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抗Rat (Rattus) 抗体:
抗Mouse (Murine) 抗体:
Cow (Bovine) Polyclonal NEDD4L Primary Antibody for WB - ABIN2774731
Raikwar, Thomas: Nedd4-2 isoforms ubiquitinate individual epithelial sodium channel subunits and reduce surface expression and function of the epithelial sodium channel. in American journal of physiology. Renal physiology 2008
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 (显示 FAM126A 抗体), possibly through triggering MAPK/ERK (显示 MAPK1 抗体)-mediated apoptosis, and Nedd4L downregulation may be a potential prognostic biomarker as well as a therapeutic target for HCC (显示 FAM126A 抗体).
evidence implicating E3 ubiquitin ligase (显示 MUL1 抗体) NEDD4L in the pathogeny of periventricular nodular heterotopia
This study demonstrated that it is possible to downregulate Kv1.3 (显示 KCNA3 抗体) channel density through activation of an E3 ubiquitin ligase (显示 MUL1 抗体) and that inhibition of the protease pathway or mutation of the Nedd4-2 catalytic site prevents Kv1.3 (显示 KCNA3 抗体) 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 (显示 XBP1 抗体) and that this is important in the induction of an appropriate autophagic response.
both Nedd4-1 (显示 NEDD4 抗体) and Nedd4-2 are important regulators for hOAT1 (显示 SLC22A6 抗体) ubiquitination, expression, and function
USP36 (显示 USP36 抗体) actions extend beyond TrkA (显示 NTRK1 抗体) because the presence of USP36 (显示 USP36 抗体) interferes with Nedd4-2-dependent Kv7.2 (显示 KCNQ2 抗体)/3 channel regulation.
NEDD4L negatively regulates PIK3CA (显示 PIK3CA 抗体) protein levels via ubiquitination and is required for the maintenance of PI3K (显示 PIK3CA 抗体)-AKT (显示 AKT1 抗体) signaling pathway.
overexpression of miR (显示 MLXIP 抗体)-93 in lung cancer cells promoted TGF-b-induced EMT (显示 ITK 抗体) 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 (显示 MLXIP 抗体)-93 in lung tumorigenesis and metastasis.
the regulation of Nedd4L protein expression may play a role in the development of ovarian cancers.
these findings suggest that regulation of Dvl (显示 DVL2 抗体) 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 (显示 TMPRSS5 抗体)-activated kinase promotes ENaC (显示 SCNN1A 抗体)-Nedd4-2 interaction, inhibiting ENaC (显示 SCNN1A 抗体) by increasing Nedd4-2-dependent ENaC (显示 SCNN1A 抗体) retrieval from the plasma membrane.
results indicate that AMPK (显示 PRKAA2 抗体) inhibits KCNQ1 (显示 KCNQ1 抗体) activity by promoting Nedd4-2-dependent channel ubiquitination and retrieval from the plasma membrane.
This study suggested that Nedd4-regulated PTEN (显示 PTEN 抗体) is a key regulator of terminal arborization in vivo.
ENaC-beta (显示 SCNN1B 抗体) regulation that occurs through IKKbeta (显示 IKBKB 抗体)-dependent Nedd4-2 phosphorylation at a recognized SGK1 (显示 SGK1 抗体) and protein kinase A target site.
Nedd4-2 knockdown ameliorates movement disorders in PD mice.
Tmbim1 (显示 TMBIM1 抗体) promoted the lysosomal degradation of toll-like receptor 4 (显示 TLR4 抗体) by cooperating with the ESCRT endosomal sorting complex to facilitate MVB formation, and the ubiquitination of Tmbim1 (显示 TMBIM1 抗体) by the E3 ubiquitin ligase (显示 MUL1 抗体) Nedd4l was required for this process.
These results identify NKCC1 (显示 SLC12A2 抗体) 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 (显示 SCNN1A 抗体)).
Three epilepsy-associated missense mutations reduce neural precursor cell expressed developmentally down-regulated gene 4 (显示 NEDD4 抗体)-2 (Nedd4-2)-mediated AMPA (显示 GRIA3 抗体) receptor GluA1 (显示 GRIA1 抗体) ubiquitination.
These findings elucidate a critical role of Mdm2 (显示 MDM2 抗体)-p53 (显示 TP53 抗体)-Nedd4-2 signaling underlying the regulation of neural network synchrony and seizure susceptibility.
We identified glutamate (显示 GRIN1 抗体) receptor subunit 1 (GluA1 (显示 GRIA1 抗体)), 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 (显示 RNF123 抗体) NEDD4L is a CREB (显示 CREB1 抗体) target gene in hepatocytes.
Nedd4-2-mediated ubiquitination of beta-ENaC (显示 SCNN1B 抗体) leading to endocytosis and degradation of apical Na(+) channels is a key feature of hypoxia-induced inhibition of transepithelial alveolar Na(+) transport.
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