WWOX, affinity purified, rabbit, 100 ug
- Known as:
- WWOX, antigenic enriched, host: rabbit, 100 ug
- Catalog number:
- RA19025-100
- Product Quantity:
- 1
- Category:
- -
- Supplier:
- Neuromi
- Gene target:
- WWOX affinity purified rabbit 100
Related genes to: WWOX, affinity purified, rabbit, 100 ug
- Gene:
- WWOX NIH gene
- Name:
- WW domain containing oxidoreductase
- Previous symbol:
- -
- Synonyms:
- FOR, WOX1, SDR41C1
- Chromosome:
- 16q23.1-q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-07-31
- Date modifiied:
- 2018-02-13
Related products to: WWOX, affinity purified, rabbit, 100 ug
Related articles to: WWOX, affinity purified, rabbit, 100 ug
- Long non-coding RNAs (lncRNAs) are increasingly acknowledged as key players in various biological processes. However, the role of these lncRNAs in the response of cnidarians to the reverse development process remains unexplored. We conducted a genome-wide analysis of lncRNAs in immortal jellyfish (Turritopsis dohrnii) to examine their response to reverse development process across a substantial dataset of 82 RNA-seq samples. We identified 8,805 high-confidence lncRNA candidates, which are characterized by a shorter average length of 640 nucleotides and fewer exons (on average 1.41), compared to mRNAs. Remarkably, 79.73% of these lncRNAs were found to be species-specific among the thirteen jellyfish species. Within 836 lncRNAs and 1,395 mRNAs that are highly correlated with the reverse development, the key genes involving DNA repair, cell cycling, differentiation, and apoptosis (e.g., Tspan4, Aifm2, Wwox, eIF3C and those of the p53 signaling pathway and the cAMP signaling pathway) exhibited progressively increasing expression levels throughout the reverse stages. Among 64 lncRNA-mRNA pairs with putative trans- and cis-regulatory effects, the lncRNA (MSTRG.37048.1) exhibited strong correlation with Tspan4, Wwox and PIGA genes during the reverse stages. Our study provides a candidate lncRNA resource and prioritizes lncRNA-associated gene pairs potentially related to life-cycle reversal in T. dohrnii. - Source: PubMed
Publication date: 2026/08/24
Ai ChunhuiHe LishengWang Yong - and are linked to hypoxia-driven metabolic and immune modulation in cancer. We examined whether the expression ratio acts as a context-dependent molecular integrator across breast cancer (BRCA) subtypes and ovarian carcinoma (OV). We analyzsed TCGA RNA-seq and clinical data from BRCA (n = 390) and OV (n = 228), using neoplasm cancer status as a proxy for disease-free survival (DFS). Patients were stratified by subtype-specific ratio cutpoints for exploratory Kaplan--Meier analyses, and the ratio was also modelled as a standardizsed continuous covariate in Cox regression. Transcriptomic, pathway, immune-cell and hormone-related profiles were examined in relation to ratio status, with all multivariable and cutpoint-based findings treated as hypothesis-generating. The ratio does not act as a uniform or strongly predictive prognostic marker but instead delineates distinct biological states whose association with DFS is modest, context-dependent and statistically fragile in TCGA. Higher ratios are linked to more favourable DFS only in basal-like and HER2-enriched BRCA, together with oxidative phosphorylation, ribosomal and reduced -linked Notch and monocyte/macrophage signatures. In luminal A BRCA and OV, lower ratios are linked to relatively favourable DFS and coincide with cytokine/JAK-STAT signalling, cytotoxic immune signatures and coordinated metabolic-endocrine programmes, whereas luminal B shows mixed immune and metabolic patterns. In this TCGA-based analysis, the ratio functions as a context-dependent molecular index of hypoxia, immune and hormone-related states rather than a strong, generalisable DFS predictor. The observed subtype-specific survival trends (high-ratio favourability in basal/HER2, low-ratio favourability in luminal A,B and OV) are non-significant and exploratory, and all ratio-based survival patterns require confirmation in independent cohorts and functional studies. - Source: PubMed
Publication date: 2026/07/28
Hammouz Raneem YMaciejek KingaBednarek Andrzej K - Approximately one-third of all human proteins transit through the secretory pathway, where the Golgi apparatus orchestrates protein modification, sorting, and distribution through highly selective vesicle budding and fusion events. Central to these processes are the Complexes Associated with Tethering Containing Helical Rods (CATCHR), multisubunit tethering complexes that coordinate vesicle docking and fusion through interactions with coiled-coil tethers (CCTs), Rab GTPases, SNAREs, and Sec1/Munc18 (SM) proteins and other trafficking factors. To define the molecular organization of Golgi CATCHR complexes, we generated the first comprehensive proximity-interaction map of the COG, GARP, and EARP tethering complexes using functional, near-endogenously expressed TurboID-tagged subunits. Comparative proximity proteomics revealed that each CATCHR complex assembles a distinct trafficking module composed of characteristic CCTs, Rab-associated proteins, SNAREs, and SM proteins, establishing a system-level framework for the spatial organization of Golgi and endosomal membrane trafficking. The COG complex preferentially associated with Golgi CCTs and the STX5-SCFD1 fusion machinery, GARP with CCDC186, and STX16-VPS45 pathway, and EARP with GRIPAP1, the VPS33B-VIPAS39 (CHEVI) complex, and RAB11-dependent recycling machinery. Beyond validating known interactions, our study identifies CCDC186 as a vesicle tether, establishes WWOX as a previously unrecognized regulator of Golgi homeostasis and glycosylation, and provides evidence that Golgi CATCHR complexes function as central organizing hubs that assemble specialized trafficking modules to coordinate vesicle tethering and membrane fusion. - Source: PubMed
Publication date: 2026/07/28
Aragon-Ramirez Walter SKhakurel AmritaPokrovskaya IrinaSumya Farhana TaherLupashin Vladimir V - Following the publication of the above article, a concerned reader drew the Editor's attention to the fact that, regarding the the western blot data shown in Fig. 4C on p. 853 for the Jurkat cell line, the p73 bands shown to portray the 72 and 96 h experiments for pGC‑FU‑WWOX were strikingly similar to the p73 bands shown to represent the 48 and 72 h experiments for pGC‑FU‑GFP. Upon assessing these data in the Editorial Office, it was concluded that the concerns of the reader were legitimate, suggesting that this figure may have been inappropriately edited. The Editor of has therefore decided that the article should be retracted from the Journal on the grounds of an overall lack of confidence in the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for drawing this matter to our attention. [International Journal of Molecular Medicine 31: 849-854, 2013; DOI: 10.3892/ijmm.2013.1289]. - Source: PubMed
Publication date: 2026/07/17
Lin DonghongCui ZhaoleiKong LingyingCheng FengXu JianpingLan Fenghua - Genome-wide association studies have predominantly implicated common variants in lung cancer susceptibility, whereas the contribution of rare non-coding variation remains incompletely defined. This study comprised 52,550 cases and 1,617,173 controls across three whole-genome sequencing (WGS) cohorts (UK Biobank, the 100,000 Genomes Project, and All of Us) and five imputed genotype-array datasets aimed to identify rare non-coding determinants of lung cancer risk. Two complementary approaches were applied: position-based single-variant testing for variants with adequate allele counts, and gene-based testing aggregating rare and ultra-rare ncRNA variants to increase power. Single-variant meta-analysis identified two novel rare non-coding variants reaching sequencing-based genome-wide significance: rs763076863 at 22q13.2 [OR (95% CI): 5.94 (3.46-10.19), P = 4.55 × 10] and rs1014871851 at 16q23.1 [OR (95% CI): 7.55 (4.50-12.67), P = 3.71 × 10]. Functional annotation-informed gene-based analyses prioritized 37 candidate ncRNAs using eQTL, expression, proteomics, prognosis, cis-Mendelian randomization drug-target evidence, and external replication. CLEC12A-AS1 ranked highest; multi-omics association and chain mediation analyses supported an indirect pathway linking CLEC12A-AS1 burden to lung cancer risk via modulation of CLEC12A. Collectively, results indicate contributions from both individually detectable rare variants and cumulative ultra-rare functional burden within ncRNA regions, highlighting the CLEC12A-AS1/CLEC12A axis as a potential biomarker and translational target. - Source: PubMed
Publication date: 2026/07/13
Zhao JingyiQiao LeiZhang YixinHong HaoFan QinhuiChristiani David CChen FengZhao YangShen Sipeng