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A critical role for the miR106b-25/NEDD4L/NOTCH1 axis in the disease.
Sgk1 stimulated OAT3 transport activity by interfering with the inhibitory effect of Nedd4-2 on the transporter. This study provides important insights into how OAT3-mediated drug elimination is regulated in vivo.
ULK1 phosphorylation at 3 different sites on the same ULK1 target region for NEDD4L is preparatory for its ubiquitylation and subsequent degradation.
WW3 and WW4 domains of Nedd4-2 are critical for its association with and modulation of the transporter.
study demonstrated significant genetic interaction on Na intake with child obesity by salt-sensitive genes variations, NEDD4L and CYP11beta2
Collectively, Nedd4L plays a tumor suppressive role in HCC, possibly through triggering MAPK/ERK-mediated apoptosis, and Nedd4L downregulation may be a potential prognostic biomarker as well as a therapeutic target for HCC.
evidence implicating E3 ubiquitin ligase NEDD4L in the pathogeny of periventricular nodular heterotopia
This study demonstrated that it is possible to downregulate Kv1.3 channel density through activation of an E3 ubiquitin ligase and that inhibition of the protease pathway or mutation of the Nedd4-2 catalytic site prevents Kv1.3 modulation.
These findings provide evidence that Nedd4-2 is up-regulated in response to endoplasmic reticulum stress by the spliced form of X-box binding protein 1 and that this is important in the induction of an appropriate autophagic response.
both Nedd4-1 and Nedd4-2 are important regulators for hOAT1 ubiquitination, expression, and function
USP36 actions extend beyond TrkA because the presence of USP36 interferes with Nedd4-2-dependent Kv7.2/3 channel regulation.
NEDD4L negatively regulates PIK3CA protein levels via ubiquitination and is required for the maintenance of PI3K-AKT signaling pathway.
overexpression of miR-93 in lung cancer cells promoted TGF-b-induced EMT through downregulation of NEDD4L. The analysis of publicly available gene expression array datasets indicates that low NEDD4L expression correlates with poor outcomes among patients with lung cancer, further supporting the oncogenic role of miR-93 in lung tumorigenesis and metastasis.
the regulation of Nedd4L protein expression may play a role in the development of ovarian cancers.
Propose regulation of placental SNAT2/LAT1 ubiquitination by mTORC1 and Nedd4-2.
Overexpression of Nedd4-2 enhanced hOAT4 ubiquitination, and inhibited hOAT4 transport activity.
Our results suggest that three screened NEDD4-2 variants do not play a leading role in the pathogenesis of photosensitive epilepsy in the Turkish population.
The mechanisms of activation and degradation of the NEDD4L:the transition from the closed to the active form is regulated by a competition of inositol 1,4,5-trisphosphate and Ca2+.
Data show that membrane protein Ndfip1 recruits E3 ubiquitin (Ub) ligase Nedd4-2 to the Golgi to target ether-a-go-go-related gene (hERG) channel for degradation while membrane protein Ndfip2 also mediates Nedd4-2 interaction with hERG in the Golgi.
Proteomics analysis of EV71-infected cells reveals the involvement of host protein NEDD4L in EV71 replication.
these findings suggest that regulation of Dvl protein levels by NEDD4L is essential for convergent extension during early Xenopus embryogenesis.
Results suggest a mechanism for epithelial Na+ channel regulation in which AMP-activated kinase promotes ENaC-Nedd4-2 interaction, inhibiting ENaC by increasing Nedd4-2-dependent ENaC retrieval from the plasma membrane.
results indicate that AMPK inhibits KCNQ1 activity by promoting Nedd4-2-dependent channel ubiquitination and retrieval from the plasma membrane.
This study suggested that Nedd4-regulated PTEN is a key regulator of terminal arborization in vivo.
ENaC-beta regulation that occurs through IKKbeta-dependent Nedd4-2 phosphorylation at a recognized SGK1 and protein kinase A target site.
NEDD4L plays a key role in the feedback regulation of cAMP signaling by limiting CRTC3 protein levels.
These findings indicate that AMPK promotes the assembly of beta1Pix, 14-3-3 proteins, and Nedd4-2 into a complex that inhibits ENaC by enhancing Nedd4-2 binding to ENaC and its degradation.
Findings indicate an important negative regulatory function for Nedd4 ubiquitin protein ligase (Nedd4-2) and Nedd4 family interacting protein 1 (Ndfip1) in IgE-dependent mast cell activity.
Data indicate that ENaC is the primary in vivo target of NEDD4-2 and that Nedd4-2 deletion is associated with hypertension on a normal Na(+) diet. Findings provide further insight into the critical function of NEDD4-2 in renal pathophysiology.
Nedd4-2 heterozygotes are hyperactive, have increased basal synaptic transmission and have enhanced sensitivity to inflammatory pain. They provide a new genetic model to study inflammatory pain.
Findings demonstrate that during a high oral salt intake the Nedd4-2-containing C2 domain protein plays a pivotal role in maintaining adaptive salt handling in the kidney.
These results suggested that Nedd4-2 with C2 domain might play a pivotal role in cardio-renal associations through post-transcriptional modification of both epithelial sodium channel and cardiac ion channels, which are critical for kidney and heart functions.
Nedd4-2 knockdown ameliorates movement disorders in PD mice.
Tmbim1 promoted the lysosomal degradation of toll-like receptor 4 by cooperating with the ESCRT endosomal sorting complex to facilitate MVB formation, and the ubiquitination of Tmbim1 by the E3 ubiquitin ligase Nedd4l was required for this process.
These results identify NKCC1 as a novel target for Nedd4L-mediated down-regulation in vivo, which modulates ion and fluid transport in the distal colon together with epithelial Na(+) channel (ENaC).
Three epilepsy-associated missense mutations reduce neural precursor cell expressed developmentally down-regulated gene 4-2 (Nedd4-2)-mediated AMPA receptor GluA1 ubiquitination.
These findings elucidate a critical role of Mdm2-p53-Nedd4-2 signaling underlying the regulation of neural network synchrony and seizure susceptibility.
We identified glutamate receptor subunit 1 (GluA1), subunit of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors as a novel substrate of Nedd4-2
The short isoform of the ubiquitin ligase NEDD4L is a CREB target gene in hepatocytes.
Nedd4-2-mediated ubiquitination of beta-ENaC leading to endocytosis and degradation of apical Na(+) channels is a key feature of hypoxia-induced inhibition of transepithelial alveolar Na(+) transport.
The first physiological evidence for an essential function of Nedd4-2 in regulating voltage-gated sodium channels in the central nervous system.
NEDD4-2 is a potent posttranslational regulator of voltage-gated sodium channels.
loss of NEDD4-2 in adult renal tubules causes a new form of mild, salt-sensitive hypertension without hyperkalemia that is characterized by upregulation of NCC, elevation of beta/gammaENaC, but not alphaENaC, and a normal Na+/K+ balance
This gene encodes a member of the Nedd4 family of HECT domain E3 ubiquitin ligases. HECT domain E3 ubiquitin ligases transfer ubiquitin from E2 ubiquitin-conjugating enzymes to protein substrates, thus targeting specific proteins for lysosomal degradation. The encoded protein mediates the ubiquitination of multiple target substrates and plays a critical role in epithelial sodium transport by regulating the cell surface expression of the epithelial sodium channel, ENaC. Single nucleotide polymorphisms in this gene may be associated with essential hypertension. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
E3 ubiquitin-protein ligase NEDD4-like
, E3 ubiquitin-protein ligase NEDD4-like protein
, ubiquitin-protein ligase Rsp5
, neural precursor cell expressed, developmentally down-regulated 4
, neural precursor cell expressed, developmentally down-regulated gene 4b