Results 21 to 30 of about 145,468 (162)
Activation of c-Jun by human cytomegalovirus UL42 through JNK activation.
PLoS ONE, 2020 c-Jun is a major component of the AP-1 transactivator complex. In this report, we demonstrated that AP-1 was activated by the expression of UL42, a human cytomegalovirus-encoded membrane protein that has two PPXY (PY) motifs and a C-terminal ...
Tetsuo Koshizuka, Naoki Inoue
doaj +1 more source
Journal of Neuroscience, 2006 Optimal management of neuropathic pain is a major clinical challenge. We investigated the involvement of c-Jun N-terminal kinase (JNK) in neuropathic pain produced by spinal nerve ligation (SNL) (L5).
Z. Zhuang +7 more
semanticscholar +1 more source
Activation of c-Jun N-terminal kinase (JNK) during mitosis in retinal progenitor cells. [PDF]
PLoS ONE, 2012 Most studies of c-Jun N-terminal Kinase (JNK) activation in retinal tissue were done in the context of neurodegeneration. In this study, we investigated the behavior of JNK during mitosis of progenitor cells in the retina of newborn rats.
Vinicius Toledo Ribas +3 more
doaj +1 more source
Baicalin modulates apoptosis via RAGE, MAPK, and AP-1 in vascular endothelial cells during invasion
Innate Immunity, 2019 Glässer’s disease, caused by Haemophilus parasuis , is a chronic disease related to an inflammatory immune response. Baicalin exerts important biological functions.
Shulin Fu +10 more
doaj +1 more source
Biomedicines, 2022 Non-alcoholic fatty liver (NAFL) is the most common chronic liver disease. Activation of mitogen-activated kinases (MAPK) cascade, which leads to c-Jun N-terminal kinase (JNK) activation occurs in the liver in response to the nutritional and metabolic ...
Robert W. M. Min +4 more
doaj +1 more source
c-Jun N-terminal Kinase (JNK) Signaling as a Therapeutic Target for Alzheimer’s Disease
Frontiers in Pharmacology, 2016 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, cell death, and regulation of cellular senescence.
Ramon Yarza +3 more
semanticscholar +1 more source
Research progress on mechanism of Schwann cells promoting peripheral nerve regeneration [PDF]
Jichu yixue yu linchuang, 2022 Schwann cells (SCs) have a strong plasticity. After peripheral nerve injury, Schwann cells dedifferentiate into repair phenotype and dominate the repair process. C-Jun N-terminal kinase, mitogen activated protein kinase(MAPK) and other signaling pathways
YANG Yi-duo, GUO Hai-dong, SHAO Shui-jin, LIU Yu-pu
doaj +1 more source
Journal of Neuroscience, 2004 The mechanisms of action of human synthetic and naturally secreted cell-derived amyloid β-peptide (Aβ)1–42 on the induction of long-term potentiation (LTP) were investigated in the medial perforant path to dentate granule cell synapses in hippocampal ...
Qin-Wen Wang +4 more
semanticscholar +1 more source
A feed-forward regulation of endothelin receptors by c-Jun in human non-pigmented ciliary epithelial cells and retinal ganglion cells. [PDF]
PLoS ONE, 2017 c-Jun, c-Jun N-terminal kinase(JNK) and endothelin B (ETB) receptor have been shown to contribute to the pathogenesis of glaucoma. Previously, we reported that an increase of c-Jun and CCAAT/enhancer binding protein β (C/EBPβ) immunohistostaining is ...
Junming Wang +4 more
doaj +1 more source
c-Jun N-terminal Kinase (JNK) Mediates Feedback Inhibition of the Insulin Signaling Cascade*
Journal of Biological Chemistry, 2003 Activation of the c-Jun N-terminal kinase (JNK) by proinflammatory cytokines inhibits insulin signaling, at least in part, by stimulating phosphorylation of rat/mouse insulin receptor substrate 1 (Irs1) at Ser307(Ser312 in human IRS1).
Yong-Hee Lee +3 more
semanticscholar +1 more source