INT83799
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
As the toxicity progressed, during 6 and 18 h post-AAP administration, the BCL-X(L) protein band shifted to a slower mobility band which might represent a phosphorylated form of BCL-X(L). | |||||||||||||||
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As the toxicity progressed, during 6 and 18 h post-AAP administration, the BCL-X(L) protein band shifted to a slower mobility band which might represent a phosphorylated form of BCL-X(L). | |||||||||||||||
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The most dramatic changes observed in this study were: (i) substantial increase in the expression of bcl-Xl in the liver by 7-day GSPE exposure alone; (ii) significant modification bcl-Xl expression by AAP alone; and (iii) dramatic inhibition of AAP-induced modification of bcl-Xl (phosphorylation?) | |||||||||||||||
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There was constitutive activation of Stat5 and detectable expression of the Stat5 target Bcl-XL in BM of both normal and polycythemic mice, with increased Stat5 phosphorylation and Bcl-XL in spleens from JAKV617F recipients, although this could in part reflect the increase in splenic myeloerythroid cells in these mice. | |||||||||||||||
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As expected levels of phosphorylated AKT, Bcl-2, Bcl-xL and survivin were significantly reduced in tumors from mice treated with the reg4 antibody compared to control. | |||||||||||||||
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JNK when activated can phosphorylate serine 62 on Bcl-xL, which effectively prevents this protein's anti-apoptotic effects [56]. | |||||||||||||||
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Because systemic treatment with the antibody reduces tumor growth and increases sensitivity to gemcitabine treatment, we used western blot analysis to monitor in tumors the influence of reg4 antibody treatment on the intracellular levels of proteins associated with apoptosis (phosphorylated AKT, Bcl-2, Bcl-xL and survivin) and cell cycle (cyclin D1). | |||||||||||||||
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Cytosol was isolated and separated by 12% SDS-PAGE and probed with tyrosine phosphorylated (p) -Bax, Bad, Bcl-2 and Bcl-xl antibodies and bands were detected. | |||||||||||||||
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The present study aims to investigate the mechanism of phosphorylation of apoptotic proteins and tests the hypothesis that the hypoxia-induced increased tyrosine phosphorylation of apoptotic proteins Bcl-2 and Bcl-xl is Ca(2+)-influx-dependent. | |||||||||||||||
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The present study aims to investigate the mechanism of phosphorylation of apoptotic proteins and tests the hypothesis that the hypoxia-induced increased tyrosine phosphorylation of apoptotic proteins Bcl-2 and Bcl-xl is Ca(2+)-influx-dependent. | |||||||||||||||
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General Comments
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