p ikk Search Results


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Bio-Techne corporation ikk epsilon/ikbke [p thr501] antibody
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ZenBio anti-phospho-ikk beta (p-ikkβ, # 347345)
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ZenBio anti-phospho-ikk alpha (p-ikkα, # 310201)
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Promega p-ikk (ser180)/ikk (ser181) antibody
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Bioworld Antibodies p-ikk-β (phospho-s180/181, bs4237)
Effects of <t>IKK-β</t> on PLA-induced MMP-9 expression in cervical cancer cells. a ‒ c SiHa ( a ), HeLa ( b ), and C-33A ( c ) cells were treated with 10 mM PLA for the indicated times, and the activation of IKK-β was then examined by Western blot analysis. d ‒ f SiHa ( d ), HeLa ( e ), and C-33A ( f ) cells were pretreated with 10 μM IMD0354 (IMD, an inhibitor of IKK-β) for 90 min and then stimulated with 10 mM PLA for an additional 24 h. The expression of MMP-9 was measured by Western blot analysis. g ‒ h HeLa ( g ) and C-33A ( h ) cells were pretreated with 10 μM PD (ERK1/2 inhibitor), LY (PI3K/Akt inhibitor), H89 (PKA inhibitor), or GF (the inhibitor of PKC) for 90 min and then stimulated with 10 mM PLA for another 24 h. The activation of IKK-β were examined by Western blot analysis. i , j HeLa ( i ) and C-33A ( j ) cells were pretreated with 10 μM PD, LY, H89, or GF for 90 min, and then stimulated with 10 mM PLA for another 24 h. The expression of MMP-9 were examined by Western blot analysis. GAPDH expression was evaluated as a loading control. One representative of three different experiments, for each of the analyses performed, is shown
P Ikk β (Phospho S180/181, Bs4237), supplied by Bioworld Antibodies, 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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ABclonal Biotechnology phosphorylated iκb kinase (p-ikk) antibody
Effects of <t>IKK-β</t> on PLA-induced MMP-9 expression in cervical cancer cells. a ‒ c SiHa ( a ), HeLa ( b ), and C-33A ( c ) cells were treated with 10 mM PLA for the indicated times, and the activation of IKK-β was then examined by Western blot analysis. d ‒ f SiHa ( d ), HeLa ( e ), and C-33A ( f ) cells were pretreated with 10 μM IMD0354 (IMD, an inhibitor of IKK-β) for 90 min and then stimulated with 10 mM PLA for an additional 24 h. The expression of MMP-9 was measured by Western blot analysis. g ‒ h HeLa ( g ) and C-33A ( h ) cells were pretreated with 10 μM PD (ERK1/2 inhibitor), LY (PI3K/Akt inhibitor), H89 (PKA inhibitor), or GF (the inhibitor of PKC) for 90 min and then stimulated with 10 mM PLA for another 24 h. The activation of IKK-β were examined by Western blot analysis. i , j HeLa ( i ) and C-33A ( j ) cells were pretreated with 10 μM PD, LY, H89, or GF for 90 min, and then stimulated with 10 mM PLA for another 24 h. The expression of MMP-9 were examined by Western blot analysis. GAPDH expression was evaluated as a loading control. One representative of three different experiments, for each of the analyses performed, is shown
Phosphorylated Iκb Kinase (P Ikk) Antibody, supplied by ABclonal Biotechnology, 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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Bioss ikk beta (tyr188) polyclonal antibody
Effects of <t>IKK-β</t> on PLA-induced MMP-9 expression in cervical cancer cells. a ‒ c SiHa ( a ), HeLa ( b ), and C-33A ( c ) cells were treated with 10 mM PLA for the indicated times, and the activation of IKK-β was then examined by Western blot analysis. d ‒ f SiHa ( d ), HeLa ( e ), and C-33A ( f ) cells were pretreated with 10 μM IMD0354 (IMD, an inhibitor of IKK-β) for 90 min and then stimulated with 10 mM PLA for an additional 24 h. The expression of MMP-9 was measured by Western blot analysis. g ‒ h HeLa ( g ) and C-33A ( h ) cells were pretreated with 10 μM PD (ERK1/2 inhibitor), LY (PI3K/Akt inhibitor), H89 (PKA inhibitor), or GF (the inhibitor of PKC) for 90 min and then stimulated with 10 mM PLA for another 24 h. The activation of IKK-β were examined by Western blot analysis. i , j HeLa ( i ) and C-33A ( j ) cells were pretreated with 10 μM PD, LY, H89, or GF for 90 min, and then stimulated with 10 mM PLA for another 24 h. The expression of MMP-9 were examined by Western blot analysis. GAPDH expression was evaluated as a loading control. One representative of three different experiments, for each of the analyses performed, is shown
Ikk Beta (Tyr188) Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Effects of IKK-β on PLA-induced MMP-9 expression in cervical cancer cells. a ‒ c SiHa ( a ), HeLa ( b ), and C-33A ( c ) cells were treated with 10 mM PLA for the indicated times, and the activation of IKK-β was then examined by Western blot analysis. d ‒ f SiHa ( d ), HeLa ( e ), and C-33A ( f ) cells were pretreated with 10 μM IMD0354 (IMD, an inhibitor of IKK-β) for 90 min and then stimulated with 10 mM PLA for an additional 24 h. The expression of MMP-9 was measured by Western blot analysis. g ‒ h HeLa ( g ) and C-33A ( h ) cells were pretreated with 10 μM PD (ERK1/2 inhibitor), LY (PI3K/Akt inhibitor), H89 (PKA inhibitor), or GF (the inhibitor of PKC) for 90 min and then stimulated with 10 mM PLA for another 24 h. The activation of IKK-β were examined by Western blot analysis. i , j HeLa ( i ) and C-33A ( j ) cells were pretreated with 10 μM PD, LY, H89, or GF for 90 min, and then stimulated with 10 mM PLA for another 24 h. The expression of MMP-9 were examined by Western blot analysis. GAPDH expression was evaluated as a loading control. One representative of three different experiments, for each of the analyses performed, is shown

Journal: Cancer Cell International

Article Title: Phenyllactic acid promotes cell migration and invasion in cervical cancer via IKK/NF-κB-mediated MMP-9 activation

doi: 10.1186/s12935-019-0965-0

Figure Lengend Snippet: Effects of IKK-β on PLA-induced MMP-9 expression in cervical cancer cells. a ‒ c SiHa ( a ), HeLa ( b ), and C-33A ( c ) cells were treated with 10 mM PLA for the indicated times, and the activation of IKK-β was then examined by Western blot analysis. d ‒ f SiHa ( d ), HeLa ( e ), and C-33A ( f ) cells were pretreated with 10 μM IMD0354 (IMD, an inhibitor of IKK-β) for 90 min and then stimulated with 10 mM PLA for an additional 24 h. The expression of MMP-9 was measured by Western blot analysis. g ‒ h HeLa ( g ) and C-33A ( h ) cells were pretreated with 10 μM PD (ERK1/2 inhibitor), LY (PI3K/Akt inhibitor), H89 (PKA inhibitor), or GF (the inhibitor of PKC) for 90 min and then stimulated with 10 mM PLA for another 24 h. The activation of IKK-β were examined by Western blot analysis. i , j HeLa ( i ) and C-33A ( j ) cells were pretreated with 10 μM PD, LY, H89, or GF for 90 min, and then stimulated with 10 mM PLA for another 24 h. The expression of MMP-9 were examined by Western blot analysis. GAPDH expression was evaluated as a loading control. One representative of three different experiments, for each of the analyses performed, is shown

Article Snippet: Blots were incubated with the indicated primary antibodies against HPV16/18 E6 (ab70), HPV16 E7 (ab30731), and HPV18 E7 (ab100953) (Abcam, London, UK) and against MMP-1 (BS1229), MMP-2 (BS1236), MMP-3 (BS6243), MMP-9 (BS1241), MMP-10 (BS7167), MMP-13 (BS6668), IκBα (BS1190), p-IκBα (phospho-S32/S36, BS4105), p65 (BS1253), p-p65 (phospho-S536, BS4138), IKK-β (BS1756), and p-IKK-β (phospho-S180/181, BS4237) (Bioworld Technology, Nanjing, China) at 4 °C overnight, followed by incubation with a goat anti-rabbit (ab6721) or rabbit anti-mouse (ab6728) IgG secondary antibody (Abcam, London, UK) for 1 h at room temperature.

Techniques: Expressing, Activation Assay, Western Blot