EPHB1(Texas Red)_CEN3q(FITC) FISH Probe
- Known as:
- EPHB1(Texas Red)_CEN3q(fluorecein) fluorescence-emitting hybridization Probe
- Catalog number:
- FA0510
- Product Quantity:
- 200 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- EPHB1(Texas Red)_CEN3q(FITC) FISH Probe
Related genes to: EPHB1(Texas Red)_CEN3q(FITC) 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: EPHB1(Texas Red)_CEN3q(FITC) FISH Probe
Related articles to: EPHB1(Texas Red)_CEN3q(FITC) FISH Probe
- A peripheral nerve sheath tumour composed predominantly of Wagner-Meissner (W-M) bodies is typically regarded as a variant of schwannoma and has been considered rare. Interestingly, a SH3PXD2A::HTRA1 fusion was found which is described in schwannomas with a so-called "serpentine" palisading pattern comprising short palisades of Schwann cells. - Source: PubMed
Publication date: 2026/08/26
Wilsher Mark JamesBerber Onur - Non-obstructive azoospermia (NOA) is a severe form of male infertility in which focal spermatogenesis may persist in otherwise functionally impaired testes. Testicular sperm extraction by microdissection (mTESE) remains the standard procedure for sperm retrieval, but its unpredictable success rate emphasizes the urgent need for reliable, non-invasive biomarkers to support clinical decision-making. Recent advances in transcriptomics have highlighted the role of circular RNAs (circRNAs), microRNAs (miRNAs), and their mRNA targets in the formation of competing endogenous RNA networks (ceRNAs) that regulate spermatogenesis. - Source: PubMed
Publication date: 2026/08/20
Babakhanzadeh EmadKhodadadian AliNazari MajidMozhdeh MahyaVahidi Mehrgardi SerajoddinJafari Mohammad HassanDehghani MohammadrezaGhafouri-Fard SoudehGhasemi Nasrin - 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