Mouse polyclonal to WDR36, Host Mouse
- Known as:
- Mouse pab WDR36, Host Mouse
- Catalog number:
- YF-PA26881
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal WDR36 Host
Related genes to: Mouse polyclonal to WDR36, Host Mouse
- Gene:
- WDR36 NIH gene
- Name:
- WD repeat domain 36
- Previous symbol:
- GLC1G
- Synonyms:
- TA-WDRP, UTP21
- Chromosome:
- 5q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2016-10-05
Related products to: Mouse polyclonal to WDR36, Host Mouse
Related articles to: Mouse polyclonal to WDR36, Host Mouse
- To synthesize the genetic architecture of primary open-angle glaucoma (POAG) across the full variant spectrum and map each genetic subtype to its clinical phenotype, IOP profile, optic nerve morphology, systemic associations, and treatment response. - Source: PubMed
Publication date: 2026/09/12
Abu-Amero Khaled KAbualkhair ShereenAlOtaibi HajarSesma Gorka - Retinal ganglion cell (RGC) loss involves p53 activation and calcium overload. The role of RNA-binding proteins like ELAVL1 in this process remains unclear. We investigated whether ELAVL1 protects retinal cells by post-transcriptionally regulating WD Repeat Domain 36 (WDR36). stress was modeled using oxygen-glucose deprivation/reperfusion (OGD/R) in R28 retinal precursor cells. acute intraocular pressure (IOP) elevation was induced in mice. We modulated gene expression with siRNA, plasmids, or AAV vectors, assessing cell death, calcium levels, and protein markers. OGD/R downregulated ELAVL1 and WDR36 protein, but not WDR36 mRNA. ELAVL1 bound WDR36 mRNA and promoted its protein translation. Overexpression of either ELAVL1 or WDR36 reduced OGD/R-induced cell death, calcium overload, and p53 pathway activation. Crucially, WDR36 knockdown abolished ELAVL1's protective effects . , AAV-mediated ELAVL1 overexpression mitigated IOP-induced retinal damage and apoptosis, which was reversed by co-knockdown of WDR36. The ELAVL1-WDR36 axis is a critical post-transcriptional mechanism that promotes retinal cell survival under acute pressure-ischemia stress by inhibiting p53 activation and calcium overload, highlighting its therapeutic potential. - Source: PubMed
Publication date: 2026/04/20
Meng QingFengNing BaoLiChen WenXiongZhang JingJingFu Jun - Our study aims to assess the utility of various next-generation sequencing (NGS) technologies and explore their role in primary glaucoma genetic research. We conducted a systematic review as of January 19, 2025, using PubMed, Scopus, and Web of Science, with study quality evaluated using the QUADAS-2 checklist. We assessed the diagnostic rates of various NGS technologies across different glaucoma subtypes. The study protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO: CRD42024614663). We included 19 studies utilizing whole exome sequencing (WES), whole genome sequencing (WGS), and panel sequencing for assessing genetic features in primary angle-closure glaucoma (PACG), primary congenital glaucoma (PCG), primary open-angle glaucoma (POAG), and juvenile open-angle glaucoma (JOAG). The overall diagnostic rate of NGS technologies was 26.2 % (95 % CI: 15.9 %-36.5 %). WES showed superior performance in PCG (46.7 %), POAG (8.9 %), and JOAG (12.4 %), while panel sequencing achieved a higher rate in PACG (56.4 %). Subtype-specific genes included CYP1B1 in PCG, MYOC in JOAG, and WDR36 in POAG/PACG. Notably, all CYP1B1 gene variant loci are concentrated in 2 specific regions on chromosome 2. This study underscores the significance of NGS in primary glaucoma genetic research, advocating for subtype-specific sequencing strategies to facilitate precise diagnosis and treatment. - Source: PubMed
Publication date: 2025/10/01
Liu YongGong DiDang KuanrongGuo JunhongYan ZhichaoShen XiaoliWang Jiantao - Pancreatic ductal adenocarcinoma (PDA) is an aggressive malignancy that lacks reliable biomarkers to guide treatment decisions. Effective prognostic tools are needed to improve its clinical management. We conducted a comprehensive proteomic analysis on 115 PDA patient samples with matched adjacent normal tissue. A 20-protein diagnostic panel was identified (LGALS1, ANXA2, LGALS3BP, CTSD, S100P, COL12A1, SFN, THBS2, CTHRC1, THBS1, SERPINB5, LAMC2, POSTN, CEACAM6, CTSE, PLEC, PKM, S100A11, TAGLN2, ALDOA). Consensus clustering analysis identified four prognostic proteomic subtypes. Subtypes with poorer prognoses exhibited upregulation of neutrophil degranulation, extracellular matrix remodeling, focal adhesion, Mesenchymal Epithelial Transition, collagen formation, and PI3K-Akt-mTOR-related pathways, indicating a predominance of basal-like and activated stromal features. In tumors with homologous recombination deficiency or Catalogue of Somatic Mutations in Cancer Signature-3, several immune-related proteins were enriched. An 18-protein (PURB, SDCBP2, CD2BP2, GALM, SERPINA3, OAS3, FAN1, ZPR1, KRT2, NUDT2, SMNDC1, SERPINA4, CUTA, WDR36, POSTN, CLEC11A, PEX14, and PI4KA) risk score was developed and validated using multicox regression analyses with LASSO regularization. The risk score demonstrated independent prognostic significance for overall survival and recurrence, and was validated in an independent proteomic dataset generated using a different proteomic technology. This study thus introduces four novel prognostic PDA subtypes, and an 18-protein risk score validated in an independent dataset, which shows promise for improving survival prediction and could serve as a valuable tool for personalized treatment guidance. - Source: PubMed
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