CUL3 Antibody
- Known as:
- CUL3 Antibody
- Catalog number:
- 32149
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CUL3 Antibody
Related genes to: CUL3 Antibody
- Gene:
- CUL3 NIH gene
- Name:
- cullin 3
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2q36.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-29
- Date modifiied:
- 2014-11-19
Related products to: CUL3 Antibody
Related articles to: CUL3 Antibody
- The tumor microenvironment (TME) domesticates macrophage function by decreasing chromatin accessibility. The activation and nuclear translocation of ATP-citrate lyase (ACLY) convert citrate to acetyl-CoA, providing a substrate necessary for histone acetylation. However, the underlying mechanisms in macrophage remodeling are poorly understood. Here, we found that saturated fatty acids (sFA), especially palmitic acid (PA), were lower in TAMs of patients with hepatocellular carcinoma (HCC). Scd1 knockout promoted PA accumulation, resulting in both primary and metastatic liver cancer retardation and overall survival improvement. Mechanisms indicated that ACLY-C893 palmitoylation via PA maintained tetramer stability against CUL3-mediated degradation, facilitating histone acetylation of M1-related genes. Notably, both dietary PA with Scd1 macrophage infusion and TAM-targeted in vivo PA/shSCD1 reprogramming improved the TME to repress HCC progression. Collectively, our research highlights the crucial role of ACLY palmitoylation in the connection between macrophage FA metabolism and histone acetylation reprogramming, which sheds light on the strategy of macrophage-based HCC immunotherapy. - Source: PubMed
Publication date: 2026/09/03
Zhao JunlongXie DongkunSi JingwenFan FanGao ChunchenYang ZhiweiYu HengchaoZhang HuanHu YiyangWang LiangCao XiuliLiang ShiqianCheng ShilinFeng LanGuan FengZhao XiaodiShang LeiNie YongzhanLiu LeiQin Hongyan - Chronic kidney disease (CKD) is characterized by proximal tubule (PT) stress, oxidative injury, and metabolic dysfunction. Human kidney single-nucleus RNA-sequencing (snRNA-seq) identified enrichment of ubiquitin-dependent protein catabolic processes in injured PT cells, suggesting activation of the ubiquitin-proteasome system during tubular stress. Because Cullin 3 (CUL3), scaffold of ubiquitin ligases, regulates oxidative stress signaling through the KEAP1-NRF2 axis, we investigated its role in PT injury and stress adaptation. - Source: PubMed
Publication date: 2026/09/02
Saritas TurgayChen LuIjaz SadafZiegler SusanneDugourd AurélienShao XiaohangUlrich JonathanKoenig ClaireFranciosa GiuliaPiga IlariaOlsen Jesper VSchneider-Kramann RebekkaMcCormick James AHayat SikanderKramann Rafael - Potassium channel tetramerization domain-containing protein 17 (KCTD17) is part of the BTB/POZ domain-containing KCTD protein family and serves as a multifunctional regulator of cellular homeostasis. As an adaptor protein associated with Cullin 3 (CUL3)-based E3 ubiquitin ligase complexes, KCTD17 plays a critical role in selective protein ubiquitination and proteasomal degradation, influencing the stability of various cellular proteins. This function links KCTD17 to numerous biological processes, including organelle dynamics, cell differentiation, intracellular signaling, metabolic regulation, stress responses, tissue remodeling, and disease progression. Notably, the effects of KCTD17 are highly context-dependent, varying with cell type, substrate availability, and pathological conditions. While recent studies have begun to uncover several pathways associated with KCTD17, its complete range of substrates, regulatory mechanisms, and physiological significance are still not fully understood. In this review, we summarize the current understanding of KCTD17's molecular functions and biological mechanisms, emphasizing its role as a proteostatic regulator. We also explore its potential relevance to human diseases and highlight key unresolved questions, such as substrate specificity, tissue-dependent functions, functional redundancy with related KCTD proteins, and therapeutic potential. Gaining a deeper understanding of KCTD17-dependent protein regulation may offer new insights into proteostasismediated cellular regulation and disease mechanisms. - Source: PubMed
Publication date: 2026/09/02
Jeong YelinGi HyunJoonJung Young HoonOh Ah-ReumKim Do-WanKim Young UnChoi Young DuKim KyeongJin - The simultaneous modulation of oxidative stress and autophagy represents a potential therapeutic strategy for amyotrophic lateral sclerosis (ALS), yet agents capable of coordinately regulating both processes remain scarce. The Keap1‑Nrf2‑ARE pathway serves as a critical hub linking redox homeostasis and autophagic regulation, making it an attractive target for ALS intervention. JWA is a stress‑responsive protein involved in cellular protection against oxidative injury, and its neuroprotective effects have been shown to depend on activation of the MEK/ERK‑Nrf2 axis. JP1 is a functional oligopeptide derived from the JWA protein that has been engineered to cross the blood-brain barrier and specifically target integrin αVβ3. Based on the link between JWA and Nrf2 signaling, we hypothesized that JP1 activates the Keap1‑Nrf2‑ARE pathway to coordinate antioxidant defense and autophagic clearance. Here, we evaluated this hypothesis in the SOD1‑G93A mouse model, a well‑established transgenic model of familial ALS, and elucidated the underlying mechanisms. - Source: PubMed
Publication date: 2026/08/25
Zhang YuLiu YaxiShi ShiyuLi QingyangHuo YaniYou PanShu MingzhuCheng XiZhang JunLiang DongZhang AihuaLu ChaoShen BinZhou JianweiNiu Qi - Dihydroorotate dehydrogenase (DHODH) is a critical enzyme involved in pyrimidine biosynthesis anda key suppressor of ferroptosis. This enzyme is commonly overexpressed in colorectal cancer (CRC), and itsupregulation facilitates the malignant progression of CRC tumors. - Source: PubMed
Publication date: 2026/08/20
Wang WeibingHu Xigang