Ask about this productRelated genes to: UBOX5 antibody
- Gene:
- UBOX5 NIH gene
- Name:
- U-box domain containing 5
- Previous symbol:
- -
- Synonyms:
- UIP5, KIAA0860, Ubce7ip5, RNF37
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2005-01-10
- Date modifiied:
- 2014-11-19
Related products to: UBOX5 antibody
Related articles to: UBOX5 antibody
- This study investigated the influence of maternal nutrient restriction and dietary melatonin supplementation on DNA methylation and gene expression in bovine placental cotyledons, with a focus on sex-specific changes. On day 160 of gestation, 29 Brangus heifers (bred to a single sire by AI) were subjected to a 2 × 2 factorial design: adequately fed (ADQ-CON, n = 7), nutrient-restricted (RES-CON, n = 7), and adequately fed or nutrient-restricted supplemented with 20 mg/d of melatonin (ADQ-MEL, n = 7; RES-MEL, n = 8). Cotyledons were collected at day 240 from 12 female and 17 male conceptuses for Methyl MiniSeq-GWBS and RNA-Seq. In RES-CON vs. ADQ-CON, 93 hypomethylated and 143 hypermethylated DMRs were identified, primarily in exonic, intronic, and promoter regions. Melatonin altered the methylation patterns of male and female cotyledons, respectively, with 203 and 460 DMRs associated with axon guidance, RHOC GTPase cycle, and BDNF signaling pathways. RES-MEL showed higher expression of the gene compared with RES-CON. Moreover, 15 DEGs (5 upregulated and 10 downregulated) were observed in the male vs. female comparison. In melatonin-treated males, , , , genes were upregulated. Thus, melatonin may modulate conceptus growth and development in a sex-specific manner. - Source: PubMed
Publication date: 2025/11/25
Rajput ShiveeliLittlejohn BrittniContreras-Correa Zully EEl Daous HalaSidelinger DarcieKing HeathArick MarkLemley Caleb - Primary angle-closure glaucoma is a major cause of irreversible blindness worldwide afflicting >20 million people. Through whole exome sequencing, we analysed the association between gene-based burden of rare, protein-altering genetic variants and disease risk in 4,667 affected individuals and 5,473 unaffected controls. We tested genes surpassing exome-wide significance (P < 2.5 × 10) for replication in a further 2,519 cases and 472,189 controls. We observed carriers of rare, protein-altering variants at UBOX5 (observed in 154 out of 7,186 affected individuals [2.1%] and in 3,975 out of 477,197 unaffected controls [0.83%]) to be associated with 2.13-fold increased risk of PACG (95%ci, 1.69 - 2.69; P = 1.25 × 10). We performed substrate trapping assays coupled with mass spectrometry and observed Binding Immunoglobulin Protein (BIP) as a key substrate for UBOX5. Biological assays showed UBOX5 acts by ubiquitinating BIP. We evaluated the functional status of 35 UBOX5 variants and observed that functionally deficient variants were enriched in affected individuals compared to controls. We validated this finding in an independent collection where 3 persons carrying functionally deficient variants were observed out of 208 cases (1.4%), whereas none were observed in 600 controls. Our findings suggest the UBOX5-BIP signalling pathway might be involved in biology of primary angle-closure glaucoma. - Source: PubMed
Publication date: 2025/08/15
Li ZhengChng Wee LingLiu ZhehaoDo TanNakano MasakazuChen Li JiaLoo YunhuaChan Anita S YTopouzis FotisNongpiur Monisha EOzaki MineoNakano SatokoKubota ToshiakiPerera Shamira AHusain RahatWong Tina T LCheng Ching-YuHo Ching LinAbu-Amero KhaledWong Hon-TymMelo Mônica Barbosa deHien Nguyen Do Thi NgocVan Trinh NguyenHuong Nguyen Thi ThanhAzhany YaakubPerez-Grossmann RodolfoChan Poemen PmStuart Kelsey VBiradar Mahantesh ISzabo AnitaAnastasopoulos EleftheriosGiannoulis Dimitrios ANtonti PanagiotaPapakonstantinou EvangeliaLambropoulos AlexandrosChatzikyriakidou AnthoulaKilintzis VassilisAyub HumairaMicheal ShaziaAung Yee YeeLeuenberger Edgar UFea AntonioMon Naing NaingAnajao AmihanBi XuezhiKok Yee JiunChong Rachel SBoey Pui-YiTan Darrell Zi JingSin Wendy Wan LingChowbay BalramKhaing Chaw ChawAung Yin MonReyes Rigo DanielPanagiotou Evangelia SMikropoulos Dimitrios GVoudouragkaki Irini CPanos Georgios DXie ZhichengChen Xiao YinLim Yi TingMeah Wee YangLee Ying ShiHo Candice Ee HuaYeo Pearlyn Mei XinIkeda YokoTokuda YuichiTanaka MasamiOmi NatsueUeno Moriode Vasconcellos José P CCosta Vital PAbe Ricardo Yde Souza Bruno BFong Guillermo BCastro Vania VFujita RicardoGuevara-Fujita Maria LAkhtar FarahAli MahmoodCatacutan Mary Ann TFelarca Irene RLiao Chona SLavia CarloThan Hlaing MayOo Khin ThidaSoe-Kyaw Phyu PFrezzotti PaoloPasutto FrancescaQuino RaquelMinn-Din ZawOo Nay LinDallorto LauraSet Saw HtooDoan Vi HuyenQamar RaheelNeto Jamil MiguelAl-Obeidan SalehTham Clement CMori KazuhikoSotozono ChieKinoshita ShigeruKonstas Anastasios GLiza-Sharmini Ahmad TajudinZenteno Juan CDo Nhu HonFoster Paul JTashiro KeiPang Chi PuiKhawaja Anthony PAung TinWang ZhenxunKhor Chiea Chuen - Long noncoding RNA (lncRNA) and N6-methyladenosine (m6A) methylation modification have recently been suggested as potential functional modulators in ovarian endometriosis, however, the function and mechanism of m6A-modified lncRNA in ovarian endometriosis remain poorly understood. In this study, we demonstrated that lncRNA UBOX5-AS1 expression was significantly elevated in ovarian endometriosis tissue and primary ectopic endometrial stromal cells. The expression of lncRNA UBOX5-AS1, which has m6A modifications, was highly positively correlated with demethylase Alk B homologous protein 5 (ALKBH5) expression and autophagy. Functional studies revealed that increased ALKBH5 and lncRNA UBOX5-AS1 expression promoted cell autophagy, proliferation, and invasion in endometriosis in vitro. LncRNA UBOX5-AS1 mediates ALKBH5-regulated autophagy, proliferation, and invasion. ALKBH5-mediated autophagy facilitates cell proliferation, migration, and invasion. In vivo, the knockdown of ALKBH5 inhibited endometriotic lesion growth. Mechanistically, we observed that ALKBH5 mediated the m6A demethylation of lncRNA UBOX5-AS1 and promoted its expression. Thus, our findings highlight that ALKBH5/lncRNA UBOX5-AS1 might serve as potential targets for ovarian endometriosis therapy in the future. In the present study, we investigated the role and potential molecular mechanism of long noncoding RNA (lncRNA) UBOX5-AS1 in ovarian endometriosis progression. Combined with the aforementioned, we proposed the hypothesis that lncRNA UBOX5-AS1 regulated by Alk B homologous protein 5 (ALKBH5)-mediated N6-methyladenosine (m6A) modification contributes to the progression of ovarian endometriosis progression. - Source: PubMed
Publication date: 2025/01/06
Liu HengweiLiang JiaxinWang XiaoliXiong WenqianZhang LingDai XinWang XiupingWang XiwenXu YingLiu Yi - Endometriosis is a debilitating gynecological condition that manifests many common malignant features, including migration and invasion. Hypoxia is a hallmark of endometriosis, characterized by endometrial cell metastasis via epithelial-mesenchymal transition (EMT). The long noncoding RNA (lncRNA) UBOX antisense RNA 1 (UBOX5-AS1) has been shown to be upregulated in ovarian endometriosis. However, the molecular mechanisms and biological functions of lncRNA UBOX5-AS1 in hypoxia-induced endometriosis EMT remain to be explored. - Source: PubMed
Liu HengweiHe HaitangZhang ZhibingWang LiliZhang LingLiu YiXiong Wenqian - Exercise-induced cardiac remodeling has aroused public concern for some time, as sudden cardiac death is known to occur in athletes; however, little is known about the underlying mechanism of exercise-induced cardiac injury. In the present study, we established an excessive exercise-induced pathologic cardiac hypertrophy model in zebrafish with increased myocardial fibrosis, myofibril disassembly, mitochondrial degradation, upregulated expression of the pathological hypertrophy marker genes in the heart, contractile impairment, and cardiopulmonary function impairment. High-throughput RNA-seq analysis revealed that the differentially expressed genes were enriched in the regulation of autophagy, protein folding, and degradation, myofibril development, angiogenesis, metabolic reprogramming, and insulin and FoxO signaling pathways. FOXO proteins may be the core mediator of the regulatory network needed to promote the pathological response. Further, PPI network analysis showed that , , , , , , , , , , , , , , , , , , , and are the hub genes that correlate with the pathogenesis of pathological cardiac hypertrophy. The underlying regulatory pathways and cardiac pressure-responsive molecules identified in the present study will provide valuable insights for the supervision and clinical treatment of pathological cardiac hypertrophy induced by excessive exercise. - Source: PubMed
Publication date: 2020/11/30
Zhou ZuoqiongZheng LanTang ChangfaChen ZhanglinZhu RunkangPeng XiyangWu XiushanZhu Ping