INT60198
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
DNA-binding activity of the transcription factor activator protein-1 (AP-1) was assessed using an electrophoretic mobility shift assay. | |||||||||||||||
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When fused with the c-jun leucine zipper domain, which binds heparin and forms homodimers, the polypeptide specifically reproduced the mitogenic and morphogenic activities of basic FGF with similar potency (EC50 = 240 pM). | |||||||||||||||
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DNA-binding activity of the transcription factor activator protein-1 (AP-1) was assessed using an electrophoretic mobility shift assay. | |||||||||||||||
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Electric mobility shift assay served for evaluation of activator protein 1 nuclear binding in HL-60 cells. | |||||||||||||||
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This suggests that Fos/Jun homo- or heterodimeric complexes may interact with the 5'-CTGCGTCAGCG-3' motif, present within the human CCK promoter. | |||||||||||||||
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The tax1 induced c-Fos protein levels and the concurrently increased association of c-Fos/c-Jun transcription factors at the AP-1 site imply a strong functional significance in the activation of proenkephalin gene expression in tax1 expressing glial cells. | |||||||||||||||
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After 1 h or 96 h of treatment, Fos and Jun protein levels were altered and the DNA-binding activity of AP-1 was increased in response to both substances. | |||||||||||||||
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After 1 h or 96 h of treatment, Fos and Jun protein levels were altered and the DNA-binding activity of AP-1 was increased in response to both substances. | |||||||||||||||
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Suppression of AP-1 was associated with altered phosphorylation of p38 mitogen-activated protein kinases. | |||||||||||||||
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DNA-binding activity of the transcription factor activator protein-1 (AP-1) was assessed using an electrophoretic mobility shift assay. | |||||||||||||||
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These data suggest enkephalin gene expression in the adrenal gland is controlled by cell-specific binding of transcription factors from the Fos/Jun families to the enkephalin CRE-2 element. | |||||||||||||||
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DNA-binding activity of the transcription factor activator protein-1 (AP-1) was assessed using an electrophoretic mobility shift assay. | |||||||||||||||
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Removal of the AP-1 binding site from the MMP-12 promoter abolished the basal and inducible expression of MMP-12 [23]. c-Jun, which is a predominant component of the AP-1 binding complex binding to the MMP-12 promoter [23], can potentially transactivate the MMP-12 promoter up to 20-fold in macrophages [18]. | |||||||||||||||
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Removal of the AP-1 binding site from the MMP-12 promoter abolished the basal and inducible expression of MMP-12 [23]. c-Jun, which is a predominant component of the AP-1 binding complex binding to the MMP-12 promoter [23], can potentially transactivate the MMP-12 promoter up to 20-fold in macrophages [18]. | |||||||||||||||
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The interference of PPARalpha/retinoid X receptor alpha with the AP-1 transcription factor elements c-Jun/c-Fos resulted in the inhibition of AP-1 binding and down-regulation of the VDUP-1 gene expression. | |||||||||||||||
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Our results provide evidence for a differential effect of chemopreventive agents such as beta-lapachone, emodin, sanguinarine and capsaicin, which significantly inhibit reporter gene expression as well as TNFalpha- and TPA-induced binding of AP-1 and NF-kappaB, whereas trans-anethole and silymarin do not produce any inhibitory effect. | |||||||||||||||
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1 promoter contains binding sites for both AP-1 and NF-? | |||||||||||||||
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1 promoter in a promoter reporter construct, with mutation of the AP-1 and NF-? | |||||||||||||||
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1 promoter contains binding sites for both AP-1 and NF-? | |||||||||||||||
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Once bound to the promoter, cFos/cJun heterodimers can recruit the SWI/SNF chromatin remodeling complex to activate transcription, whereas homodimers or heterodimers consisting of other family members lack this ability [194]. | |||||||||||||||
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