phospho p70s6k ser371  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho p70s6k ser371
    Phospho P70s6k Ser371, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phospho p70s6k ser371/product/Cell Signaling Technology Inc
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    anti phospho ser371 p70s6k  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho ser371 p70s6k
    Anti Phospho Ser371 P70s6k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1 ap rabbit polyclonal anti phospho ser371 p70s6k cellsignaling  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc 1 ap rabbit polyclonal anti phospho ser371 p70s6k cellsignaling
    1 Ap Rabbit Polyclonal Anti Phospho Ser371 P70s6k Cellsignaling, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti phospho ser371 p70s6k  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho ser371 p70s6k

    Anti Phospho Ser371 P70s6k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "TIAR and FMRP shape pro-survival nascent proteome of leukemia cells in the bone marrow microenvironment"

    Article Title: TIAR and FMRP shape pro-survival nascent proteome of leukemia cells in the bone marrow microenvironment

    Journal: iScience

    doi: 10.1016/j.isci.2023.106543


    Figure Legend Snippet:

    Techniques Used: Purification, shRNA, Transduction, Recombinant, Reporter Assay, Lysis, Plasmid Preparation, Software

    rabbit polyclonal anti phospho ser371 p70s6k  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit polyclonal anti phospho ser371 p70s6k

    Rabbit Polyclonal Anti Phospho Ser371 P70s6k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit polyclonal anti phospho ser371 p70s6k/product/Cell Signaling Technology Inc
    Average 86 stars, based on 1 article reviews
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    rabbit polyclonal anti phospho ser371 p70s6k - by Bioz Stars, 2024-07
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    1) Product Images from "TIAR and FMRP shape pro-survival nascent proteome of leukemia cells in the bone marrow microenvironment"

    Article Title: TIAR and FMRP shape pro-survival nascent proteome of leukemia cells in the bone marrow microenvironment

    Journal: iScience

    doi: 10.1016/j.isci.2023.106543


    Figure Legend Snippet:

    Techniques Used: Purification, shRNA, Transduction, Recombinant, Reporter Assay, Lysis, Plasmid Preparation, Software

    anti phospho p70s6k ser371  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho p70s6k ser371
    Anti Phospho P70s6k Ser371, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti phospho p70s6k ser371/product/Cell Signaling Technology Inc
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    p p70s6k  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p p70s6k
    Effects of LIF on the expression and activation of <t>AKT/mTOR/p70S6k</t> signaling pathway components after AOH. (A) Representative western blotting images, and semi-quantitative analysis of the (B) p-AKT/AKT, (C) p-mTOR/mTOR and (D) <t>p-p70S6K/p70S6K</t> ratios. * P<0.05, # P<0.001, n=3/group. AOH, acute ocular hypertension; LIF, leukemia inhibitory factor; p-, phosphorylated; <t>p70S6K,</t> ribosomal protein S6 kinase.
    P P70s6k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Protective effect of leukemia inhibitory factor on the retinal injury induced by acute ocular hypertension in rats"

    Article Title: Protective effect of leukemia inhibitory factor on the retinal injury induced by acute ocular hypertension in rats

    Journal: Experimental and Therapeutic Medicine

    doi: 10.3892/etm.2022.11717

    Effects of LIF on the expression and activation of AKT/mTOR/p70S6k signaling pathway components after AOH. (A) Representative western blotting images, and semi-quantitative analysis of the (B) p-AKT/AKT, (C) p-mTOR/mTOR and (D) p-p70S6K/p70S6K ratios. * P<0.05, # P<0.001, n=3/group. AOH, acute ocular hypertension; LIF, leukemia inhibitory factor; p-, phosphorylated; p70S6K, ribosomal protein S6 kinase.
    Figure Legend Snippet: Effects of LIF on the expression and activation of AKT/mTOR/p70S6k signaling pathway components after AOH. (A) Representative western blotting images, and semi-quantitative analysis of the (B) p-AKT/AKT, (C) p-mTOR/mTOR and (D) p-p70S6K/p70S6K ratios. * P<0.05, # P<0.001, n=3/group. AOH, acute ocular hypertension; LIF, leukemia inhibitory factor; p-, phosphorylated; p70S6K, ribosomal protein S6 kinase.

    Techniques Used: Expressing, Activation Assay, Western Blot

    antibodies against total p70s6k  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc antibodies against total p70s6k
    Western blotting analysis of phosphorylated <t>P70S6K</t> ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).
    Antibodies Against Total P70s6k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Vascular Endothelial Growth Factor Receptor-3 Directly Interacts with Phosphatidylinositol 3-Kinase to Regulate Lymphangiogenesis"

    Article Title: Vascular Endothelial Growth Factor Receptor-3 Directly Interacts with Phosphatidylinositol 3-Kinase to Regulate Lymphangiogenesis

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0039558

    Western blotting analysis of phosphorylated P70S6K ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).
    Figure Legend Snippet: Western blotting analysis of phosphorylated P70S6K ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).

    Techniques Used: Western Blot, Concentration Assay, Inhibition

    p p70s6k  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p p70s6k
    A. EGFR is autophosphorylated in ER H2170 and downregulated in H358-E4 resistant cell lines. p-mTOR (S2448) and its downstream signaling protein <t>phospho-p70S6K</t> (T389) are upregulated in both resistant cell lines. H2170 and H358 parental and resistant cell lines were starved overnight in 0.5% BSA and then treated with or without 7.0 µM of erlotinib for 24 hours and cells were stimulated with 10 ng/mL of EGF for 2.5 minutes. Higher concentrations of erlotinib were used since these NSCLC cell lines have no EGFR TK mutation. Autophosphorylation of EGFR on Y1068 was seen in the absence of EGF in ER H2170 cells which was not seen in ER H358-E4 cells. Upregulation of p-mTOR and its downstream protein phosho-p70S6K (T389) is seen in H2170 resistant lines +/− erlotinib. ER H2170 cells show increased EGFR phosphorylation +/− EGF. Upregulation of p-ERK (2–5-fold) was also seen in ER H2170 and H358 cells in +/− erlotinib B. To confirm autophosphorylation of EGFR, cells were plated on chamber slides, allowed to adhere for 24 hours and then starved overnight. Cells were then treated with +/− EGF for 15 minutes, fixed with acetone: methanol and visualized with p-EGFR (Y1068) primary antibody and anti rabbit DyLight secondary antibody (Thermo Fisher Scientific) (green) or Hoechst dye for nuclear staining (blue) on a Zeiss Axio Observer Z1 fluorescent microscope. Graph showing relative average total cell fluorescence units per 8 microscopic fields. There was a 3.8-fold increase in fluorescence when comparing parental to resistant cells in the absence of EGF in H2170 cells.
    P P70s6k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Alternative Signaling Pathways as Potential Therapeutic Targets for Overcoming EGFR and c-Met Inhibitor Resistance in Non-Small Cell Lung Cancer"

    Article Title: Alternative Signaling Pathways as Potential Therapeutic Targets for Overcoming EGFR and c-Met Inhibitor Resistance in Non-Small Cell Lung Cancer

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0078398

    A. EGFR is autophosphorylated in ER H2170 and downregulated in H358-E4 resistant cell lines. p-mTOR (S2448) and its downstream signaling protein phospho-p70S6K (T389) are upregulated in both resistant cell lines. H2170 and H358 parental and resistant cell lines were starved overnight in 0.5% BSA and then treated with or without 7.0 µM of erlotinib for 24 hours and cells were stimulated with 10 ng/mL of EGF for 2.5 minutes. Higher concentrations of erlotinib were used since these NSCLC cell lines have no EGFR TK mutation. Autophosphorylation of EGFR on Y1068 was seen in the absence of EGF in ER H2170 cells which was not seen in ER H358-E4 cells. Upregulation of p-mTOR and its downstream protein phosho-p70S6K (T389) is seen in H2170 resistant lines +/− erlotinib. ER H2170 cells show increased EGFR phosphorylation +/− EGF. Upregulation of p-ERK (2–5-fold) was also seen in ER H2170 and H358 cells in +/− erlotinib B. To confirm autophosphorylation of EGFR, cells were plated on chamber slides, allowed to adhere for 24 hours and then starved overnight. Cells were then treated with +/− EGF for 15 minutes, fixed with acetone: methanol and visualized with p-EGFR (Y1068) primary antibody and anti rabbit DyLight secondary antibody (Thermo Fisher Scientific) (green) or Hoechst dye for nuclear staining (blue) on a Zeiss Axio Observer Z1 fluorescent microscope. Graph showing relative average total cell fluorescence units per 8 microscopic fields. There was a 3.8-fold increase in fluorescence when comparing parental to resistant cells in the absence of EGF in H2170 cells.
    Figure Legend Snippet: A. EGFR is autophosphorylated in ER H2170 and downregulated in H358-E4 resistant cell lines. p-mTOR (S2448) and its downstream signaling protein phospho-p70S6K (T389) are upregulated in both resistant cell lines. H2170 and H358 parental and resistant cell lines were starved overnight in 0.5% BSA and then treated with or without 7.0 µM of erlotinib for 24 hours and cells were stimulated with 10 ng/mL of EGF for 2.5 minutes. Higher concentrations of erlotinib were used since these NSCLC cell lines have no EGFR TK mutation. Autophosphorylation of EGFR on Y1068 was seen in the absence of EGF in ER H2170 cells which was not seen in ER H358-E4 cells. Upregulation of p-mTOR and its downstream protein phosho-p70S6K (T389) is seen in H2170 resistant lines +/− erlotinib. ER H2170 cells show increased EGFR phosphorylation +/− EGF. Upregulation of p-ERK (2–5-fold) was also seen in ER H2170 and H358 cells in +/− erlotinib B. To confirm autophosphorylation of EGFR, cells were plated on chamber slides, allowed to adhere for 24 hours and then starved overnight. Cells were then treated with +/− EGF for 15 minutes, fixed with acetone: methanol and visualized with p-EGFR (Y1068) primary antibody and anti rabbit DyLight secondary antibody (Thermo Fisher Scientific) (green) or Hoechst dye for nuclear staining (blue) on a Zeiss Axio Observer Z1 fluorescent microscope. Graph showing relative average total cell fluorescence units per 8 microscopic fields. There was a 3.8-fold increase in fluorescence when comparing parental to resistant cells in the absence of EGF in H2170 cells.

    Techniques Used: Mutagenesis, Staining, Microscopy, Fluorescence

    Cells were starved overnight and then treated with or without 8.0 µM SU11274 for 24 hours. Cells were stimulated with 40 ng/mL of HGF for 2.5 minutes after which western blot analysis was performed. Downregulation of p-c-Met (Y1003) was seen in both cell lines. Upregulation of p-p70S6kinase (S371) was observed in SR H2170 cells. Upregulation of p-4E-BP1 (T37/46) was also observed in both cells lines +/− SU11274.
    Figure Legend Snippet: Cells were starved overnight and then treated with or without 8.0 µM SU11274 for 24 hours. Cells were stimulated with 40 ng/mL of HGF for 2.5 minutes after which western blot analysis was performed. Downregulation of p-c-Met (Y1003) was seen in both cell lines. Upregulation of p-p70S6kinase (S371) was observed in SR H2170 cells. Upregulation of p-4E-BP1 (T37/46) was also observed in both cells lines +/− SU11274.

    Techniques Used: Western Blot

    p p70s6k  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p p70s6k
    TMEM16A ameliorated autophagy-meditated vascular remodeling by reducing VPS34 activity. (A-C) Western blot analysis of the phosphorylation of AKT, mTOR (A), <t>p70S6K,</t> and 4EBP1 (B) and the expression of VPS34 (C) in aortas from TM SMC Tg and TM con mice following AngII infusion for 4 weeks. (D) Bar charts showing VPS34 kinase activity in aorta homogenates. **P < 0.01 vs. sham + TM con ; ##P < 0.01 vs. AngII + TM con . Statistical significance was determined by one-way ANOVA. n = 6 mice/ group. (E) TM con or TM SMC Tg mice were injected intraperitoneally with 3-MA (100 µg/kg) or rapamycin (1 mg/kg), respectively, at 2 weeks after AngII infusion, and then continuously dosed once per day for 2 weeks. Representative images of Ki67 staining and hematoxylin-eosin staining of aortic sections are shown. Scale bars, 25 µm (upper panel), 200 µm (middle panel) or 50 µm (lower panel). (F) Quantification of cross-sectional areas (CSAs). **P < 0.01 vs. sham + TM con ; ##P < 0.01 vs. AngII + TM con ; &&P < 0.01 vs. AngII + TM SMC Tg , one-way ANOVA. n = 6 mice/ group. (G) Cells were infected with Ad-Lacz or Ad-TM for 48 h and then transfected with VPS34 plasmid in the presence of AngII for 24 h. Cell proliferation was determined by performing BrdU assays. (H) Proliferation of MASMCs transfected with scr.RNA or TM siRNA following AngII and SAR405 (1 µmol/L) treatment for 24 h. **P < 0.01 vs. control; ##P < 0.01 vs. AngII; &&P < 0.01 vs. AngII + Ad-TM or AngII + TM siRNA, one-way ANOVA. n = 6.
    P P70s6k, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 96 stars, based on 1 article reviews
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    1) Product Images from "TMEM16A ameliorates vascular remodeling by suppressing autophagy via inhibiting Bcl-2-p62 complex formation"

    Article Title: TMEM16A ameliorates vascular remodeling by suppressing autophagy via inhibiting Bcl-2-p62 complex formation

    Journal: Theranostics

    doi: 10.7150/thno.41028

    TMEM16A ameliorated autophagy-meditated vascular remodeling by reducing VPS34 activity. (A-C) Western blot analysis of the phosphorylation of AKT, mTOR (A), p70S6K, and 4EBP1 (B) and the expression of VPS34 (C) in aortas from TM SMC Tg and TM con mice following AngII infusion for 4 weeks. (D) Bar charts showing VPS34 kinase activity in aorta homogenates. **P < 0.01 vs. sham + TM con ; ##P < 0.01 vs. AngII + TM con . Statistical significance was determined by one-way ANOVA. n = 6 mice/ group. (E) TM con or TM SMC Tg mice were injected intraperitoneally with 3-MA (100 µg/kg) or rapamycin (1 mg/kg), respectively, at 2 weeks after AngII infusion, and then continuously dosed once per day for 2 weeks. Representative images of Ki67 staining and hematoxylin-eosin staining of aortic sections are shown. Scale bars, 25 µm (upper panel), 200 µm (middle panel) or 50 µm (lower panel). (F) Quantification of cross-sectional areas (CSAs). **P < 0.01 vs. sham + TM con ; ##P < 0.01 vs. AngII + TM con ; &&P < 0.01 vs. AngII + TM SMC Tg , one-way ANOVA. n = 6 mice/ group. (G) Cells were infected with Ad-Lacz or Ad-TM for 48 h and then transfected with VPS34 plasmid in the presence of AngII for 24 h. Cell proliferation was determined by performing BrdU assays. (H) Proliferation of MASMCs transfected with scr.RNA or TM siRNA following AngII and SAR405 (1 µmol/L) treatment for 24 h. **P < 0.01 vs. control; ##P < 0.01 vs. AngII; &&P < 0.01 vs. AngII + Ad-TM or AngII + TM siRNA, one-way ANOVA. n = 6.
    Figure Legend Snippet: TMEM16A ameliorated autophagy-meditated vascular remodeling by reducing VPS34 activity. (A-C) Western blot analysis of the phosphorylation of AKT, mTOR (A), p70S6K, and 4EBP1 (B) and the expression of VPS34 (C) in aortas from TM SMC Tg and TM con mice following AngII infusion for 4 weeks. (D) Bar charts showing VPS34 kinase activity in aorta homogenates. **P < 0.01 vs. sham + TM con ; ##P < 0.01 vs. AngII + TM con . Statistical significance was determined by one-way ANOVA. n = 6 mice/ group. (E) TM con or TM SMC Tg mice were injected intraperitoneally with 3-MA (100 µg/kg) or rapamycin (1 mg/kg), respectively, at 2 weeks after AngII infusion, and then continuously dosed once per day for 2 weeks. Representative images of Ki67 staining and hematoxylin-eosin staining of aortic sections are shown. Scale bars, 25 µm (upper panel), 200 µm (middle panel) or 50 µm (lower panel). (F) Quantification of cross-sectional areas (CSAs). **P < 0.01 vs. sham + TM con ; ##P < 0.01 vs. AngII + TM con ; &&P < 0.01 vs. AngII + TM SMC Tg , one-way ANOVA. n = 6 mice/ group. (G) Cells were infected with Ad-Lacz or Ad-TM for 48 h and then transfected with VPS34 plasmid in the presence of AngII for 24 h. Cell proliferation was determined by performing BrdU assays. (H) Proliferation of MASMCs transfected with scr.RNA or TM siRNA following AngII and SAR405 (1 µmol/L) treatment for 24 h. **P < 0.01 vs. control; ##P < 0.01 vs. AngII; &&P < 0.01 vs. AngII + Ad-TM or AngII + TM siRNA, one-way ANOVA. n = 6.

    Techniques Used: Activity Assay, Western Blot, Expressing, Injection, Staining, Infection, Transfection, Plasmid Preparation

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    Cell Signaling Technology Inc phospho p70s6k ser371
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    Effects of LIF on the expression and activation of <t>AKT/mTOR/p70S6k</t> signaling pathway components after AOH. (A) Representative western blotting images, and semi-quantitative analysis of the (B) p-AKT/AKT, (C) p-mTOR/mTOR and (D) <t>p-p70S6K/p70S6K</t> ratios. * P<0.05, # P<0.001, n=3/group. AOH, acute ocular hypertension; LIF, leukemia inhibitory factor; p-, phosphorylated; <t>p70S6K,</t> ribosomal protein S6 kinase.
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    Western blotting analysis of phosphorylated <t>P70S6K</t> ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).
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    Image Search Results


    Journal: iScience

    Article Title: TIAR and FMRP shape pro-survival nascent proteome of leukemia cells in the bone marrow microenvironment

    doi: 10.1016/j.isci.2023.106543

    Figure Lengend Snippet:

    Article Snippet: Rabbit polyclonal anti-phospho Ser371-p70S6K , CellSignaling , Cat #9208.

    Techniques: Purification, shRNA, Transduction, Recombinant, Reporter Assay, Lysis, Plasmid Preparation, Software

    Effects of LIF on the expression and activation of AKT/mTOR/p70S6k signaling pathway components after AOH. (A) Representative western blotting images, and semi-quantitative analysis of the (B) p-AKT/AKT, (C) p-mTOR/mTOR and (D) p-p70S6K/p70S6K ratios. * P<0.05, # P<0.001, n=3/group. AOH, acute ocular hypertension; LIF, leukemia inhibitory factor; p-, phosphorylated; p70S6K, ribosomal protein S6 kinase.

    Journal: Experimental and Therapeutic Medicine

    Article Title: Protective effect of leukemia inhibitory factor on the retinal injury induced by acute ocular hypertension in rats

    doi: 10.3892/etm.2022.11717

    Figure Lengend Snippet: Effects of LIF on the expression and activation of AKT/mTOR/p70S6k signaling pathway components after AOH. (A) Representative western blotting images, and semi-quantitative analysis of the (B) p-AKT/AKT, (C) p-mTOR/mTOR and (D) p-p70S6K/p70S6K ratios. * P<0.05, # P<0.001, n=3/group. AOH, acute ocular hypertension; LIF, leukemia inhibitory factor; p-, phosphorylated; p70S6K, ribosomal protein S6 kinase.

    Article Snippet: The antibodies of cleaved-caspase-3 (cat. no. 9579), PARP (cat. no. 9542), AKT (cat. no. 9272), p-AKT (cat. no. 31957), mTOR (cat. no. 2972), p-mTOR (cat. no. 5536), p70S6K (cat. no. 9202) and p-p70S6K (cat. no. 9208) were purchased from Cell Signaling Technology, Inc., whilst the antibodies of STAT3 (cat. no. APR13562G) and p-STAT3 (cat. no. APR11162G) were bought from Santa Cruz Biotechnology, Inc. After washing with TBS + 1% Tween 20 three times, the membranes were incubated with an HRP-conjugated goat anti-rabbit IgG secondary antibody (1:10,000; cat. no. 172-1050; Bio-Rad Laboratories, Inc.) for 2 h at room temperature.

    Techniques: Expressing, Activation Assay, Western Blot

    Western blotting analysis of phosphorylated P70S6K ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).

    Journal: PLoS ONE

    Article Title: Vascular Endothelial Growth Factor Receptor-3 Directly Interacts with Phosphatidylinositol 3-Kinase to Regulate Lymphangiogenesis

    doi: 10.1371/journal.pone.0039558

    Figure Lengend Snippet: Western blotting analysis of phosphorylated P70S6K ( A, top left ) and eNOS (S1177) ( B, top left ) in prostatic LECs following 15 minute stimulation with ligand: VEGF-C (100 ng/ml), VEGF-A (100 ng/ml), VEGF-C156S (250 ng/ml), VEGF-D (250 ng/ml) and VEGF-E (100 ng/ml). Time- and concentration-dependent phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, top right ), and PLCγ1 (Tyr783) ( C, top left ) in LECs in response to VEGF-C. The effect of inhibition of VEGFR-3 (hF4-3C5), VEGFR-2 (IMC-1121b) or VEGFR-1 (IMC-18F1) on phosphorylation of P70S6K ( A, bottom left ), eNOS (S1177) ( B, bottom left ); and VEGFR-3 (hF4-3C5) on PLCγ1 (Tyr783) ( C, bottom right ) on LEC response to VEGF-C (100 ng/ml). The effect of AS252424, LY294002, PD98059, and U-73122 on phosphorylation of P70S6K ( A, top right ), eNOS (S1177) ( B, bottom right ), and PLCγ1 (Tyr783) ( C, bottom right ) on LECs in response to VEGF-C. The effect of VEGF-C on phosphorylation of PLCγ2 (Tyr759, Tyr1217) in LECs ( C, bottom left ). Control serum-free vehicle treated LEC lysate is indicated by ‘0′ in all blots. n = 3. Densitometry analysis is shown under each blot in italics; where integrated intensity of phosphorylated molecules was firstly compared to that of the total target protein for each sample, and then expressed as fold change in integrated density compared to either serum-free (A, top left and right panels ; B, top left and right panels ; C, top and bottom left panels ) or VEGF-C treated control samples (A, bottom left and right panels ; B, bottom left and right panels ; C, bottom and bottom left panels ).

    Article Snippet: Antibodies against total P70S6K (Clone: 49D7, Cat. no. 9208), mTOR (Cat. no. 2972), eNOS (Clone: 49G3, Cat. no. 9586), PLCγ1 (Clone: D9H10, Cat. no. 5690), PLCγ2 (Cat. no. 3872), Erk1/2 (Clone: 137F5; Cat. no. 4695), and Akt (Cat. no. 9272) were purchased from Cell Signaling Technology (MA).

    Techniques: Western Blot, Concentration Assay, Inhibition