INT200670
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
/Akt2 expression on the phosphorylation of GSK3? | |||||||||||||||
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We used the PDGF-BB isoform in all experiments in this study because PDGF-B chain expression is induced after peripheral nerve injury [25], neurons throughout the CNS contain the PDGF-B chain [26], and the PDGF-B chain activates both PDGFR? | |||||||||||||||
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l, as a vehicle control) was intrathecally administered 30 min before PDGF-BB (10 pmol/10 ? | |||||||||||||||
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Furthermore, applying PDGF-BB (50 ng/ml) to primary cultured microglial cells enhanced the immunofluorescence for p-PDGFR? | |||||||||||||||
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However, in the patient, we observed LOH deletion in AKT1, under-expression of AKT2, mTOR, elF4E, and over-expression of the negative regulators eIF4EBP1 and NKX3-1. | |||||||||||||||
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Our study demonstrated that HDAC inhibitors, such as valproic acid and butyrate, induce apoptosis in HeLa cervical cancer cells by inhibition of gene expression of Akt1 and Akt2. | |||||||||||||||
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Treatment of HeLa cells with HDAC inhibitors such as valproic acid and butyrate leads to inhibition of Akt1 and Akt2 expression, consequently to deactivation of cellular Akt (Fig. 1 and 2). | |||||||||||||||
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As shown in Fig. 5C, both valproic acid and butyrate decreased the levels of Akt1 and Akt2 mRNA to a certain degree, but not significantly. | |||||||||||||||
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We, for the first time, show that the down-regulation of Akt activity is a consequence of inhibition of Akt1 and Akt2 expression by valproic acid and butyrate. | |||||||||||||||
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Mutations in AKT family members and their correlation with other gene alterations are found in endometrial carcinoma, including AKT2 (D399N), AKT2 (D32H) and AKT3 (E438D) mutations. | |||||||||||||||
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Mutations in AKT family members and their correlation with other gene alterations are found in endometrial carcinoma, including AKT2 (D399N), AKT2 (D32H) and AKT3 (E438D) mutations. | |||||||||||||||
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Mutations in AKT family members and their correlation with other gene alterations are found in endometrial carcinoma, including AKT2 (D399N), AKT2 (D32H) and AKT3 (E438D) mutations. | |||||||||||||||
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Akt1 is the predominant isoform in most tissues while Akt2 is highly expressed in skeletal muscle, heart, liver and kidney [22,23]. | |||||||||||||||
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Valproic acid treatment also reduced the levels of the Akt1 and Akt2 mRNA, but to a lesser degree (Fig. 1B). | |||||||||||||||
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, Akt2/PKB? | |||||||||||||||
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Akt3 is the most abundant of Akt isoforms, about 2 and 4 fold more than Akt1 and Akt2 respectively (Fig. 1C), which is not a normal Akt isoform expression pattern for cervical epithelial cells. | |||||||||||||||
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However, in the patient, we observed LOH deletion in AKT1, under-expression of AKT2, mTOR, elF4E, and over-expression of the negative regulators eIF4EBP1 and NKX3-1. | |||||||||||||||
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As shown in Fig. 1B, following 16 hours of butyrate treatment, the levels of Akt1 and Akt2 mRNA were reduced by about 70% and 50% respectively as compared to untreated control cells. | |||||||||||||||
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Here we report that the induction of cancer cell apoptosis by HDAC inhibitors, such as valproic acid and butyrate, is achieved through inhibition of gene expression of Akt1 and Akt2, pro-survival factors involved in many cell signalling pathways. | |||||||||||||||
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Taken together, these data suggest that the down-regulation of Akt activity by HDAC inhibitors, such as valproic acid and butyrate, is achieved through inhibition of gene expression of Akt1 and Akt2.
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General Comments
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