Jong-Hee Lee

TL;DR: Results demonstrate that activation of PKCδ triggers degradation of MKP-1 through the ubiquitin-proteasome pathway, thereby contributing to persistent activation of ERK1/2 under glutamate-induced oxidative toxicity.

TL;DR: It is demonstrated for the first time that Cdk5 interacts with p53 and increases its stability through posttranslational regulation, leading to accumulation of p53, particularly in the nucleus, which helps define the mechanisms underlying neuronal apoptosis occurring as a result of Cdk 5-mediated p53 stabilization and transcriptional activation.

TL;DR: It is found that RA treatment of SK‐N‐BE(2)C, human neuroblastoma cells, increased the expression of Cdk5 and its neuron specific activator p35 through the extracellular‐signal‐regulated kinase1/2 and cAMP‐dependent protein kinase A (PKA) pathway and plays a critical role in the RA‐induced neuronal differentiation.

TL;DR: A critical role is identified in neuronal death induced by DNA damage upon mitomycin C treatment and evidence that the ERK signaling regulates Cyclin‐dependent kinase 5 (Cdk5) activity and stability of tumor suppressor p53 is provided.

TL;DR: The data presented here suggest that white adipocytes express at least two different types of P2Y receptors and that activation of P 2Y11 receptor might be involved in inhibition of leptin production and stimulation of lipolysis, suggesting that purinergic transmission can play an important role in white adipocyte physiology.