Ask about this productRelated 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
- Accurate evaluation of HER2 status is critical for the targeted management of invasive ductal carcinoma (IDC) of the breast; however, resolving equivocal immunohistochemistry (IHC) results remains a significant clinical challenge. This study aims to comparatively evaluate IHC, fluorescence in situ hybridization (FISH), and quantitative polymerase chain reaction (qPCR) for precise HER2 assessment, while mapping the broader genetic landscape of aggressive IDC subtypes using whole-exome sequencing (WES). - Source: PubMed
Publication date: 2026/05/11
Balar ShilpaJoshi EshaRawal RakeshSaiyad HiramHaque MoquitulDesai Urja - Co-directional (CD) transcription-replication conflicts (TRCs) arise when the DNA replication and transcription machineries progress along the same DNA template. Although generally considered less severe than head-on (HO) TRCs, CD TRCs are now recognized as frequent and actively regulated events that influence genome stability. The Cullin 3-Potassium channel tetramerization domain containing 10 (KCTD10) ubiquitin ligase complex functions as a bivalent sensor that detects CD collisions and directs the nonproteolytic ubiquitination of the elongation factor TCEA2, transiently remodeling RNA polymerase II to permit replisome bypass. This sensing-driven remodeling reframes CD TRCs as dynamic decision nodes where replication and transcription priorities are continuously negotiated, highlighting how conflict geometry, ubiquitin signaling, and genome maintenance are functionally integrated. - Source: PubMed
Publication date: 2026/05/13
Chen BinKloeber Jake AHuang JinzhouLou Zhenkun - Ischemia/reperfusion (IR) enhances oxidative stress, leading to myocardial injury. Although Perm1 promotes cytoprotective mechanisms, the underlying mechanisms are poorly understood. Cysteine oxidation of Keap1 alleviates Cul3-mediated ubiquitination/degradation of Nrf2 and promotes antioxidant transcription. Here we show that Perm1 activates Nrf2 through cysteine oxidation of Keap1 and stabilization of Nrf2. Endogenous Perm1 was downregulated during IR, whereas the rescue of Perm1 reduced IR injury. Downregulation of Perm1 exacerbated oxidative stress, whereas upregulation of Perm1 alleviated it, accompanied by downregulation and upregulation of Nrf2-regulated antioxidant genes, respectively. Perm1 promoted oxidation of cysteine residues in Keap1, possibly through thiol-disulfide exchange reactions, which decreases Keap1-Nrf2 interaction and inhibits Cul3-mediated degradation of Nrf2. We identified Cys121 and Cys746 in Perm1 as critical for Keap1 oxidation and cardioprotection. Thus, Perm1 induces cysteine oxidation of Keap1, thereby conferring myocardial resistance to IR injury by inducing Nrf2 stabilization and transcriptional activation of antioxidant genes. - Source: PubMed
Publication date: 2026/05/12
Oka Shin-IchiHuang Chun-YangMatsushita MasatoTitus Allen SamNakada YasukiMukai RisaVeera SamtaMourad YoussefYehia GhassanRomanienko PeterTian YiminZhai PeiyongSadoshima Junichi - Nuclear factor erythroid 2-related factor 2 (NRF2), a redox-sensitive transcription factor, is a master regulator of cellular adaptation to diverse types of stressors. Under basal conditions, the regulation of NRF2 is governed by Kelch-like ECH-associated protein 1 (KEAP1), an adaptor subunit of the CUL3-based E3 ubiquitin ligase, which promotes the ubiquitination and subsequent degradation of NRF2. However, when electrophilic or oxidative stressors alter the conformation of the KEAP1-NRF2 complex, KEAP1 loses its regulatory control over newly synthesized NRF2, leading to its accumulation and nuclear translocation, where it exerts transcriptional activity. NRF2 stability and activity are also shaped by a broader spectrum of protein-protein interactions (PPIs), including recently emerging regulators such as peptidyl prolyl isomerase (PIN1). Significantly, many of these dynamic PPI networks are regulated by post-translational modifications (PTMs), which, in turn, can be governed by these PPIs. While major PTMs such as phosphorylation and ubiquitination constitute the central regulatory processes, atypical or less-characterized modifications, including SUMOylation and O-GlcNAcylation, are gaining increasing attention for their tissue and condition-specific roles. This review compiles the latest structural and functional evidence on well-known as well as understudied PTMs and PPIs of NRF2, emphasizing the dynamic interplay between these regulatory mechanisms in shaping NRF2 signaling under physiological and stress conditions. - Source: PubMed
Publication date: 2026/05/05
Ozleyen AdemKulabas Seda SavranogluNovak MiroslavCichoń MilenaHeras Cristina Matas De LasHonda TadashiDoveston Richard GDinkova-Kostova Albena TGrochot-Przeczek AnnaTumer Tugba Boyunegmez - KLHL15 encodes Kelch-like protein 15, an adapter for the Cullin3 (CUL3) E3 ubiquitin ligase complex. CUL3 variants are linked to developmental disorders and epilepsy. However, the association between KLHL15 variants and epilepsy is unclear. This study aimed to explore the association of KLHL15 with epilepsy. - Source: PubMed
Publication date: 2026/05/01
Zhang Si-QiLao Zhi-HongLiu Wen-HuiWang Peng-YuZhu Zhong-YanQu Yi-BoWen Qian-RuDing YanMeng Heng