IndraLab
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"AKT signaling is important in endothelial-to-mesenchymal transition and myofibroblastic transformation in fibroblasts from the heart and lungs.32, 33 miR-486 may upregulate AKT activity through negative regulation of PTEN expression.43 The phosphoinositide phosphatase PTEN converts PIP3 to PIP2 and thereby negatively modulates AKT activity,31 thus downregulation of PTEN can upregulate AKT phosphorylation.43, 53 We evaluated the role of the AKT pathway in mediating alpha-SMA expression induced by miR-486 mimic."
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"Di-Poi et al. suggested that PPARbeta and delta activation increases the expression of 3-phosphoinositide-dependent-protein kinae 1 (PDPK1) and integrin linked kinase (ILK), and decreases the expression of PTEN, causing increased phosphorylation of AKT, leading to antiapoptotic signaling and enhanced cell survival [XREF_BIBR]."
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"Here, we report that Pten (-/-) mouse blood contains 25% more platelets than Pten (+/+) blood and that PTEN deficiency significantly shortened the bleeding time, increased the sensitivity of platelets to collagen induced activation and aggregation, and enhanced phosphorylation of Akt at Ser473 in response to collagen."
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"To verify the proposed signaling mechanisms for spiral ganglion defects in Pax2 Cre/+; Pten loxP and loxP mice, we examined whether Pten deficiency (XREF_SUPPLEMENTARY) upregulates Ser473 phosphorylation of Akt and triggers Ser9 phosphorylation of GSK3beta (pGSK3beta) in the PI3K signaling cascade."
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"The data in XREF_FIG and XREF_SUPPLEMENTARY (repeat experiments) also show that the extent of Akt S473 phosphorylation induced in the cells upon rescue by P110 * or Pten ablation is moderate and closer to that seen in resting mature B cells than B cells activated by BCR engagement or even just exposed to serum containing culture medium."
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"However, a recent report by Rodrik-Outmezguine et al. showed that phosphorylation of AKT at the Thr308 site and of the AKT substrates including PRAS40, GSK-3beta and FOXO1/3 are only transiently repressed by mTORKIs in PIK3CA mutant (MCF7, BT474) and PTEN deficient (MDA-MB-468) breast cancer cell lines [XREF_BIBR]."
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"To verify the proposed signaling mechanisms for spiral ganglion defects in Pax2 Cre/+; Pten loxP and loxP mice, we examined whether Pten deficiency (XREF_SUPPLEMENTARY) upregulates Ser473 phosphorylation of Akt and triggers Ser9 phosphorylation of GSK3beta (pGSK3beta) in the PI3K signaling cascade."
"Ectopic expression of wild-type PTEN in MCF-7 epithelial breast cancer cells resulted in universal inhibition of Akt phosphorylation in response to stimulation by diverse growth factors and selective inhibition of MEK/extracellular signal-regulated kinase (ERK) phosphorylation stimulated by insulin or insulin-like growth factor 1 (IGF-1)"