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Validated All-in-One™ qPCR Primer for NEDD4L(NM_015277.5) Search again
Product ID:
HQP005996
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
NEDD4-2, NEDD4.2, PVNH7, RSP5, hNEDD4-2
Gene Description:
NEDD4 like E3 ubiquitin protein ligase
Target Gene Accession:
NM_015277.5(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- Candidate gene for autosomal dominant orthostatic hypotensive disorder.
- This ubiquitin-protein ligase is expressed in mouse mandibular salivary duct cells and regulates the amiloride-sensitive Na+ conductance in these cells.
- The ubiquitin ligase NEDD4L is a candidate gene for essential hypertension on both functional and genetic grounds
- Alternate transcripts of Nedd4-2 may interact with ENaC differently. hNedd4-2 has role in regulation of ENaC. Protein domains are important for Nedd4-2 function.
- Identification of multiple splice forms and 5' variants of Nedd4l. 5' variants inhibit ENaC-mediated Na+ transport when reconstituted in FRT epithelia. Other splice forms encode Nedd4L isoforms with 2 to 4 WW domains having varying affinity for ENaC.
- Results describe the isolation of three new NEDD4L transcripts designated NEDD4Lf, NEDD4Lg and NEDD4Lh, which encode different forms of the NEDD4L protein.
- SGK1 stimulates the NaPi IIb, at least in part, by phosphorylating and thereby inhibiting Nedd4-2 binding to its target.
- The differential phosphorylation status between wild-type and mutant Nedd4-2 provides an explanation for the different potential to inhibit ENaC activity.
- cAMP regulates ENaC in part by phosphorylation and inhibition of Nedd4-2. Moreover, Nedd4-2 is a central convergence point for kinase regulation of Na(+) transport.
- Nedd4-2 phosphorylation induces SGK ubiquitination and degradation
- Significant association between several SNPs and hypertension in US whites, Greek whites, and African-Americans. Genetic variation in NEDD4L may play role in development or progression of some forms of hypertension.
- 14-3-3 inhibits the interaction between the WW domains of hNedd4-2 and the PY motif of the epithelial Na(+) channel, ENaC
- genetic NEDD4L variation affecting cross-sectional and longitudinal blood pressure is possibly as a consequence of altered NEDD4L interaction with ENaC
- Study identified three NEDD4-2 missense changes in highly conserved residues (S233L, E271A and H515P) in families with photosensitive generalized epilepsy.
- Nedd4-2 binds to and ubiquitinates ENaC at the cell surface, which targets surface ENaC for degradation, and thus, reduces epithelial Na(+) transport.
- G-protein-coupled receptor kinase 2 interacts not only with epithelial Na(+) channels, but also with both Nedd4 and Nedd4-2
- The human Nedd4L gene, especially the evolutionarily new isoform I, is a candidate gene for hypertension.
- Our results support rs3865418 but not rs4149601 polymorphism of NEDD4L gene implicated in the prevalence of hypertension in Chinese Hans.
- These observations suggest that NEDD4L and possibly other NEDD4-like proteins can ubiquitylate and activate ESCRT-I to function in virus budding.
- budding of various HIV-1 L-domain mutants is dramatically enhanced by ectopic Nedd4-2s, a native isoform with a truncated C2 domain.
- Nedd4-2 reduces the half-life of epithelial sodium channel subunits and enhances the ubiquitination of alpha, beta, and gamma epithelial sodium channels
- WW domains of Nedd4-2 bind (weakly) to a PY motif (LPXY) located within its own HECT domain and inhibit auto-ubiquitination. HECT PY-motif mutation does not affect ubiquitination or down-regulation of a known Nedd4-2 substrate, ENaC.
- Nedd4-2 differentially interacts with and regulates TTYH1-3
- Physiological interaction between the ADD1 and WNK1-NEDD4L pathways influences the effects of variants in these genes on sodium-related BP regulation.