pho akt Search Results


phos pho akt ser473  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc phos pho akt ser473
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pho akt signaling pathway kit  (Cell Signaling Technology Inc)
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Pho Akt Signaling Pathway Kit, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit anti pho akt cell signaling  (Cell Signaling Technology Inc)
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rabbit anti pho enos cell signaling  (Cell Signaling Technology Inc)
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Rabbit Anti Pho Enos Cell Signaling, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti-pho-akt  (Cell Signaling Technology Inc)
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<t>AMPK-</t> <t>α</t> 1-knockdown THP-1 cells exhibit impairments of TLR4-mediated signal, leading to activation of NF-κB and AP-1. ( a and b ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were transfected with either pBIIx-Luc ( a ) or AP-1-luc ( b ) together with Renilla luciferase vector. After 24 h, cells were treated with or without LPS (10 ng/ml) for 6 h, and then analyzed for luciferase activity. Results are expressed as the fold induction in luciferase activity relative to that of untreated cells. Error bars indicate ±S.D. of triplicate samples. ( c–f ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were treated with or without LPS (10 ng/ml) for 1 h, and then analyzed for DNA-binding activities for NF-KB, p65 ( c ) and p50 ( d ), and AP-1, c-Fos ( e ) and c-Jun ( f ), components as described in Materials and Methods. Results are expressed as the fold increase relative to that of wt THP-1 transfected with mock. Error bars indicate ±S.D. of triplicate samples. ( g ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for different times as indicated. The lysates were examined by western blotting with anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, <t>anti-pho-AKT,</t> and anti-AKT antibodies. Immunoblotting with anti-GAPDH antibody was performed to generate a control for gel loading. ( h ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for 9 h, and then analyzed for productions of TNF- α , and IL-1 β , and IL-6 in supernatants using ELISA method. Error bars indicate ±S.D. of triplicate samples. * P <0.05, ** P <0.01, *** P <0.001
Anti Pho Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pho-akt(ser 473) antibody  (Cell Signaling Technology Inc)
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<t>AMPK-</t> <t>α</t> 1-knockdown THP-1 cells exhibit impairments of TLR4-mediated signal, leading to activation of NF-κB and AP-1. ( a and b ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were transfected with either pBIIx-Luc ( a ) or AP-1-luc ( b ) together with Renilla luciferase vector. After 24 h, cells were treated with or without LPS (10 ng/ml) for 6 h, and then analyzed for luciferase activity. Results are expressed as the fold induction in luciferase activity relative to that of untreated cells. Error bars indicate ±S.D. of triplicate samples. ( c–f ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were treated with or without LPS (10 ng/ml) for 1 h, and then analyzed for DNA-binding activities for NF-KB, p65 ( c ) and p50 ( d ), and AP-1, c-Fos ( e ) and c-Jun ( f ), components as described in Materials and Methods. Results are expressed as the fold increase relative to that of wt THP-1 transfected with mock. Error bars indicate ±S.D. of triplicate samples. ( g ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for different times as indicated. The lysates were examined by western blotting with anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, <t>anti-pho-AKT,</t> and anti-AKT antibodies. Immunoblotting with anti-GAPDH antibody was performed to generate a control for gel loading. ( h ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for 9 h, and then analyzed for productions of TNF- α , and IL-1 β , and IL-6 in supernatants using ELISA method. Error bars indicate ±S.D. of triplicate samples. * P <0.05, ** P <0.01, *** P <0.001
Pho Akt(Ser 473) Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti phos pho akt  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc anti phos pho akt
<t>AMPK-</t> <t>α</t> 1-knockdown THP-1 cells exhibit impairments of TLR4-mediated signal, leading to activation of NF-κB and AP-1. ( a and b ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were transfected with either pBIIx-Luc ( a ) or AP-1-luc ( b ) together with Renilla luciferase vector. After 24 h, cells were treated with or without LPS (10 ng/ml) for 6 h, and then analyzed for luciferase activity. Results are expressed as the fold induction in luciferase activity relative to that of untreated cells. Error bars indicate ±S.D. of triplicate samples. ( c–f ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were treated with or without LPS (10 ng/ml) for 1 h, and then analyzed for DNA-binding activities for NF-KB, p65 ( c ) and p50 ( d ), and AP-1, c-Fos ( e ) and c-Jun ( f ), components as described in Materials and Methods. Results are expressed as the fold increase relative to that of wt THP-1 transfected with mock. Error bars indicate ±S.D. of triplicate samples. ( g ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for different times as indicated. The lysates were examined by western blotting with anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, <t>anti-pho-AKT,</t> and anti-AKT antibodies. Immunoblotting with anti-GAPDH antibody was performed to generate a control for gel loading. ( h ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for 9 h, and then analyzed for productions of TNF- α , and IL-1 β , and IL-6 in supernatants using ELISA method. Error bars indicate ±S.D. of triplicate samples. * P <0.05, ** P <0.01, *** P <0.001
Anti Phos Pho Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pho akt  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc pho akt
<t>AMPK-</t> <t>α</t> 1-knockdown THP-1 cells exhibit impairments of TLR4-mediated signal, leading to activation of NF-κB and AP-1. ( a and b ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were transfected with either pBIIx-Luc ( a ) or AP-1-luc ( b ) together with Renilla luciferase vector. After 24 h, cells were treated with or without LPS (10 ng/ml) for 6 h, and then analyzed for luciferase activity. Results are expressed as the fold induction in luciferase activity relative to that of untreated cells. Error bars indicate ±S.D. of triplicate samples. ( c–f ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were treated with or without LPS (10 ng/ml) for 1 h, and then analyzed for DNA-binding activities for NF-KB, p65 ( c ) and p50 ( d ), and AP-1, c-Fos ( e ) and c-Jun ( f ), components as described in Materials and Methods. Results are expressed as the fold increase relative to that of wt THP-1 transfected with mock. Error bars indicate ±S.D. of triplicate samples. ( g ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for different times as indicated. The lysates were examined by western blotting with anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, <t>anti-pho-AKT,</t> and anti-AKT antibodies. Immunoblotting with anti-GAPDH antibody was performed to generate a control for gel loading. ( h ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for 9 h, and then analyzed for productions of TNF- α , and IL-1 β , and IL-6 in supernatants using ELISA method. Error bars indicate ±S.D. of triplicate samples. * P <0.05, ** P <0.01, *** P <0.001
Pho Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti pho akt ser473  (Proteintech)
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Proteintech anti pho akt ser473
<t>AMPK-</t> <t>α</t> 1-knockdown THP-1 cells exhibit impairments of TLR4-mediated signal, leading to activation of NF-κB and AP-1. ( a and b ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were transfected with either pBIIx-Luc ( a ) or AP-1-luc ( b ) together with Renilla luciferase vector. After 24 h, cells were treated with or without LPS (10 ng/ml) for 6 h, and then analyzed for luciferase activity. Results are expressed as the fold induction in luciferase activity relative to that of untreated cells. Error bars indicate ±S.D. of triplicate samples. ( c–f ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were treated with or without LPS (10 ng/ml) for 1 h, and then analyzed for DNA-binding activities for NF-KB, p65 ( c ) and p50 ( d ), and AP-1, c-Fos ( e ) and c-Jun ( f ), components as described in Materials and Methods. Results are expressed as the fold increase relative to that of wt THP-1 transfected with mock. Error bars indicate ±S.D. of triplicate samples. ( g ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for different times as indicated. The lysates were examined by western blotting with anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, <t>anti-pho-AKT,</t> and anti-AKT antibodies. Immunoblotting with anti-GAPDH antibody was performed to generate a control for gel loading. ( h ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for 9 h, and then analyzed for productions of TNF- α , and IL-1 β , and IL-6 in supernatants using ELISA method. Error bars indicate ±S.D. of triplicate samples. * P <0.05, ** P <0.01, *** P <0.001
Anti Pho Akt Ser473, supplied by Proteintech, 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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anti phos pho rxrxxs t  (Cell Signaling Technology Inc)
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<t>AMPK-</t> <t>α</t> 1-knockdown THP-1 cells exhibit impairments of TLR4-mediated signal, leading to activation of NF-κB and AP-1. ( a and b ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were transfected with either pBIIx-Luc ( a ) or AP-1-luc ( b ) together with Renilla luciferase vector. After 24 h, cells were treated with or without LPS (10 ng/ml) for 6 h, and then analyzed for luciferase activity. Results are expressed as the fold induction in luciferase activity relative to that of untreated cells. Error bars indicate ±S.D. of triplicate samples. ( c–f ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were treated with or without LPS (10 ng/ml) for 1 h, and then analyzed for DNA-binding activities for NF-KB, p65 ( c ) and p50 ( d ), and AP-1, c-Fos ( e ) and c-Jun ( f ), components as described in Materials and Methods. Results are expressed as the fold increase relative to that of wt THP-1 transfected with mock. Error bars indicate ±S.D. of triplicate samples. ( g ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for different times as indicated. The lysates were examined by western blotting with anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, <t>anti-pho-AKT,</t> and anti-AKT antibodies. Immunoblotting with anti-GAPDH antibody was performed to generate a control for gel loading. ( h ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for 9 h, and then analyzed for productions of TNF- α , and IL-1 β , and IL-6 in supernatants using ELISA method. Error bars indicate ±S.D. of triplicate samples. * P <0.05, ** P <0.01, *** P <0.001
Anti Phos Pho Rxrxxs T, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti pho akt antibody  (Proteintech)
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Proteintech anti pho akt antibody
FIGURE 6 SP140 inhibitor suppress glioma progress <t>and</t> <t>TRIM22/PI3K/AKT</t> signaling pathway. (A) Coexpression analysis of TRIM22 and SP family in TCGA glioma database. (B) The mRNA and protein expression level of TRIM22 in different cell lines. (C) The mRNA and protein expression level of TRIM22 in U87 and U251 after GSK761 intervention. (D) CCK-8 analysis showed cell proliferation in U87 and U251 after GSK761 intervention. (E, F) Wound-healing assay showed cell migration in U87 and U251 after GSK761 intervention. (G, H) Transwell invasion assay showed cell invasion in U87 and U251 after GSK761 intervention. (I) The mRNA expression level of TRIM22 after GSK761 treatment. (J) Western Blot analysis showed PI3K/AKT signaling pathway changes after GSK761 intervention. *p < .05, **p < .01, ns indicates no significance.
Anti Pho Akt Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


AMPK- α 1-knockdown THP-1 cells exhibit impairments of TLR4-mediated signal, leading to activation of NF-κB and AP-1. ( a and b ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were transfected with either pBIIx-Luc ( a ) or AP-1-luc ( b ) together with Renilla luciferase vector. After 24 h, cells were treated with or without LPS (10 ng/ml) for 6 h, and then analyzed for luciferase activity. Results are expressed as the fold induction in luciferase activity relative to that of untreated cells. Error bars indicate ±S.D. of triplicate samples. ( c–f ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were treated with or without LPS (10 ng/ml) for 1 h, and then analyzed for DNA-binding activities for NF-KB, p65 ( c ) and p50 ( d ), and AP-1, c-Fos ( e ) and c-Jun ( f ), components as described in Materials and Methods. Results are expressed as the fold increase relative to that of wt THP-1 transfected with mock. Error bars indicate ±S.D. of triplicate samples. ( g ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for different times as indicated. The lysates were examined by western blotting with anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, anti-pho-AKT, and anti-AKT antibodies. Immunoblotting with anti-GAPDH antibody was performed to generate a control for gel loading. ( h ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for 9 h, and then analyzed for productions of TNF- α , and IL-1 β , and IL-6 in supernatants using ELISA method. Error bars indicate ±S.D. of triplicate samples. * P <0.05, ** P <0.01, *** P <0.001

Journal: Cell Death & Disease

Article Title: AMP-activated protein kinase- α 1 as an activating kinase of TGF- β -activated kinase 1 has a key role in inflammatory signals

doi: 10.1038/cddis.2012.95

Figure Lengend Snippet: AMPK- α 1-knockdown THP-1 cells exhibit impairments of TLR4-mediated signal, leading to activation of NF-κB and AP-1. ( a and b ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were transfected with either pBIIx-Luc ( a ) or AP-1-luc ( b ) together with Renilla luciferase vector. After 24 h, cells were treated with or without LPS (10 ng/ml) for 6 h, and then analyzed for luciferase activity. Results are expressed as the fold induction in luciferase activity relative to that of untreated cells. Error bars indicate ±S.D. of triplicate samples. ( c–f ) The wt THP-1 and AMPK- α 1 KD THP-1 cells were transfected with or without hAMPK- α 1 vector. Twenty-four hours after transfection, cells were treated with or without LPS (10 ng/ml) for 1 h, and then analyzed for DNA-binding activities for NF-KB, p65 ( c ) and p50 ( d ), and AP-1, c-Fos ( e ) and c-Jun ( f ), components as described in Materials and Methods. Results are expressed as the fold increase relative to that of wt THP-1 transfected with mock. Error bars indicate ±S.D. of triplicate samples. ( g ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for different times as indicated. The lysates were examined by western blotting with anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, anti-pho-AKT, and anti-AKT antibodies. Immunoblotting with anti-GAPDH antibody was performed to generate a control for gel loading. ( h ) The wt THP-1 and AMPK- α 1-knockdown (AMPK- α 1 KD ) THP-1 cells were treated with or without LPS (10 ng/ml) for 9 h, and then analyzed for productions of TNF- α , and IL-1 β , and IL-6 in supernatants using ELISA method. Error bars indicate ±S.D. of triplicate samples. * P <0.05, ** P <0.01, *** P <0.001

Article Snippet: Antibodies used were anti-pho-AMPK- α 1 (Ser485), anti-pho-AMPK- α 1 (Thr172/Thr174), anti-pho-TAK1, anti-TAK1, anti-IκB α , anti-pho-p38, anti-p38, anti-pho-JNK, anti-JNK, anti-pho-AKT, anti-AKT, anti-Myc, anti-Flag, anti-GAPDH (Cell Signaling, Beverly, MA, USA), and anti-AMPK- α 1 antibodies (Abcam, Cambridge, MA, USA).

Techniques: Activation Assay, Transfection, Plasmid Preparation, Luciferase, Activity Assay, Binding Assay, Western Blot, Enzyme-linked Immunosorbent Assay

FIGURE 6 SP140 inhibitor suppress glioma progress and TRIM22/PI3K/AKT signaling pathway. (A) Coexpression analysis of TRIM22 and SP family in TCGA glioma database. (B) The mRNA and protein expression level of TRIM22 in different cell lines. (C) The mRNA and protein expression level of TRIM22 in U87 and U251 after GSK761 intervention. (D) CCK-8 analysis showed cell proliferation in U87 and U251 after GSK761 intervention. (E, F) Wound-healing assay showed cell migration in U87 and U251 after GSK761 intervention. (G, H) Transwell invasion assay showed cell invasion in U87 and U251 after GSK761 intervention. (I) The mRNA expression level of TRIM22 after GSK761 treatment. (J) Western Blot analysis showed PI3K/AKT signaling pathway changes after GSK761 intervention. *p < .05, **p < .01, ns indicates no significance.

Journal: Brain and behavior

Article Title: SP140 inhibitor suppressing TRIM22 expression regulates glioma progress through PI3K/AKT signaling pathway.

doi: 10.1002/brb3.3465

Figure Lengend Snippet: FIGURE 6 SP140 inhibitor suppress glioma progress and TRIM22/PI3K/AKT signaling pathway. (A) Coexpression analysis of TRIM22 and SP family in TCGA glioma database. (B) The mRNA and protein expression level of TRIM22 in different cell lines. (C) The mRNA and protein expression level of TRIM22 in U87 and U251 after GSK761 intervention. (D) CCK-8 analysis showed cell proliferation in U87 and U251 after GSK761 intervention. (E, F) Wound-healing assay showed cell migration in U87 and U251 after GSK761 intervention. (G, H) Transwell invasion assay showed cell invasion in U87 and U251 after GSK761 intervention. (I) The mRNA expression level of TRIM22 after GSK761 treatment. (J) Western Blot analysis showed PI3K/AKT signaling pathway changes after GSK761 intervention. *p < .05, **p < .01, ns indicates no significance.

Article Snippet: The primary antibodies used in this study were anti-PI3K antibody (67121-1-Ig, Proteintech), anti-AKT antibody (60203-2-Ig, Proteintech), anti-pho-AKT antibody (80455-1-RR, Proteintech), anti-TRIM22 antibody (ab68071, Abcam).

Techniques: Expressing, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Invasion Assay, Western Blot