Ask about this productRelated genes to: RBX1 antibody
- Gene:
- RBX1 NIH gene
- Name:
- ring-box 1
- Previous symbol:
- -
- Synonyms:
- ROC1, RNF75, BA554C12.1
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-29
- Date modifiied:
- 2017-12-06
Related products to: RBX1 antibody
Related articles to: RBX1 antibody
- Tubo-ovarian, high-grade serous carcinoma (HGSC) is the most lethal gynecological malignancy, with limited targeted therapies and poor outcomes. Heterozygous loss of occurs in approximately 81% of HGSCs and drives chromosome instability and cellular transformation. Here, we identify as a novel synthetic lethal (SL) interactor of in clinically relevant fallopian tube secretory epithelial cell models. Genetic silencing or pharmacologic inhibition of CDK2 with siRNA duplexes or SNS-032, respectively, selectively reduced viability and induced cytotoxicity in cells, with significantly lower EC values compared to controls. Importantly, in two malignant HGSC cell lines (COV362 and OVCAR-3), we further observed that silencing or SNS-032 treatment in combination with silencing induced significant reductions in cell numbers, thereby extending the SL interaction to established HGSC models. Mechanistically, SNS-032 treatment led to increased DNA double-strand breaks and apoptosis, as evidenced by increased numbers of γ-H2AX foci and cleaved Caspase-3 signal intensities. To our knowledge, this is the first demonstration of a SL interaction that exploits a heterozygous disease state in HGSC. These findings highlight CDK2 inhibition as a promising precision medicine strategy for -deficient tumors, broaden the applicability of SL approaches beyond homozygous gene loss, and provide strong preclinical rationale for further therapeutic development. - Source: PubMed
Publication date: 2026/04/28
Farrell Ally CLam Lukas AChen HelenNeudorf Nicole MSajesh Babu VLepage Chloe CLichtensztejn ZeldaMcManus Kirk J - Intervertebral disc degeneration (IDD) is a major cause of low back pain, yet the biological effects of commonly used non-steroidal anti-inflammatory drugs (NSAIDs) on disc cells remain poorly understood. Celecoxib is widely prescribed for IDD-related pain, but its direct influence on IDD has not been systematically examined. Here, we identify a concentration-dependent biphasic effect of celecoxib on nucleus pulposus (NP) cells and uncover the mechanism that converts celecoxib from protective to detrimental. Using interleukin-1β-stimulated NP cells and rat IDD models, we show that low-dose celecoxib (≤20 µm) suppresses inflammation and preserves extracellular matrix (ECM). In contrast, high-dose celecoxib (>20 µm) activates a previously unrecognized heat shock protein 90 (HSP90)/RING-box protein 1 (RBX1)/cuproptosis axis, leading to copper accumulation, mitochondrial stress, and ECM degradation. Mechanistically, elevated celecoxib induces HSP90 upregulation, which stabilizes RBX1 by reducing its K48-linked ubiquitination. Accumulated RBX1 promotes ATPase copper transporting beta (ATP7B) and its regulator copper metabolism domain containing 1 (COMMD1) degradation, thereby triggering cuproptosis. Pharmacologic inhibition of HSP90 or cuproptosis effectively reverses the detrimental effects of high-dose celecoxib in vivo. Together, these findings define a strict therapeutic window for celecoxib in IDD and reveal a novel HSP90/RBX1-mediated cuproptosis pathway that mediates its dual effects. - Source: PubMed
Publication date: 2026/05/04
Guo YoufengXiao HongjuBa ShenghaoZhou YuWang BijunYu BinHuang YufengZhao HaihongChen Zhefan StephenShen NaBa ZhaoyuWu Desheng - RING box Protein 1 (Rbx1) is a RING-domain protein that serves as the catalytic core of the SKP1-Cullin1-F-box (SCF) ubiquitin ligase complex. It is implicated in the ubiquitination process during plant self-incompatibility, growth, and abiotic stress responses. Two Arabidopsis Rbx1 homologous genes, designated ClRbx1-1 and ClRbx1-2, were identified in the genome of 'Xiangshui' lemon. Both ClRbx1 genes are highly expressed in pollen, furthermore, their expression was generally upregulated under self-pollination compared to cross-pollination conditions. Additionally, under simulated salt stress, the expression of ClRbx1 in leaves increased overall. The result of yeast two-hybrid showed that ClRbx1-1 could interact with several proteins associated with self-incompatibility and stress-responses, including Cullin1-2, S-RNase, S-RNase, Ubc12, AP1M2, and Peroxidase25. Yeast three-hybrid assays further demonstrated that ClRbx1-1 interacts with both Cullin1-2 and SKP1-6/SKP1-14 to assemble a canonical SCF complex. Notably, Ubc12 is highly expressed in pollen and its expression level is higher under self-pollination than under cross-pollination. This suggests that ClRbx1-1, cooperating with Ubc12, might function to regulate the self-incompatibility response via the RUB (related to ubiquitin) modification pathway. Overexpression of ClRbx1 in Arabidopsis resulted in dwarfism, and significantly improved salt stress tolerance. Overexpression of ClRbx1 in 'Xiangshui' lemon, achieved via Agrobacterium rhizogenes mediated hairy root transformation, led to a significant increase in salt stress tolerance. In summary, this study collectively elucidates the critical functions of ClRbx1 in self-incompatibility and salt stress response in 'Xiangshui' lemon, laying a solid foundation for further dissection of the molecular mechanisms by which the SCF complex mediates self-incompatibility and abiotic stress in plants. - Source: PubMed
Publication date: 2026/04/30
Nai YiLi YuzeZhang YuexingLuo CongYang TianLan MoyingWei JumeiLi MingqingWu WentingPeng LonghuiHuang GuixiangHe XinHua - This study aims to explore the anti-inflammatory mechanism of Anwulignan (AN) by integrating proteomics, molecular docking, and in vitro cell models. - Source: PubMed
Publication date: 2026/04/26
Tang BinglanQin LangQin BenLi RilunOu ChunliMo Dandan - - Source: PubMed
Publication date: 2026/04/28
Xu DebinYu JichunYang YutingDu YunyanLu HongchengZhang ShouhuaFeng QianYu YiHao LiangShao JunChen Leifeng