NEDD8 Antibody
- Known as:
- NEDD8 Antibody
- Catalog number:
- 32194
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- NEDD8 Antibody
Related genes to: NEDD8 Antibody
- Gene:
- NEDD8 NIH gene
- Name:
- NEDD8 ubiquitin like modifier
- Previous symbol:
- -
- Synonyms:
- Nedd-8
- Chromosome:
- 14q12
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-21
- Date modifiied:
- 2019-04-04
Related products to: NEDD8 Antibody
Related articles to: NEDD8 Antibody
- Polycystic ovary syndrome (PCOS) is a common and complex endocrine and metabolic disorder whose etiology has not yet been fully elucidated. Emerging research has revealed an association between PCOS pathogenesis and post-translational modifications of proteins. However, the effect of neddylation on PCOS pathogenesis has not been investigated. In this study, key proteins of the neddylation pathway (Nedd8, neddylation-activating enzyme (NAE), and Cullin-1/2/3) were significantly upregulated in the granulosa cells of patients with PCOS; this was accompanied by enhanced apoptosis (increased Bax and Caspase-3, decreased Bcl-2) and elevated expression of the androgen synthesis-related proteins, namely: androgen receptor (AR) and Cytochrome P450 Family 17 Subfamily A Member 1(CYP17A1). In the in vitro DHT-induced PCOS KGN cell model, key neddylation pathway proteins (Nedd8, NAE, and Cullin-1) were upregulated. Overexpression of Nedd8 and inhibition of neddylation by MLN4924 promoted apoptosis. However, inhibition of neddylation by MLN4924 reversed AR/CYP17A1 protein expression. In a rat model of PCOS, MLN4924 treatment significantly suppressed the expression of Nedd8, NAE, and Cullin-1/2/3 in the ovarian tissue, restored estrous cycles, alleviated ovarian morphological abnormalities (characterized by increased corpora lutea and reduced cystic follicles), and decreased serum testosterone and LH levels. MLN4924 significantly promoted ovarian granulosa cell apoptosis, but reduced the expression of androgen synthesis-related proteins. Together, these findings indicate the unrecognized role of neddylation in PCOS, while highlighting that MLN4924 represents a potential therapeutic approach for PCOS treatment. - Source: PubMed
Publication date: 2026/09/30
Qin XiaoweiLuo TingSong HaixiaLiu YunyunZhang XuminQin QinLiu Jianrong - Accumulating evidence suggests that neddylation contributes to tumor initiation and progression. Nonetheless, its biological functions and regulatory mechanisms in lung adenocarcinoma (LUAD) remain poorly understood. - Source: PubMed
Peng XiaogangXiang GuangmingSun Gengyun - Kidney renal clear cell carcinoma (KIRC) is characterized by malignant progression, inflammatory signaling, and therapeutic resistance. This study investigated whether MLN4924, a selective NEDD8-activating enzyme inhibitor, suppresses KIRC progression through coordinated regulation of Cullin1 neddylation, PSMB10 expression, and NF-κB signaling. - Source: PubMed
Publication date: 2026/09/27
Liu DequanSu JingChen FengLiu LeiQi XiaochenWang QifeiWu GuangzhenSun HuijunZhu ZhanmengChe Xiangyu - Type I interferon (IFN-I) signaling is crucial for antiviral innate immunity. F-box protein-mediated ubiquitination regulates this pathway. FBXO11 positively regulates IFN-I signaling via TRAF3 K63-linked ubiquitination, but whether other F-box proteins act synergistically during HBV infection remains unknown. This study investigates FBXO32 expression and function in HBV infection, and whether FBXO11 and FBXO32 synergistically activate innate immunity through a NEDD8-dependent mechanism. - Source: PubMed
Publication date: 2026/09/03
Li LiqiangTao ShunZhang YunfeiZeng ZihanLi LiangZhang Jun - Ovarian cancer (OV) is a highly lethal gynecological tumor, often developing platinum chemotherapy resistance and treatment failure. With their diverse and complex structures, natural products offer potential solutions to drug resistance. This study systematically examines chaetocin's effects on cisplatin-resistant OV cells and its underlying molecular mechanisms. We utilized a cell counting Kit-8, transwell assays, flow cytometry, immunohistochemistry, and western blotting to evaluate chaetocin's effects on cisplatin-resistant OV cells. Proteomic analysis and bioinformatics were utilized to identify the molecular targets of chaetocin, which were validated via cell transfection and co-immunoprecipitation. Additionally, a cisplatin-resistant OV xenograft model was developed for in vivo studies. Chaetocin suppressed the malignancy of cisplatin-resistant OV cells in a dose-dependent manner to suppress cell proliferation, impede cell migration and invasion, and induce both cell apoptosis and cell cycle arrest. Furthermore, in vivo studies showed that chaetocin inhibited tumor growth in a cisplatin-resistant OV xenograft model. In terms of mechanism, chaetocin induced ferroptosis in these cells, inhibiting TFRC ubiquitination and upregulating its expression by reducing the levels of cullin1 and its neddylation binding (cullin1-NEDD8). Our study uncovers a previously unrecognized mechanism: Chaetocin induces ferroptosis by inhibiting TFRC neddylation to upregulate its expression in OV. Unlike its known role as an SUV39H1 inhibitor, chaetocin functions through the neddylation-TFRC-ferroptosis axis, a pathway not previously linked to this compound. Moreover, while neddylation has recently been reported to regulate ferroptosis via SLC7A11, our study reveals an entirely distinct mechanism involving TFRC-mediated iron transport. This epigenetic regulation stabilizes TFRC, sensitizing resistant cells to ferroptosis, providing a dual-mechanistic insight not found in existing literature. By linking chaetocin's gene regulation to iron-dependent cell death, we offer new insights and potential therapies for cisplatin-resistant OV. - Source: PubMed
Publication date: 2026/09/14
Xie HanfeiDai WuminSun LuGong WangangZhu TaoZhang Yingli