Serum and glucocorticoid inducible kinase 1 modulates mitochondrial dysfunction and oxidative stress in doxorubicin-induced cardiomyocytes by regulating Hippo pathway via Neural precursor cell-expressed developmentally down-regulated 4 type 2.
The data revealed that maternal immune activation impedes offspring's dendrite development and causes depressive like behaviors by upregulating ISG15 and suppressing NEDD4/Rap2A signaling.
NEDD4-1 levels were decreased after ischemia-reperfusion (I/R) and increased after ischemic preconditioning in rat heart tissue and in H9c2 cardiomyocytes. Overexpression activated the Akt pathway and regulated apoptosis-related proteins in H9c2 cardiomyocytes attenuating SI/R-induced cell apoptosis and caspase 3/7 activities. Overexpression attenuated myocardial apoptosis after I/R.
histone methyltransferase Ehmt2 (G9a) led to the loss of repressive histone methylation at the Nedd4-1 promoter and the transcriptional activation of Nedd4
In thyroid FRTL-5 cells activation of the cyclic AMP pathway increases the association of Nedd4 with IRS-2 thereby enhancing IRS-2-mediated signalling and cell proliferation induced by IGF-I.
Results in two evolutionarily distant model organisms strongly suggests that Nedd4 is a modifier of alpha-synuclein pathobiology and thus a potential target for neuroprotective therapies
COMMD1 modulates Na(+) transport in epithelial cells through regulation of ENaC cell surface expression and this effect is likely mediated via Nedd4-2.
NEDD4-1-mediated PTEN ubiquitination is crucial in the regulation of PI3K/Akt signaling by PTEN during the neuronal response to zinc which may represent a common mechanism in neurodegeneration
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