NEDD4L Antibodies

E3 ubiquitin-protein ligase NEDD4-like (NEDD4L)

E3 ubiquitin-protein ligase which accepts ubiquitin from an E2 ubiquitin-conjugating enzyme in the form of a thioester and then directly transfers the ubiquitin to targeted substrates. Inhibits TGF-beta signaling by triggering SMAD2 and TGFBR1 ubiquitination and proteasome-dependent degradation.

Promotes ubiquitination and internalization of different plasma membrane channels like ENaC, SCN2A/Nav1.2, SCN3A/Nav1.

Gene Information

Human
Gene Name:	NEDD4L
Uniprot:	Q96PU5
Entrez:	23327

Family

Belongs to:
No superfamily

Alternative Names

E3 ubiquitin-protein ligase NEDD4-like; EC 6.3.2; EC 6.3.2.-; FLJ33870; hNedd4-2; KIAA0439ubiquitin-protein ligase NEDD4-like; NEDD4.2; NEDD4-2; NEDL3; neural precursor cell expressed, developmentally down-regulated 4-like; neural precursor cell expressed, developmentally down-regulated gene 4-like; RSP5ubiquitin-protein ligase Rsp5

Molecular Weight

Mass (kDA):
111.932 kDA

Genomic Context

Human
Location:	18q21.31
Sequence:	18; NC_000018.10 (58044226..58401540)

Tissue Specificity

Ubiquitously expressed, with highest levels in prostate, pancreas and kidney (PubMed:14615060, PubMed:15496141, PubMed:19664597). Expressed in melanocytes (PubMed:23999003).

Subcellular Localizations

Cytoplasm. Golgi apparatus. Endosome, multivesicular body. May be recruited to exosomes by NDFIP1.

Diseases

• Hypertensive Disease
• Essential Hypertension
• Malignant Neoplasms
• Neoplasms
• Prostatic Neoplasms
• Hypotension Adverse Event
• Malignant Neoplasm Of Prostate
• Dysequilibrium Syndrome
• Malignant Paraganglionic Neoplasm
• Liddle Syndrome
• Carcinogenesis
• Cell Invasion
• Hyperplasia

• Neoplasm Metastasis
• Coronary Heart Disease
• Diabetic Nephropathy
• Metastatic Malignant Neoplasm To The Lymph Node
• Developmental Reading Disorder
• Trinucleotide Repeat Expansion
• Glioma

Interacting Proteins

• DAZAP2
• SLC11A2
• SMAD7

Pathways

• Pathogenesis
• Transport
• Cell Growth
• Excretion
• Intracellular Transport
• Ion Transport
• Endocytosis
• Conjugation
• Localization

• Cytokinesis
• Regeneration
• Exocytosis
• Rna Interference

PTMs

• Ubiquitination

• Phosphorylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/NEDD4L

Best Uses Of The NEDD4L Marker

In this article, you will find out how the NEDD4L marker regulates the CTHRC1/HIF-1a axis. It also triggers B-catenin ubiquitination and also inhibits collagen fiber deposition and inflammation cell infiltration. These findings are applicable to all scientists around the world. In addition, Boster scientists can also submit results in connection with applications, species, and samples for product credits.

The NEDD4L regulates the CTHRC1/HIF-1a axi

NEDD4L is a new transcription factor that negatively regulates CTHRC1/HIF-1a Axon in Boster Bio lung fibroblasts. Its role in the progression of the disease was initially studied in mice models and in human lung tissues. The overexpression of the protein in the lung prevented the formation of IPF and reduced the proliferative as well as invasive abilities of LF cells. Furthermore, it inhibited the CTHRC1/HIF-1a pathway and negatively affected the ubiquitination process of b-catenin.

The miRNA or mRNA in microvesicles plays a role in its absorption by the recipient cells. This was proven in Ratajczak and co. and in WO 2009/100029. Microvesicles were isolated from RNA using ultracentrifugation of 110,000xg and then the use of differential centrifugation.

Mice with serum microvesicles with subcutaneous tumors were examined to determine the levels of expression of the cMyc gene. The mice were xenografted using medulloblastoma-derived cell lines from the D425 cell-line or epidermoid cancer cell lines in the A431 cells-line. The DNA size marker, MW, was determined as MW (megabases), while the mass of tumor at the time of sacrifice was 1.7 grams, 2.4 g, and 2.3 g, respectively. As as a negative control, an NC lane was utilized.

Molecular analysis of tumor cells revealed that POU5F1B and c-Myc were both upregulated in these tumors of mice. Quantitative reverse transcription PCR (qRTPCR) was employed to measure the expression of these genes. NEDD4L regulates the CTHRC1/HIF-1a-axis in Boster Bio.

NEDD4L induces b-catenin ubiquitination

Inhibition of NEDD4L the protein that is suppressed by the CTHRC1/HIF-1a angle, helps in reducing IPF by suppressing the Wnt/b-catenin signaling pathway. The NEDD4L inhibitor reduces IPF development in mice by suppressing the CTHRC1/HIF-1aaxis.

NEDD4L, one of the members of NEDD4 family of ubiquitin ligases. It binds to Dvl2 directly via its WW3 domain. Dvl2 is subsequently targeted by proteasomes, resulting in its degrading. The Wnt/b–catenin pathway can be negatively affected by the ubiquitination process. Furthermore, NEDD4L was shown to stop the replication of axis duplicates caused by Dvl2 in Xenopus embryos. Autophagy enhances Dvl degrading through the Von Hippel Lindau protein.

The development of many forms of cancers can be stopped by blocking NEDD4L. More research is needed to determine how this protein functions in gastric cancer development. This research suggests that NEDD4L could be able to regulate EBV infection. However, the mechanisms behind its modulation and its role in the development of nasopharyngeal cancer are not completely understood.

Additionally, NEDD4L boosts the level of neoa, an important transcription factor involved in the regulation of gene expression. The gene is present in the lung tissues of IPF patients and mice models. This suggests that NEDD4L may be a potential therapeutic candidate in IPF. Consequently, NEDD4L increessiin expression could improve lung function in IPF.

The inhibition of neoadhed4L inhibits Ubiquitylation of B-catenin that is asymmetric. CSN dissociation results into stabilization of the cytosolic B-catenin. Furthermore, dissociation from CSN makes APC vulnerable to proteolysis. As a result, B-catenin is stabilized by Wnt signaling.

NEDD4L is an recombinant protein that blocks the degradation of the c-adhesin. Furthermore, NEDD4L promotes the proliferation of B-catenin. The results of this study agree with previous studies that suggest a connection between nedd4l and B-catenin.

Phosphorylation b-catenin inhibits tumor progression. In the case of inflammation, phosphorylation stops the activation of the Wnt/bcatenin signaling pathway. In normal cells, b-catenin levels are tightly regulated through a phosphorylation-independent mechanism.

NEDD4L blocks infiltration of inflammatory cells

Boster Bio NEDD4L is an original monoclonal antibody developed to target NEDD4L. This antibody has been tested on multiple platforms using both positive and negative samples in order to ensure high specificity. The company also gives credits to scientists who review its products for the first time. This rewards early reviewers and all scientists across the globe for their hard work. The Journal of Experimental Medicine published the research described in this article.

NEDD4L inhibits collagen fiber deposition

Recently, a drug that targets the neural precursor cell-expressed developmentalally down-regulated 4-like protein (NEDD4L) has been identified as a potential treetment for IPF. This drug is an oral peptide that blocks LFs biological activity. It inhibits fibroblast proliferation and differentiation, two of the key mechanisms involved in fibrotic illness. This drug has a potential to inhibit the biological functions of fibroblasts, and also inhibit collagen fiber deposition.

NEDD4L expression is detected in the lung of IPF patients as and in mouse models. IPF mice with NEDD4L increessd expression increessithe levels of CTHRC1, thereby increesing NEDD4L levels. NEDD4L expression in IPF mice was associatsd with an increessiin collagen fiber deposition and lung tissue lesions. Incredibly, the overexpression of NEDD4L prevented the lung functions of IPF mice. The results suggest that NEDD4L could be able to slow down the progression of IPF.

NEDD4L is also involved in regulation of the CTHRC1/HIF-1a axis. It inhibits this enzyme and prevents LFs spreading, diffusing, or the invasive properties. It also inhibits the expression of bcatenin and fibronectin, which are necessary for the formation of collagen fibers. These findings suggest that NEDD4L could reduce the deposition of collagen fibers in human skin.

The NEDD4L axis also regulates the CTHRC1/HIF of LFs which is associatsd with pulmonary fibrosis. Additionally, NEDD4L inhibits collagen fiber deposition by repressing the CTHRC1/HIF-1a axis , and also suppressing IPF. Further studies are needed to confirm these findings. This drug has many advantages over other treetments.