The c-Jun N-terminal kinases (JNKs), as members of the mitogen-activated protein kinase
(MAPK) family, mediate eukaryotic cell responses to a wide range of abiotic and biotic stress …

The c-Jun N-terminal kinases (JNKs), with its members JNK1, JNK2, and JNK3, is a
subfamily of (MAPK) mitogen-activated protein kinases. JNK signaling regulates a wide …

Abstract NMDA (N-methyl-d-aspartate) receptors (NMDARs) play a central role in excitotoxic
neuronal death caused by ischemic stroke, but NMDAR channel blockers have failed to be …

Excitotoxicity, the specific type of neurotoxicity mediated by glutamate, may be the missing
link between ischemia and neuronal death, and intervening the mechanistic steps that lead …

c-Jun N-terminal kinases (JNKs) are a family of protein kinases that play a central role in
stress signaling pathways implicated in gene expression, neuronal plasticity, regeneration …

T cell antigen receptor (TCR) signaling drives distinct responses depending on the
differentiation state and context of CD8+ T cells. We hypothesized that access of signal …

Obesity contributes to the development of type 2 diabetes, but the underlying mechanisms
are poorly understood. Using cell culture and mouse models, we show that obesity causes …

The JNKs are master protein kinases that regulate many physiological processes, including
inflammatory responses, morphogenesis, cell proliferation, differentiation, survival and …

The c-Jun N-terminal kinases (JNKs) are members of a larger group of serine/threonine
(Ser/Thr) protein kinases from the mitogen-activated protein kinase family. JNKs were …

Neuronal death in cerebral ischemia is largely due to excitotoxic mechanisms, which are
known to activate the c-Jun N-terminal kinase (JNK) pathway. We have evaluated the …