Human Polyclonal NEDD4 Ab
- Known as:
- Human Polyclonal NEDD4 Antibody
- Catalog number:
- a0552
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal NEDD4
Related genes to: Human Polyclonal NEDD4 Ab
- Gene:
- NEDD4 NIH gene
- Name:
- NEDD4 E3 ubiquitin protein ligase
- Previous symbol:
- -
- Synonyms:
- KIAA0093, MGC176705, NEDD4-1, RPF1
- Chromosome:
- 15q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-21
- Date modifiied:
- 2019-04-04
- Gene:
- NEDD4L NIH gene
- Name:
- NEDD4 like E3 ubiquitin protein ligase
- Previous symbol:
- -
- Synonyms:
- KIAA0439, RSP5, NEDD4-2
- Chromosome:
- 18q21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-14
- Date modifiied:
- 2019-04-04
Related products to: Human Polyclonal NEDD4 Ab
Related articles to: Human Polyclonal NEDD4 Ab
- Central nervous system astrocytes have an intricate, highly branched morphology. Proper development of perisynaptic astrocyte processes is necessary for tripartite synapse formation and function. However, cellular pathways orchestrating this development are largely unknown. Neuroligins (NLs) 1-3 regulate astrocyte morphogenesis via transcellular adhesions with neuronal neurexins. Here, we found an astrocytic NL2-based mechanism governing morphogenesis. Through structure and function studies, we identified a WW-binding motif within the NL2 intracellular domain required for astrocyte morphogenesis. Using cell-specific in vivo proximity labeling (iBioID), we found that each NL displays distinct protein-protein interactions within astrocytes, distinct from the neuronal NL2-binding partners. From these data, we identified a role for WW domain-containing E3 ubiquitin ligase Nedd4l in astrocyte morphogenesis. Biochemical assays revealed Nedd4l ubiquitinates and stabilizes NL2, and this ubiquitination is required for astrocyte morphogenesis. This study shows that NLs have nonoverlapping roles in controlling astrocyte growth and uncovers a molecular mechanism of how NL2 mediates astrocyte morphogenesis. - Source: PubMed
Publication date: 2026/06/01
Sakers KristinaRamirez Juan JElazar NimrodNagendren LeykashreeSoderblom ErikEroglu Cagla - Atherosclerotic plaque instability is linked to dysregulated cellular stress responses and protein homeostasis within the vascular wall. RNA-binding motif protein 47 (RBM47) modulates mRNA stability and protein expression, but its contribution to the regulation of plaque stability and associated cellular injury has not been fully elucidated. - Source: PubMed
Publication date: 2026/05/24
Xiang JiaQin ZhenghongLiu YunrunTan SongwenTong Guoxiang - Liver fibrosis is characterized by excessive extracellular matrix deposition and hepatic stellate cell (HSC) activation, driven by chronic liver injury and inflammation. Macrophages play dual roles in fibrogenesis; the dynamic balance between pro-fibrotic and anti-fibrotic subsets is critical in determining the progression or regression of the disease. NEDD4L, an E3 ubiquitin ligase, is well-known to be involved in cell biological processes by promoting protein degradation, yet its role in macrophages and liver fibrosis remains poorly understood. - Source: PubMed
Publication date: 2026/03/17
He YanghuanGe ShujunLing ShijiaYang SitingYang FeiranLiu XinyiDong SiyueChen YingfenZhang ZilingZhou YueHwang SeonghwanKim Seung-JinWang PengHe YongChen Yuanwen - Seizure is one of the common comorbidities in Alzheimer's disease (AD). Seizures in AD have been shown to occur more often with early-onset disease, particularly when there is a familial presenilin I (PS1) mutation or abnormal expression of amyloid precursor protein (APP). AD patients with seizures have been associated with a faster decline in cognitive functions. However, it remains unclear how seizures exacerbate neurodegeneration in AD. Here, we showed that, using a kainic acid-induced acute seizure model, mitochondrial function is enhanced and the reactive oxygen species (ROS) are reduced in the brain of wild-type (WT) mice but not in an AD mouse model, APP/PS1 mice. These data suggest a lack of protective mechanism following seizures in APP/PS1 mice. Mechanistically, we found that an E3 ubiquitin ligase, the neural precursor cell-expressed developmentally downregulated protein 4-like (Nedd4-2), is elevated but stays dephosphorylated in APP/PS1 mice upon seizure inductions. Immunocytochemistry and sub-cellular fractionation experiments demonstrate an interaction between Nedd4-2 and mitochondria. Unbiased proteomics analysis suggests that Nedd4-2 regulates the expression of multiple mitochondrial proteins including one of the key mitochondrial outer membrane proteins, Mitofusin 2 (MFN2). Upon seizure induction, Nedd4-2 exhibits elevated interaction with mitochondria and downregulates MFN2 in APP/PS1 mice but not in WT mice. These data suggest that seizures aggravate mitochondrial dysfunction in AD, and Nedd4-2, which acts as a negative mitochondrial regulator, contributes to this effect. Altogether, our findings illustrate a potential mechanism by which seizures exacerbate neurodegeneration in AD and suggest Nedd4-2 as a novel therapeutic target for AD patients with comorbid seizures. - Source: PubMed
Wang YingxinZhu JiuheLizarazo SimonLee Kwan YoungWong OliviaAzim SophiaYook YeeunKumar VipendraTsai Nien-Pei - Allergic rhinitis (AR) is a chronic inflammatory disorder characterized by type 2 T helper (Th2) cell-dominant immune responses. NEDD4 like E3 ubiquitin protein ligase (NEDD4L) plays a role in regulating T cell activation and Th cell differentiation. Dipeptidyl peptidase 4 (DPP4) is involved in Th2 inflammatory responses in AR. In this study, NEDD4L was found to be downregulated in peripheral blood CD4-enriched T cells from AR patients. In a BALB/c mouse model of AR, established by intraperitoneal sensitization with 25 μg ovalbumin (OVA) followed by intranasal challenge with 500 μg OVA, NEDD4L expression was also reduced in splenic T cells enriched in CD4 populations. T cell-specific overexpression of NEDD4L, achieved via tail vein injection of lentivirus carrying the CD3δ promoter, significantly alleviated AR symptoms, as shown by reduced sneezing and nose-wiping frequency, and decreased serum levels of OVA-specific immunoglobulin E (IgE) and histamine. Moreover, NEDD4L overexpression attenuated nasal mucosal thickening, inflammatory cell infiltration, and goblet cell hyperplasia. In vitro, lentiviral-mediated NEDD4L overexpression in T cells, enriched in CD4 populations, is associated with suppression of Th2-linked inflammation, as indicated by decreased GATA-binding protein 3 (GATA-3) and JunB proto-oncogene (JunB) protein levels, reduced secretion of Th2 cytokines, and a lower proportion of CD4IL-4 cells. Mechanistically, NEDD4L ubiquitinates DPP4 at the K583 site to promote its degradation, and DPP4 overexpression reversed the anti-inflammatory effects of NEDD4L. Collectively, NEDD4L is consistent with acting as a negative regulator of Th2-linked inflammation, potentially via ubiquitination-mediated degradation of DPP4. - Source: PubMed
Publication date: 2026/04/09
Lv PingLi DandanSong WeiWang Jizhe