRC-3 and ICAM-1 protein levels in 16 atherosclerotic plaques and plaque-adjacent vasculature in the lower limb aorta. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05.

    Journal: International Journal of Biological Sciences

    Article Title: SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment

    doi: 10.7150/ijbs.74864

    Figure Lengend Snippet: SRC-3 increases ICAM-1 expression during atherosclerosis development. (A) KEGG enrichment pathway analysis and (B) Gene Ontology (GO) biological process analysis of mRNA profiles in the aortas of SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice after WD feeding for 12 weeks. (C) Selected genes involved in leukocyte recruitment and proinflammatory markers are shown as a heat map. (D) The mRNA level of ICAM-1 in the aortas of SRC-3 -/- ApoE -/- mice was significantly decreased after WD feeding for 12 weeks. (E) The protein level of ICAM-1 in the aortas of SRC-3 +/+ ApoE -/- and SRC-3 -/- ApoE -/- mice after WD feeding for 12 weeks. Each lane represents a pooled sample of three representative mice. (F) Western blot analysis of SRC-3 and ICAM-1 in 16 atherosclerotic plaques and plaque-adjacent vasculature in the lower limb aorta of accident patients. N represents plaque-adjacent vasculature in the lower limb aorta; AS represents atherosclerotic plaques in the lower limb aorta. (G) Correlation between SRC-3 and ICAM-1 protein levels in 16 atherosclerotic plaques and plaque-adjacent vasculature in the lower limb aorta. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05.

    Article Snippet: Anti-SRC-3 antibodies (C-20, sc-7216) and anti-p65 (D14E12, #8284) antibodies were purchased from Santa Cruz Biotechnology and Cell Signaling Technology, respectively.

    Techniques: Expressing, Western Blot, Two Tailed Test

    SRC-3 regulates ICAM-1 expression via enhancing NF-κB signaling. (A) The protein levels of SRC-3 and ICAM-1 in SRC-3 siRNA-transfected HUVECs were significantly reduced compared with those in scrambled siRNA-transfected HUVECs after TNFα or IL-1β treatment. (B) The mRNA level of ICAM-1 in the SRC-3 siRNA-transfected HUVECs was markedly decreased after TNFα or IL-1β treatment. (C) ICAM-1 promoter activity was reduced in SRC-3 siRNA-transfected HUVECs after TNFα or IL-1β treatment. (D) SRC-3 cooperated with p65 to enhance the activity of the NF-κB reporter (upper panel) and ICAM-1 promoter (lower panel). (E) NF-κB binding site mutation abolished NF-κB-mediated ICAM-1 promoter activity. (F) The recruitment of SRC-3 and p65 was significantly reduced in SRC-3 siRNA-transfected HUVECs after TNFα or IL-1β treatment (right panel). Position of the subfragments detected by ChIP assays (left panel). (G) The SRC-3 siRNA-transfected HUVECs monolayer exhibited a significantly decreased number of adhered (upper panel) and transmigrated (lower panel) THP-1 cells after TNFα or IL-1β treatment. (H) Western blot showing ICAM-1 overexpression in SRC-3 siRNA-transfected HUVECs. (I) ICAM-1 overexpression in SRC-3 siRNA-transfected HUVECs rescued monocyte attachment to HUVECs and monocyte transendothelial migration after TNFα or IL-1β treatment. The data represent the mean ± SEM of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01;***, P <0.001.

    Journal: International Journal of Biological Sciences

    Article Title: SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment

    doi: 10.7150/ijbs.74864

    Figure Lengend Snippet: SRC-3 regulates ICAM-1 expression via enhancing NF-κB signaling. (A) The protein levels of SRC-3 and ICAM-1 in SRC-3 siRNA-transfected HUVECs were significantly reduced compared with those in scrambled siRNA-transfected HUVECs after TNFα or IL-1β treatment. (B) The mRNA level of ICAM-1 in the SRC-3 siRNA-transfected HUVECs was markedly decreased after TNFα or IL-1β treatment. (C) ICAM-1 promoter activity was reduced in SRC-3 siRNA-transfected HUVECs after TNFα or IL-1β treatment. (D) SRC-3 cooperated with p65 to enhance the activity of the NF-κB reporter (upper panel) and ICAM-1 promoter (lower panel). (E) NF-κB binding site mutation abolished NF-κB-mediated ICAM-1 promoter activity. (F) The recruitment of SRC-3 and p65 was significantly reduced in SRC-3 siRNA-transfected HUVECs after TNFα or IL-1β treatment (right panel). Position of the subfragments detected by ChIP assays (left panel). (G) The SRC-3 siRNA-transfected HUVECs monolayer exhibited a significantly decreased number of adhered (upper panel) and transmigrated (lower panel) THP-1 cells after TNFα or IL-1β treatment. (H) Western blot showing ICAM-1 overexpression in SRC-3 siRNA-transfected HUVECs. (I) ICAM-1 overexpression in SRC-3 siRNA-transfected HUVECs rescued monocyte attachment to HUVECs and monocyte transendothelial migration after TNFα or IL-1β treatment. The data represent the mean ± SEM of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01;***, P <0.001.

    Article Snippet: Anti-SRC-3 antibodies (C-20, sc-7216) and anti-p65 (D14E12, #8284) antibodies were purchased from Santa Cruz Biotechnology and Cell Signaling Technology, respectively.

    Techniques: Expressing, Transfection, Activity Assay, Binding Assay, Mutagenesis, Western Blot, Over Expression, Migration, Two Tailed Test

    Pharmacological inhibition of SRC-3 reduces atherosclerosis. (A) The protein levels of SRC-3, ICAM-1 and p-p65 in bufalin-treated HUVECs were significantly reduced compared with those in vehicle-treated HUVECs after TNFα or IL-1β treatment. The bufalin-treated HUVECs monolayer resulted in a dramatically decreased number of adhered (upper panel) and transmigrated (lower panel) THP-1 cells after TNFα or IL-1β treatment. (B-C) ApoE -/- mice were administered vehicle or bufalin (1.0 mg/kg, six times a week) by intraperitoneal injection for 13 weeks concomitant with WD feeding. (B) Dosing regimen (ApoE -/- prevention model). (C) Representative images of en face Oil Red O-stained aortas from ApoE -/- mice treated with vehicle or bufalin (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (D) The protein levels of SRC-3 and ICAM-1 in the aortas of ApoE -/- mice treated with bufalin were significantly reduced in the ApoE -/- prevention model. (E-F) ApoE -/- mice were fed a WD for 10 weeks and then treated with vehicle or bufalin (1.0 mg/kg, six times a week) by intraperitoneal injection for 13 weeks concomitant with WD feeding. (E) Dosing regimen (ApoE -/- regression model). (F) Representative images of en face Oil Red O-stained aortas from ApoE -/- mice treated with vehicle or bufalin (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (G) The protein levels of SRC-3 and ICAM-1 in the aortas of ApoE -/- mice treated with bufalin were significantly reduced in the ApoE -/- regression model. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01;***, P <0.001.

    Journal: International Journal of Biological Sciences

    Article Title: SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment

    doi: 10.7150/ijbs.74864

    Figure Lengend Snippet: Pharmacological inhibition of SRC-3 reduces atherosclerosis. (A) The protein levels of SRC-3, ICAM-1 and p-p65 in bufalin-treated HUVECs were significantly reduced compared with those in vehicle-treated HUVECs after TNFα or IL-1β treatment. The bufalin-treated HUVECs monolayer resulted in a dramatically decreased number of adhered (upper panel) and transmigrated (lower panel) THP-1 cells after TNFα or IL-1β treatment. (B-C) ApoE -/- mice were administered vehicle or bufalin (1.0 mg/kg, six times a week) by intraperitoneal injection for 13 weeks concomitant with WD feeding. (B) Dosing regimen (ApoE -/- prevention model). (C) Representative images of en face Oil Red O-stained aortas from ApoE -/- mice treated with vehicle or bufalin (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (D) The protein levels of SRC-3 and ICAM-1 in the aortas of ApoE -/- mice treated with bufalin were significantly reduced in the ApoE -/- prevention model. (E-F) ApoE -/- mice were fed a WD for 10 weeks and then treated with vehicle or bufalin (1.0 mg/kg, six times a week) by intraperitoneal injection for 13 weeks concomitant with WD feeding. (E) Dosing regimen (ApoE -/- regression model). (F) Representative images of en face Oil Red O-stained aortas from ApoE -/- mice treated with vehicle or bufalin (left panel). Quantification of the plaque areas of aortas (right panel). The data represent the mean ± SEM. (G) The protein levels of SRC-3 and ICAM-1 in the aortas of ApoE -/- mice treated with bufalin were significantly reduced in the ApoE -/- regression model. The data represent the mean ± SEM. The results are representative of three independent experiments. P values were calculated by unpaired two-tailed Student's t-test. *, P <0.05; **, P <0.01;***, P <0.001.

    Article Snippet: Anti-SRC-3 antibodies (C-20, sc-7216) and anti-p65 (D14E12, #8284) antibodies were purchased from Santa Cruz Biotechnology and Cell Signaling Technology, respectively.

    Techniques: Inhibition, Injection, Staining, Two Tailed Test

    Schematic model of the mechanism by which SRC-3 accelerates atherosclerosis development. SRC-3 promotes atherosclerosis development by increasing ICAM-1 transcription by enhancing the function of NF-κB in endothelial cells to promote macrophage recruitment. SRC-3 depletion or pharmacological inhibition of SRC-3 by bufalin ameliorates atherosclerosis development through decreasing endothelial ICAM-1 expression and macrophage recruitment via reduction of NF-κB function.

    Journal: International Journal of Biological Sciences

    Article Title: SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment

    doi: 10.7150/ijbs.74864

    Figure Lengend Snippet: Schematic model of the mechanism by which SRC-3 accelerates atherosclerosis development. SRC-3 promotes atherosclerosis development by increasing ICAM-1 transcription by enhancing the function of NF-κB in endothelial cells to promote macrophage recruitment. SRC-3 depletion or pharmacological inhibition of SRC-3 by bufalin ameliorates atherosclerosis development through decreasing endothelial ICAM-1 expression and macrophage recruitment via reduction of NF-κB function.

    Article Snippet: Anti-SRC-3 antibodies (C-20, sc-7216) and anti-p65 (D14E12, #8284) antibodies were purchased from Santa Cruz Biotechnology and Cell Signaling Technology, respectively.

    Techniques: Inhibition, Expressing

    Histology and immunohistochemistry (IHC) of ALCL tumor samples. (A, B) Histology of ALCL tumor samples (HE staining). (A) The classic type of ALCL. The tumor cells are large with abundant cytoplasm and manifest prominent nucleoli with an eccentrically located and pleomorphic nucleus of kidney-shape. (B) ALCL of small cell type. The tumor cells are small in size, with abundant cytoplasm and prominent nucleoli. (C to H) IHC staining of ALCL tumor samples (EnVision staining). Expression of ALK, p-AKT, p-mTOR, p-4E-BP1, and p-p70S6K eIF4E was assessed. (C, D) IHC staining with ALK1 antibody. (C) The tumor cells show cytoplasmic and nuclear staining. (D) The tumor cells manifest cytoplasmic staining only. (E) IHC staining with Thr308p-AKT antibody. The tumor cells show cytoplasmic and nuclear staining. (F) IHC staining with Ser2448p-mTOR antibody. The tumor cells show cytoplasmic staining. (G) IHC staining with Thr70p-4E-BP1 antibody. The tumor cells show cytoplasmic staining. (H) IHC staining with Thr421p-p70S6K antibody. The tumor cells show cytoplasmic staining. All images were captured at 400× magnification.

    Journal: BMC Cancer

    Article Title: Prognostic significance and therapeutic potential of the activation of anaplastic lymphoma kinase/protein kinase B/mammalian target of rapamycin signaling pathway in anaplastic large cell lymphoma

    doi: 10.1186/1471-2407-13-471

    Figure Lengend Snippet: Histology and immunohistochemistry (IHC) of ALCL tumor samples. (A, B) Histology of ALCL tumor samples (HE staining). (A) The classic type of ALCL. The tumor cells are large with abundant cytoplasm and manifest prominent nucleoli with an eccentrically located and pleomorphic nucleus of kidney-shape. (B) ALCL of small cell type. The tumor cells are small in size, with abundant cytoplasm and prominent nucleoli. (C to H) IHC staining of ALCL tumor samples (EnVision staining). Expression of ALK, p-AKT, p-mTOR, p-4E-BP1, and p-p70S6K eIF4E was assessed. (C, D) IHC staining with ALK1 antibody. (C) The tumor cells show cytoplasmic and nuclear staining. (D) The tumor cells manifest cytoplasmic staining only. (E) IHC staining with Thr308p-AKT antibody. The tumor cells show cytoplasmic and nuclear staining. (F) IHC staining with Ser2448p-mTOR antibody. The tumor cells show cytoplasmic staining. (G) IHC staining with Thr70p-4E-BP1 antibody. The tumor cells show cytoplasmic staining. (H) IHC staining with Thr421p-p70S6K antibody. The tumor cells show cytoplasmic staining. All images were captured at 400× magnification.

    Article Snippet: Rabbit polyclonal antibodies specific for Thr308p-AKT (p-AKT), Ser2448p-mTOR (p-mTOR), Thr70p-4E-BP1 (p-4E-BP1), and Thr421p-p70S6K1 (p-p70S6K1) (Cell Signaling Technology, Beverly, MA) were used.

    Techniques: Immunohistochemistry, Staining, Expressing

    Relationship between expression of  p-4E-BP1  and p-p70S6K and activation of ALK, AKT, and mTOR

    Journal: BMC Cancer

    Article Title: Prognostic significance and therapeutic potential of the activation of anaplastic lymphoma kinase/protein kinase B/mammalian target of rapamycin signaling pathway in anaplastic large cell lymphoma

    doi: 10.1186/1471-2407-13-471

    Figure Lengend Snippet: Relationship between expression of p-4E-BP1 and p-p70S6K and activation of ALK, AKT, and mTOR

    Article Snippet: Rabbit polyclonal antibodies specific for Thr308p-AKT (p-AKT), Ser2448p-mTOR (p-mTOR), Thr70p-4E-BP1 (p-4E-BP1), and Thr421p-p70S6K1 (p-p70S6K1) (Cell Signaling Technology, Beverly, MA) were used.

    Techniques: Expressing, Activation Assay, Significance Assay

    Overexpression of NPM-ALK activated the AKT/mTOR pathway. Overexpression of NPM-ALK in BaF3 cells induced hyper-activation of the AKT/mTOR pathway, as demonstrated by hyperphosphorylation of AKT and downstream molecules of mTOR: 4E-BP1 and p70SK6.

    Journal: BMC Cancer

    Article Title: Prognostic significance and therapeutic potential of the activation of anaplastic lymphoma kinase/protein kinase B/mammalian target of rapamycin signaling pathway in anaplastic large cell lymphoma

    doi: 10.1186/1471-2407-13-471

    Figure Lengend Snippet: Overexpression of NPM-ALK activated the AKT/mTOR pathway. Overexpression of NPM-ALK in BaF3 cells induced hyper-activation of the AKT/mTOR pathway, as demonstrated by hyperphosphorylation of AKT and downstream molecules of mTOR: 4E-BP1 and p70SK6.

    Article Snippet: Rabbit polyclonal antibodies specific for Thr308p-AKT (p-AKT), Ser2448p-mTOR (p-mTOR), Thr70p-4E-BP1 (p-4E-BP1), and Thr421p-p70S6K1 (p-p70S6K1) (Cell Signaling Technology, Beverly, MA) were used.

    Techniques: Over Expression, Activation Assay

    Schematic presentation of mechanisms of gartanin’s action in induction of autophagy and apoptosis. (1) Gartanin activates AMPK α and inhibits AKT activation, which causes down-regulation of p70S6 and 4E-BP1 leading to autophagy; (2) Gartanin down-regulates Bcl-2 and up-regulates p53, PUMA and Bax, which results in activation of Caspase-3 and PARP cleavages to induce apoptosis.

    Journal: Nutrition and cancer

    Article Title: The effect of gartanin, a naturally- occurring xanthone in mangosteen juice, on the mTOR pathway, autophagy, apoptosis and the growth of human urinary bladder cancer cell Lines

    doi: 10.1080/01635581.2013.785011

    Figure Lengend Snippet: Schematic presentation of mechanisms of gartanin’s action in induction of autophagy and apoptosis. (1) Gartanin activates AMPK α and inhibits AKT activation, which causes down-regulation of p70S6 and 4E-BP1 leading to autophagy; (2) Gartanin down-regulates Bcl-2 and up-regulates p53, PUMA and Bax, which results in activation of Caspase-3 and PARP cleavages to induce apoptosis.

    Article Snippet: Antibodies for phospho-AMP-activated protein kinase α (AMPKα), AMPKα, phospho-4E-BP1, 4E-BP1, phospho-rpS6, phospho-ACC, ACC, Caspase 3, PARP, phospho-mTOR, mTOR, TSC1, TSC2, p21, p70S6, phospho-p70S6, and p62 were purchased from Cell Signaling Technologies (Beverly, MA).

    Techniques: Activation Assay

    Selected antibodies, fluorescence intensities and Log 2 FC in protein & phosphoprotein quantities in T15 and JIMT-1 relative to SKBR3.

    Journal: Frontiers in Endocrinology

    Article Title: PKC-mediated phosphorylation and activation of the MEK/ERK pathway as a mechanism of acquired trastuzumab resistance in HER2-positive breast cancer

    doi: 10.3389/fendo.2022.1010092

    Figure Lengend Snippet: Selected antibodies, fluorescence intensities and Log 2 FC in protein & phosphoprotein quantities in T15 and JIMT-1 relative to SKBR3.

    Article Snippet: PI3K/mTOR , 4E-BP1 - phosphoThr70 , Cell Signaling , 9455 , Rb pAb , 754 , 119 , 164 , 2.66 , 0.46.

    Techniques: Fluorescence