Human Exportin 1,XPO1 ELISA Kit
- Known as:
- Human Exportin 1,XPO1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- dl-xpo1-hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Wuxi donglin
- Gene target:
- Human Exportin 1 XPO1 ELISA Kit
Related genes to: Human Exportin 1,XPO1 ELISA Kit
- Gene:
- XPO1 NIH gene
- Name:
- exportin 1
- Previous symbol:
- -
- Synonyms:
- CRM1, CRM-1, emb
- Chromosome:
- 2p15
- Locus Type:
- gene with protein product
- Date approved:
- 1998-05-12
- Date modifiied:
- 2019-03-12
Related products to: Human Exportin 1,XPO1 ELISA Kit
Related articles to: Human Exportin 1,XPO1 ELISA Kit
- Glioblastoma multiforme (GBM) is the most aggressive primary brain tumor with high resistance and recurrence rate. Here we present a novel combination therapy composed of Selinexor, a selective nuclear export (XPO1) inhibitor, and 5-aminolevulinic acid (5-ALA), a protoporphyrin IX (PpIX) precursor. Selected drugs act through two distinct mechanisms of action: Selinexor retains tumor suppressor proteins within the nucleus, while 5-ALA, after being converted to PpIX, induces oxidative stress upon light exposure. Intracellular accumulation of PpIX in U-87 MG cells peaked at 4 h and co-administration of the drugs to U-87 MG cells yielded strong synergism with substantially reduced doses of 5-ALA and Selinexor up to ∼140- and ∼ 29-fold, respectively. Conversely, very strong antagonism was observed in the control cell line. While the highest mitochondrial H₂O₂ production was measured following 5-ALA induced photodynamic therapy (PDT), Selinexor reduced H₂O₂ level. The strong synergistic interaction between the two drugs enhanced therapeutic outcome by suppressing cell migration and inducing apoptosis with markedly lower drug doses. These findings suggest that the combination therapy of Selinexor and 5-ALA/PDT may increase the chances of successful GBM treatment compared to monotherapy alone. - Source: PubMed
Publication date: 2026/06/01
Güler S İremDemircioglu E EsmaYıldırım SenaAbdallah Sarah OsamaEroğlu EmrahErdem S Sibel - Nucleophosmin 1 (NPM1) gene aberrations are among the most common genetic alterations in acute myeloid leukemia (AML). NPM1 mutations (NPM1c), detected in 30-40% of adult AML cases, are well-characterized and associated with distinct clinical and molecular features. In contrast, NPM1 rearrangements (NPM1-r), involving rare fusion partners such as MLF1, CCDC28A, HAUS1, and RARA, are much less common and have historically been poorly understood. However, recent studies have begun to shed light on the molecular mechanisms and clinical characteristics of NPM1-r AML, revealing overlapping features with NPM1c-AML. Both types share key leukemogenic mechanisms, including cytoplasmic mislocalization of NPM1, interaction with XPO1, and sustained HOX gene expression, which drive leukemic transformation. NPM1-r AML may exhibit unique clinical characteristics, including a higher prevalence in younger patients and potentially a poorer prognosis, although further validation in larger cohorts is needed. Therapeutic strategies targeting XPO1 and Menin, which have shown promise in NPM1c-AML, may also hold potential for NPM1-r AML. Continued research is essential to further elucidate the biology of this rare AML subtype and to establish optimized treatment strategies. - Source: PubMed
Publication date: 2026/06/05
Shimosato YukoGoyama Susumu - Richter transformation of Chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) into classic Hodgkin lymphoma (CHL-RT) is rare and remains incompletely understood. Two histologic subtypes are recognized: type 1 (CLL/SLL with scattered Hodgkin/Reed-Sternberg (HRS) cells) and type 2 (HRS cells within a polymorphous inflammatory background). In this multi-institutional study of 77 patients with CHL-RT (27 type 1 and 50 type 2), we characterized immune evasion markers, / copy number alterations, tumor microenvironment, and performed targeted next-generation sequencing on 37 CLL/SLL samples. HRS cells in CHL-RT displayed immune-evasion phenotypes similar to de novo CHL, though PD-L1 expression was lower in type 1 cases. gain/polysomy were frequent (83.3%). CLL/SLL with CHL-RT harbored increased mutations in , and versus reference CLL/SLL. Similar mutational profiles, demographics, and survival outcomes support a biological continuum between type 1 and type 2 CHL-RT, with distinct genetic features in CLL/SLL predisposing to CHL transformation. - Source: PubMed
Publication date: 2026/05/20
Yan MingfeiParikh Sameer ASampaio De Melo Michelly KHampel Paul JAleynick NathanielChan AlexanderEren Ozgur CanLopez KatherineCohen AlexaRoshal MikhailLim Megan SBoiocchi LeonardoDogan AhmetZhang YanmingSinha SutapaRabe Kari GKay Neil EJaffe Elaine SKing Rebecca LXiao Wenbin - Multiple myeloma (MM) remains the second most common hematologic malignancy, necessitating the identification of novel therapeutic targets. MM is characterized by a distinct epigenetic landscape driven by aberrant chromatin activation and super-enhancer addiction. The transcriptional co-activator p300 acts as a critical "writer" of this landscape by depositing H3K27ac marks. In this study, we hypothesized that targeting the histone acetyltransferase (HAT) activity of p300 with the selective inhibitor A485 would collapse this oncogenic chromatin network and induce lethality in MM cells. - Source: PubMed
Xu HongWu WenqiJiang YananWang JinhuanZhai YixinZhao Zhigang - Diffuse malignant peritoneal mesothelioma (DMPM) is a rare and aggressive malignancy with limited therapeutic options and poor clinical outcomes. While metabolic reprogramming, including altered lipid metabolism, is a recognized hallmark of cancer, its contribution to DMPM progression and treatment response remains poorly understood. - Source: PubMed
Publication date: 2026/05/21
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