Ask about this productRelated genes to: MXI1 antibody
- Gene:
- MXI1 NIH gene
- Name:
- MAX interactor 1, dimerization protein
- Previous symbol:
- -
- Synonyms:
- MXD2, MAD2, MXI, bHLHc11
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-16
- Date modifiied:
- 2016-10-05
Related products to: MXI1 antibody
Related articles to: MXI1 antibody
- Early onset preeclampsia (EOPE), a complex complication of pregnancy, is a major contributor to maternal and fetal morbidity and mortality. The only symptom consistently observed in EOPE is new maternal hypertension. Other symptoms vary among patients, posing challenges for early detection. There are currently no clinically accepted molecular markers other than FLT1, which is highly upregulated and displays a small change in its splicing ratio in EOPE placentas. However, an exhaustive search for changes in transcript use in EOPE has not been performed. - Source: PubMed
Publication date: 2026/07/17
Grinshpan NufarMizrachi TehilaLianski SapirZarivach RazGoldman-Wohl DebraBeharier OferShay Tal - Myeloid antigen-presentation dysfunction is a central but incompletely translated immune state in hepatocellular carcinoma (HCC). This study aimed to develop a compact prognostic and recurrence model directly anchored in single-cell-defined myeloid antigen-presentation loss. - Source: PubMed
Publication date: 2026/07/04
Tan YeXiang JingxuanWang ZehanWang YuChen AidongWu Qiwen - Glioblastoma (GBM), the most aggressive primary brain tumor, develops within a tumor microenvironment (TME) dominated by tumor-associated macrophages (TAMs) that critically influence disease progression. Through single-cell RNA sequencing (scRNA-seq) and bioinformatic analysis, we delineated macrophage heterogeneity within the GBM TME and identified a distinct VCAN⁺ macrophage subpopulation. Pseudotime trajectory analysis revealed these cells at the terminal stage of macrophage differentiation, where they exhibit enhanced granulocyte migration and chemotaxis pathways and exhibit a pro-tumorigenic phenotype that diverges from classical M1/M2 polarization. These VCAN⁺ macrophages displayed a distinct polarization state driven by tumor necrosis factor-α (TNF-α), contributing to both a pro-inflammatory and an immunosuppressive TME. CellChat analysis demonstrated their pivotal role in intercellular communication-predominantly mediating crosstalk with GBM tumor cells, endothelial cells, and CD8⁺ T cells via SPP1 signaling: SPP1 binding to CD44 on tumor cells enhances their invasiveness, while its interaction with CD47 on CD8⁺ T cells inhibits anti-tumor immunity. Transcriptional regulatory network analysis identified that CDX2 and MXI1 serve as key transcription factors modulating VCAN⁺ macrophage function and maintaining their specific polarization and homeostasis. Through machine learning, we identified seven hub genes-C1QA, C1QC, C3, CCL4, CD44, SERPINE1, and TREM2 (all highly expressed in VCAN⁺ macrophages and involved in their polarization or intercellular communication)-and constructed an effective GBM prognostic model (AUC = 0.83 in validation cohort), underscoring their roles in immune regulation, extracellular matrix remodeling, and VCAN⁺ macrophage-mediated tumor progression. Further studies with larger cohorts and functional validation will clarify this subpopulation's therapeutic potential and spatial distribution patterns. - Source: PubMed
Publication date: 2026/05/09
Guo JiaxinZhu ZhanshengTong NanyangXu DingdingZhang HuanLin ChenshiWan GuipingWang YameiZhou QingqingXia Liang - Immune checkpoint blockade (ICB) therapy has shown limited efficacy in ovarian cancer (OC). PTEN loss is a common driver in OC, yet its impact on ICB efficacy remains poorly understood. Utilizing the single-cell RNA sequencing data and performing multiplex immunohistochemical staining on treatment-naive OC clinical specimens, we showed that PTEN reduction resulted in an immunosuppressive tumor microenvironment associated with upregulated B7H3. Mechanistically, PTEN depletion activates mTORC2, which phosphorylates FOXO1/3, thereby inhibiting their transcriptional activity and reducing MXI1 expression. This, in turn, diminishes the inhibitory effect on c-Myc, leading to enhanced c-Myc transcriptional activity and subsequent upregulation of B7H3. Notably, in mouse models, anti-B7H3 therapy exhibits heightened effectiveness in OC with PTEN loss. This enhanced response can be abrogated by removing CD8 T cells. Our findings elucidate an immune evasion mechanism in PTEN-loss OC and suggest B7H3 blockade as a potent therapeutic strategy specifically for these tumors. - Source: PubMed
Publication date: 2026/03/31
Wang ZhenJin NingLi XinMa XinyanFeng YuqingYin KangDuan ShicanPan WenJiang Jin-KaiLei Le-LinQian Yi-YuZheng XuleiGao Qing-LeiLiu DanXia Yu - RRAS, a gene encoding a small monomeric GTPase that controls cell adhesion and migration, has been linked to leukemogenesis. However, its function in acute megakaryoblastic leukemia (AMKL), a rare type of acute myeloid leukemia, remains indistinct. Here, we explored the potential and mechanism of RRAS in the immune escape of AMKL. Human AMKL cells M-07e and UT-7 were infected using lentiviruses and co-cultured with CD8 T cells. An AMKL mouse model was constructed by tail vein injection of the mouse AMKL cells with genetic intervention. RRAS expression and ERK-1/2 phosphorylation were enhanced, and MXI1 was reduced in M-07e and UT-7 cells. RRAS knockdown and MXI1 or FUBP3 overexpression inhibited AMKL cell viability and promoted the anti-tumor immunity of CD8 T cells and apoptosis of AMKL cells. Knockdown of RRAS or overexpression of FUBP3 decreased the infiltration and aggregation of megakaryocytes in the bone marrow, liver, and spleen of AMKL mice, which were rescued by MXI1 knockdown or RRAS overexpression. MXI1 inhibited the MAPK signaling by recruiting NCOR1/2, Sin3A/B, and HDAC1 to co-repress RRAS transcription. FUBP3 stabilized MXI1 to block RRAS-mediated ERK signaling. Overall, we provide evidence of an unrevealed axis FUBP3/MXI1/RRAS/MAPK in the CD8 T cell immunity in AMKL. - Source: PubMed
Publication date: 2025/12/22
Zhu YingLiu JinyingZeng JiqiangLiu ZhiruiYan ZhiminZhang ShanrongLuo HuixiWu ZhipengLu JiaweiQiu FangYe JunsongLu Chen