Ask about this productRelated genes to: CUL2 Blocking Peptide
- Gene:
- CUL2 NIH gene
- Name:
- cullin 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 10p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-29
- Date modifiied:
- 2016-10-05
Related products to: CUL2 Blocking Peptide
Related articles to: CUL2 Blocking Peptide
- Six new copper(ii) complexes with general molecular formula [CuL1(Phen)] (1), [CuL2(Phen)] (2), [CuL3(Phen)] (3), [CuL1(DM-Phen)] (4), [CuL2(DM-Phen)] (5) and [CuL3(DM-Phen)] (6) (L = ()-1-(((4-chloro-2-hydroxyphenyl)imino)methyl)naphthalen-2-ol (L1), ()-1-(((2-hydroxy-5-methylphenyl)imino)methyl)naphthalen-2-ol (L2), ()-1-(((2-hydroxy-4-nitrophenyl)imino)methyl)naphthalen-2-ol (L3), Phen = 1,10-phenanthroline and DM-Phen = 2,9-dimethyl-1,10-phenanthroline) have been synthesized and characterized by spectroscopic as well as crystallographic techniques. Molecular structures of 2, 4, 5 and 6 revealed that they are mononuclear species where the copper(ii) center is five-coordinated to a pair of oxygen atoms as well as one nitrogen atom from the ligands (L1-L3) and to a pair of nitrogen atoms from the auxiliary ligand (Phen or DM-Phen) conforming to a distorted square pyramid. The binding affinities of ligands L1-L3 and copper(ii) complexes 1-6 with calf thymus DNA (ctDNA) and bovine serum albumin (BSA) were evaluated using UV-visible absorption spectroscopy. For ctDNA, all compounds showed hypochromism and bathochromic shifts suggesting intercalative binding, with values ranging from 1.49 × 10 to 2.74 × 10 M. The complexes exhibited 3-18-fold higher affinity than ligands, especially those with 2,9-dimethyl-1,10-phenanthroline coligands. BSA titrations of complexes 1-6 revealed hyperchromic shifts at ∼280 nm, with values of 9.59 × 10 to 2.41 × 10 M. These moderate-to-strong bindings were enhanced by lipophilic substituents that promote hydrophobic and π-stacking interactions in protein pockets. All of the compounds inhibit α-amylase better than acarbose with complex 5 (IC = 0.274 mM) showing the highest activity. For the α-glucosidase assay, only complexes 2 (IC = 0.055 mM) and 4 (IC = 0.054 mM) outshined acarbose (IC = 0.059 mM) while other compounds showed moderate to good α-glucosidase inhibition activity. Antioxidant activities of the free ligands showed better activity than that of the metal complexes with none of the compounds performing better than quercetin in all of the assays explored for this study. - Source: PubMed
Publication date: 2026/04/10
Oladipo Segun DAdeleke Adesola AOlofisan Kolawole AOmondi BernardLuckay Robert C - Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths globally. Although the hypoxia-inducible factor 1A (HIF1A) pathway is crucial in HCC progression, its regulatory mechanisms remain unclear as mutations in its primary regulator, von Hippel-Lindau tumor suppressor (), are rare in HCC. We aimed to elucidate the role of proliferation and apoptosis adaptor protein 15 (PEA15), identified through proteomic analysis, as a regulator of the VHL/HIF1A pathway and a therapeutic target in HCC. Proteomic and genomic analyses of over 1,000 HCC samples were conducted, identifying amplification. Functional validation involved in vitro and in vivo assays, including gene knockdown, ectopic expression, and antisense oligonucleotide (ASO) therapy in xenograft models. Protein interactions were assessed using immunoprecipitation and ubiquitination assays. We identified 3 clinically distinct HCC subtypes and found that was selectively amplified and highly expressed in the mesenchymal (MES) subtype, which exhibited the poorest prognosis. acted as a regulator of the VHL/HIF1A pathway and a key oncogene in HCC. The amplification of was significantly associated with the poor survival of HCC patients. Moreover, by interacting with the β-domain of VHL, PEA15 promoted HCC cell proliferation and migration by inhibiting VHL's interaction with the VHL/elongin C (ELOC)/elongin B (ELOB)/cullin 2 (CUL2) E3 ligase complex, destabilizing the complex and consequently activating HIF1A. Importantly, pharmacologically inhibiting PEA15 using ASO drugs attenuated tumor burden and restored VHL function in a xenograft mouse model. This study identified as a potential oncogene in HCC, regulating the VHL/HIF1A axis and driving tumor progression. Targeting using ASOs offers a promising therapeutic strategy for HCC, particularly in the MES subtype. These findings provide a basis for further exploration of -targeted therapies to improve HCC outcomes. - Source: PubMed
Publication date: 2026/04/08
Jeong Yun SeongShin Ji-HyunKim Soo MiSohn Bo HwaYim Sun YoungKim Ji HoonShim Jae JunLee Sung HwanChun Yun ShinLee Sunyoung SDai HuiKaseb AhmedKang Koo JeongEltzschig Holger KMacLeod A RobertLuo XiaolinRevenko AlexeyKim YoungsooLee Ju-Seog - Staphylococcus aureus infection can cause severe lung injury and inflammation, with mechanisms including excessive activation of the NF-κB pathway and disruption of the epithelial barrier. The role of host regulatory factors in this process remains unclear. - Source: PubMed
Publication date: 2026/04/01
Zhou XiangyuZhao ZhuyunWang Ke - The ubiquitin-proteasome system (UPS) represents an evolutionarily conserved machinery governing proteostasis through spatiotemporal regulation of protein degradation. While spermatogenesis involves multilayered regulatory mechanisms spanning translation to dynamic post-translational modifications (PTMs), the identity of UPS-associated E3 ligases orchestrating germ cell-specific protein turnover remains elusive. Here, we identify a testis-specific E3 ubiquitin ligase complex comprising elongin B/C, Cullin-2 (CUL2), RING-box protein-1 (RBX1), and SOCS box protein ASB9, designated ECS. Genetic ablation of ECS in mice via ubiquitous Asb9 knockout (KO) or spermatid-specific elongin B/C conditional KO disrupts spermiogenesis and compromises fertility. Mechanistic studies reveal that ECS engages tubulin beta 4 A (TUBB4A) through substrate recognition, catalyzing K48-linked polyubiquitination at lysine 379 (K379) to promote proteasomal degradation. Notably, Tubb4a knock-in (KI) mice phenocopy the spermiogenesis defects observed upon ECS deficiency. Clinically, we identify three hemizygous missense variants in X-linked ASB9 among Chinese males with idiopathic infertility. Male mice bearing orthologous ASB9 variant exhibit oligoasthenoteratozoospermia (OAT) and subfertility, mirroring human phenotypes. Taken together, our findings establish ECS as an important regulator of spermatogenic proteostasis and provide mechanistic insights into UPS-mediated tissue-specific degradation, while implicating ASB9 variants in male infertility pathogenesis. - Source: PubMed
Publication date: 2026/02/24
Wu TiantianTu ChaofengFeng YuxuanQu WenyingChen JinyiWu HuanGao WenxinXu BingyaYu XianglingBao MingyuanXu JinfuZhou NianchaoHu HaoyueJiang BingXie QingsongMeng LanlanTan ChenLin GeShen CongChen XiaGuo YueshuaiZhou TaoLiang YutingHua RongCao YunxiaLiu MingxiYu JunHuang XiaoyanTan Yue-QiuZheng Bo - Pancreatic cancer (PC) is characterized by high chemoresistance and poor prognosis. CUL2, a scaffold protein of E3 ubiquitin ligases, has been implicated in tumor progression, but its role in PC remains unclear. - Source: PubMed
Publication date: 2025/12/16
Yu KuiChen LiLiZhong YongWang YangZhu NaWang DaohengYao WenyanBai HaoranYang LijuanQi Dachuan