20p Subtelomere(R6G) FISH Probe
- Known as:
- 20p Subtelomere(R6G) fluorescence-emitting hybridization Probe
- Catalog number:
- FE0178
- Product Quantity:
- 20 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- 20p Subtelomere(R6G) FISH Probe
Related genes to: 20p Subtelomere(R6G) FISH Probe
- Gene:
- SH3PXD2A NIH gene
- Name:
- SH3 and PX domains 2A
- Previous symbol:
- SH3MD1
- Synonyms:
- FISH, KIAA0418
- Chromosome:
- 10q24.33
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-01
- Date modifiied:
- 2016-10-05
Related products to: 20p Subtelomere(R6G) FISH Probe
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated1 MATAL PROBE Tip1 metal probe tip (marked as 19-160-03)1 PLASTIC PROBE TIP1,1'-Dioctadecyl-3,3,3',3'-tetramethylindodicarbocyanine perchlorate, Red fluorescent membrane probe, 10mg1,1'-Dioctadecyl-3,3,3',3'-tetramethylindodicarbocyanine perchlorate, Red fluorescent membrane probe, 10mg1,1'-Dioctadecyl-3,3,3',3'-tetramethylindotricarbocyanine iodide, DiR, A lipophilic near-IR (NIR) fluorescent membrane probe used for labeling cells f1,1'-Dioctadecyl-3,3,3',3'-tetramethylindotricarbocyanine iodide, DiR, A lipophilic near-IR (NIR) fluorescent membrane probe used for labeling cells for long term analysis, 25mg1,1'_Dioctadecyl_3,3,3',3'_tetramethylindodicarbocyanine perchlorate, Red fluorescent membrane probe, 10mg1-[4-(Dimethylamino)phenyl]-6-phenylhexatriene (DMA-DPH), Fluorescent probe of lipid bilayer structure and dynamics, 100mg1-[4-(Dimethylamino)phenyl]-6-phenylhexatriene (DMA-DPH), Fluorescent probe of lipid bilayer structure and dynamics, 100mg10% Fish Gelatin Blocking Buffer Related articles to: 20p Subtelomere(R6G) FISH Probe
- Preeclampsia (PE) is a multifaceted pregnancy disorder marked by impaired trophoblast invasion and placental ischemia. Although common, dependable noninvasive biomarkers and the underlying molecular mechanisms responsible for trophoblast dysfunction are still not fully understood. In this study, we applied an integrated multi-omics strategy to uncover reliable placenta-derived circulating biomarkers and to define the functional contribution of the novel hub gene AIF1L to the pathogenesis of PE. - Source: PubMed
Publication date: 2026/07/29
Chen YinlongZhan WenliShen KePeng ManqingZheng Qingliang - Although historically associated with the inactivation of the gene, a minority of schwannomas have recently been found to exhibit fusion transcripts, such as , , or fusions. Herein, we report a large retroperitoneal schwannoma exhibiting a fusion. Histologically, this tumor contained distinctive large epithelioid cells with granular cytoplasm, but also exhibited degenerative features often associated with schwannoma, such as perivascular hyalinization and hemosiderin deposition. The cells were positive for SOX10, showed robust TRIM63 expression, and were focally positive for HMB45. Methylation profiling confirmed that the tumor was of Schwann cell differentiation. Following complete surgical resection, the patient has experienced no recurrence to date. As MiT family translocation-associated renal cell carcinoma and alveolar soft part sarcoma can also exhibit a fusion, awareness of this rare schwannoma subtype is vital in ensuring it is not mistaken for a more aggressive neoplasm. - Source: PubMed
Publication date: 2026/05/06
Perry Kyle DMehra RohitLeathersich AnnAbdulfatah EmanRottmann DouglasSchechter ShulaMcHugh JonathanNarayan Suguna PAngeles Christina VChugh RashmiConway KyleBrown Noah - The lncRNA SH3PXD2A-AS1 drives therapy resistance in non-small cell lung cancer (NSCLC) through mA-mediated PD-L1 overexpression, representing a novel molecular toxicology paradigm. In the present work, the functional significance of SH3PXD2A-AS1 in orchestrating immune escape and malignant progression of NSCLC was systematically examined. Integrating TCGA analyses with cell and mouse studies, we found that SH3PXD2A-AS1 was elevated in NSCLC and associated with features of an immunosuppressive tumor microenvironment. Multi-omics profiling, RNA pull-down/RIP, and promoter-reporter assays revealed that SH3PXD2A-AS1 interacts with the transcription factor MYBL2 to drive transcriptional activation of WTAP, a core component of the mA writer complex. This axis enhanced mA modification of PD-L1 mRNA, stabilizing PD-L1 and dampening CD8 T-cell responses. Silencing SH3PXD2A-AS1 reduced MYBL2/WTAP/PD-L1 signaling, decreased malignant phenotypes in vitro, and restored antitumor T-cell activity in humanized mouse models, whereas enforced MYBL2 or WTAP expression counteracted these effects. Collectively, these findings define an lncRNA-transcription factor-epitranscriptomic checkpoint that sustains PD-L1-mediated immune escape in NSCLC, and nominate SH3PXD2A-AS1 and its MYBL2/WTAP partners as potential biomarkers and therapeutic targets to improve responses to immune checkpoint inhibition. - Source: PubMed
Wu SiyanChen JuanHan YuDong YuanShi HaiLiu PingchuangChen YunfengYuan JieqingCui Wenjie - The HCLS1-Binding Protein 3 (HS1BP3) interacts with the SH3 domain of cortactin (CTTN), a protein that contributes to a malignant phenotype in cancers. Here, we demonstrate that high expression of HS1BP3 is associated with reduced survival for gastric adenocarcinoma and triple negative breast carcinoma patients and that HS1BP3 is specifically upregulated in these cancers. We mapped the HS1BP3-cortactin interaction site to the third proline-rich region (PRR3.1) of HS1BP3 and show that this interaction is important for cancer cell proliferation, extracellular matrix degradation and secretion. HS1BP3 expression was found to correlate with expression of the invadopodia scaffold protein TKS5 and we show that the localisation of TKS5 inside multivesicular endosomes is increased in cells expressing an HS1BP3 PRR3.1 mutant. Overall, our results highlight the importance of the direct interaction between HS1BP3 and cortactin in cancer development by regulating cell proliferation, secretion and invasion, which may provide an explanation for the negative correlation between HS1BP3 levels and the survival of gastric adenocarcinoma and triple negative breast cancer patients. - Source: PubMed
Publication date: 2026/04/10
Løchen Arja ArnesenSøreng KristianeVeroni ChiaraTrachsel-Moncho LauraAsp NaghamGaupset RobinLyckander Lars GustavKnævelsrud HeleneEftang LarsSimonsen Anne - Epigenetic alterations, particularly DNA methylation, play a crucial role in the progression of oral squamous cell carcinoma (OSCC) from oral leukoplakia (OL). However, the molecular mechanisms driving this transition remain poorly understood. Using interpretable machine learning (IML) on genome-wide methylation data from 118 samples (22 OL, 74 OSCC, and 22 controls), we identified 20 key CpG sites among 820 193 loci through SHAP (SHapley Additive exPlanations) analysis. Notably, cg19853638, cg25393842, cg01743793, and cg10784570 mapped to pivotal genes such as TNFRSF19, ALOX5, and SH3PXD2A, which regulate cell morphology, inflammatory pathways, and immune responses- critical processes influencing OSCC malignancy and progression. To assess generalizability and confirm the robustness of classifier, the predictive model was validated on an independent Taiwanese cohort (GSE38532) profiled on a different array platform, achieving 98.8% accuracy and ROC-AUC of 0.999 demonstrating robust cross-population performance. Furthermore, cross-omics integration with an independent transcriptomic dataset (GSE31056) identified eight genes, including ALOX5, FOXP1, and VTI1A, showing consistent methylation and expression patterns, underscoring their biological relevance. Our findings highlight the functional relevance of SH3PXD2A, TNFRSF19, and ALOX5 in OSCC pathophysiology: SH3PXD2A mediates cell migration and invasion, TNFRSF19 is involved in survival signaling, and ALOX5 regulates inflammatory responses. These multi-layered analyses provide novel insights into epigenetic mechanisms underlying OL to OSCC progression and highlight candidate biomarkers with strong translational potential. By combining IML based methylation modeling with external and cross-omics validation, this study advances the development of reliable, interpretable biomarkers for precision oral cancer diagnostics and management. - Source: PubMed
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