IndraLab

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Phosphorylated AKT activates cell differentiation. 6 / 6
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"Taken together, our results demonstrate that over-expression of CHL1 inhibits the activation of Rho GTPases, of related p38 and JNK MAPK pathways, and of p-Akt inducing cell apoptosis and differentiation."
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"Moreover, loss of METTL3 leads to increased levels of phosphorylated AKT, which contributes to the differentiation promoting effects of METTL3 depletion."
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"Moreover, IGFBP2 increased phosphorylation of c-Jun N-terminal kinase (p-JNK) and p-Akt, and activated JNK or Akt signaling significantly promoted adipogenic differentiation of MSCs."
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"Previous reports are consistent with our results showing increased p-Akt expression during matrix induced osteogenic differentiation."
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"Furthermore, we showed that nutrient deprivation reduced the level of phosphorylated Akt in the resting zone and that exogenous IGF-1 restored the phosphorylated Akt level and stimulated differentiation of the pooled chondroprogenitors, decreasing their numbers."
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"Upregulating p-AKT could increase the neuronal differentiation from mouse cochlear neural stem cells."
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