Ask about this productRelated genes to: XPO1 antibody
- 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: XPO1 antibody
Related articles to: XPO1 antibody
- KRAS G12C-mutant advanced non-small cell lung cancer (NSCLC) is currently treated with KRAS G12C covalent inhibitors, such as sotorasib, or RAS (ON) G12-selective inhibitors; however, response rates and progression-free survival remain limited, with recurrence occurring in most patients. Although mechanisms of resistance in KRAS G12C cell lines are multifarious, they have been attributed to EGFR activation and Aurora kinase A (AURKA) signaling via Ras-related nuclear protein (Ran). Ran-GTP cooperates with Exportin-1 (XPO1), which has been identified as essential in KRAS-mutant NSCLC cells. - Source: PubMed
Publication date: 2026/08/17
González JèssicaCai XuetingDiao WenjingRoué GaëlValència-Clua KevinOlmo-González DanielGonzález-Cao MaríaJain AnishaJantus-Lewintre EloisaGiménez-Capitán AnaMolina-Vila Miguel AngelCodony-Servat JordiCao PengRosell Rafael - Despite being the initial intervention of choice, revascularization for myocardial ischemia-reperfusion (I/R) injury remains constrained, making the exploration of novel therapeutic targets imperative. Alpha-kinase 1 (ALPK1) knockdown mitigates ischemic brain injury, whereas its function in cardiac I/R injury requires further investigation. Nur77 knockout (Nur77 KO) mice, with more severe post-acute myocardial infarction (post-AMI) cardiac dysfunction, fibrosis and hypertrophy than C57BL/6 mice, underwent 45 min LAD ligation plus 4 h reperfusion for modeling and genetic ALPK1 knockdown's impacts on this injury were examined in hypoxic AC16 cardiomyocytes via siRNA silencing, pharmacological ferroptosis rescue and siRNA-resistant ALPK1 plasmid functional recovery assays. The results demonstrated that genetic ALPK1 knockdown resulted in an improvement in cardiac function, the amelioration of pathological changes, a reduction in infarct size, and the suppression of apoptosis of myocardial cells in Nur77 KO mice post-I/R. Furthermore, genetic ALPK1 knockdown was observed to suppress lipid peroxidation and ferroptosis, while concomitantly activating Nrf2/HO-1 pathway in Nur77 KO mice post-I/R. Furthermore, genetic ALPK1 knockdown was observed to inhibit apoptosis and ferroptosis in vitro and pharmacological rescue experiments confirmed ferroptosis as the core downstream cell death pathway of ALPK1. ALPK1 was observed to interact with XPO1, thereby inhibiting XPO1 degradation. Moreover, XPO1 overexpression impeded the impact of ALPK1 knockdown on cell survival, lipid peroxidation, and ferroptosis. ALPK1 represents a potential novel target for pharmacological intervention in the treatment of myocardial I/R injury. - Source: PubMed
Publication date: 2026/08/14
Liu YueHu RuisiWang YantengWang YingxiZhao QiheGuan WenweiWang Difei - Myelodysplastic syndrome with biallelic TP53 inactivation (MDS-biTP53) patients represents an ultra-high-risk subgroup with dismal outcomes. Even after allogeneic hematopoietic stem cell transplantation (allo-HSCT), relapse rates remain extremely high and survival is poor. This preliminary case series reports the outcomes of 8 consecutive patients with MDS-biTP53 who received a novel sequential therapy of decitabine (DAC) combined with the XPO-1 inhibitor selinexor, followed by allo-HSCT at a single center between September 2024 and December 2025. At a median follow-up of 7.3 months (95% CI, 4.2-10.4 months) from HSCT, median overall survival (OS) and relapse-free survival (RFS) were not reached. At last follow-up, 7/8 patients remained alive (OS 87.5%) and 6/8 were relapse-free (RFS 75%), with one relapse (12.5%). This patient successfully achieved a second complete remission following preemptive therapy with low-dose decitabine combined with donor lymphocyte infusion and remained in remission at the last follow-up. Two patients developed serious infections during the peritransplant period. One patient with pre-transplant intestinal colonization of carbapenem-resistant Enterobacteriaceae (CRE) ultimately died due to CRE bloodstream infection followed by intestinal graft-versus-host-disease (GVHD). Overall treatment-related toxicity was deemed manageable, and the incidence of grade III-IV acute GVHD was 25% (2/8). This preliminary study provides encouraging evidence that sequential decitabine and selinexor therapy followed by allo-HSCT may improve outcomes with acceptable toxicity in patients with ultra-high-risk MDS-biTP53. However, these findings are limited by the small sample size, relatively short follow-up, and retrospective, single-center design. Confirmation in larger prospective trials is warranted. - Source: PubMed
Publication date: 2026/08/10
Ren YanlingLang WeiXu YuMei ChenHuang XianboWang ShashaQian JiejingTong Hongyan - XPO1/CRM1 (also known as Exportin-1) is best known as a RanGTP-dependent nuclear export receptor and has been explored as a therapeutic target in various diseases, including acute myeloid leukemia (AML). Emerging evidence, however, indicates that XPO1 is also detectable on chromatin at active regulatory regions, including the HOX clusters and the MEIS1 locus-key transcriptional nodes in multiple AML subtypes. Recent studies support a "pre-bound XPO1 platform" model in which genetically diverse leukemia drivers, such as nucleoporin (NUP98/NUP214) fusions and mutant NPM1 (NPM1c), are recruited to these loci via phenylalanine-glycine (FG) repeat-XPO1 or nuclear export signal (NES)-XPO1 interactions, coupled with partner-encoded chromatin contacts. This dual engagement may stabilize locus-restricted assemblies and lower the threshold for liquid-liquid phase separation (LLPS)-linked condensate formation that sustains aberrant HOX/MEIS-driven transcriptional programs. By reframing XPO1 from a nuclear export receptor to a chromatin-associated interaction hub, this perspective provides a framework for understanding transcriptionally addicted AML subtypes and highlights opportunities to selectively target chromatin-associated XPO1 functions in HOX/MEIS-driven AML. - Source: PubMed
Publication date: 2026/08/07
Oka Masahiro - During tumor progression, cells within the solid tumor core experience substantial mechanical crowding (solid stress). Although HDAC6 is a key regulator of cell survival and motility, its spatial regulation under physical crowding remains poorly understood. Here, using HeLa cell monolayers as a model, we show that mechanical crowding promotes the redistribution of HDAC6 from the nucleus to the cytoplasm, whereas fluid shear stress induces the opposite response and favors nuclear accumulation. Expanded immunofluorescence analyses across multiple fields, together with nuclear/cytoplasmic fractionation, support this crowding-associated shift in HDAC6 localization. Transcriptomic profiling further revealed broad remodeling under crowded conditions, including suppression of translation- and cytoskeleton-related programs and enrichment of a candidate export-related signature involving XPO1. Biochemical validation confirmed XPO1 protein expression under crowded conditions, and pharmacological inhibition of XPO1 attenuated the crowding-associated redistribution of HDAC6, supporting a functional role for XPO1 activity in this process. In addition, crowding was accompanied by the upregulation of invasion-associated markers, including MMP9 and Vimentin, suggesting the emergence of a pro-invasive transcriptional state. Together, these findings identify HDAC6 nucleo-cytoplasmic redistribution as a mechanically responsive event under crowding and support the involvement of XPO1 in this adaptation. - Source: PubMed
Publication date: 2026/07/28
Li ShukaiDu Jing