Ask about this productRelated genes to: FXR1 antibody
- Gene:
- FXR1 NIH gene
- Name:
- FMR1 autosomal homolog 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 3q26.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-16
- Date modifiied:
- 2016-10-05
Related products to: FXR1 antibody
Related articles to: FXR1 antibody
- Histone lactylation is an epigenetic modification triggered by lactate produced during glycolysis. In cancer, histone lactylation can coordinate metabolic and epigenetic states to promote tumor development and progression. Here, we identified circ2891 as a driver of metabolic reprogramming and histone lactylation in colorectal cancer (CRC). In patients, circ2891 was aberrantly upregulated in tumors and correlated with poor outcomes. Elevated circ2891 potentiated aerobic glycolysis and lactate production in CRC cells, supporting enhanced cell proliferation and tumor growth. Mechanistically, circ2891 specifically interacted with the m6A reader FXR1 and facilitated its phase separation, which stabilized PGK1 and ENO1 mRNAs by enhancing the recognition of their m6A modification sites. Consequently, elevated PGK1 and ENO1 led to increased aerobic glycolysis and drove histone lactylation, thereby transcriptionally activating the RNA helicase DDX21 to promote CRC progression. Simultaneously targeting circ2891 and histone lactylation suppressed patient-derived organoid and xenograft tumor growth. Together, these findings show that circ2891 promotes CRC by stabilizing PGK1/ENO1 via phase separation of FXR1, boosting glycolysis and histone lactylation to activate expression of DDX21. Targeting circ2891 offers a promising therapeutic strategy enhancing clinical outcomes. - Source: PubMed
Publication date: 2026/08/05
Jiang TaoLiu JianquanHu QihangQi JunwenLiu BowenMa NingXu YixinZhang LongChen JunnanSong Jun - Viruses must subvert host responses to facilitate successful infection. While most antiviral responses are associated with interferons, stress granules (SG) are another barrier to viral infection by inducing translation arrest. To combat SG activity, viruses have evolved mechanisms to disrupt formation and disassemble these complexes. Our prior studies identified residues in SARS-CoV-2 NSP3 (Y138/F145) and nucleocapsid (F17) that independently antagonize SG activity. Disrupting these key residues in NSP3 or nucleocapsid attenuated viral replication, but only modestly impacted pathogenesis suggesting overlap in SG antagonism partially compensate for the individual losses. In this study, we evaluated a SARS-CoV-2 mutant (YF/F17A) that combines the NSP3 and N mutations. We find that loss of both SG antagonizing functions attenuates SARS-CoV-2 replication . While no changes are seen in type I IFN sensitivity, attenuation corresponds to increased induction of SGs. Importantly, the SARS-CoV-2 YF/F17A mutant has significant attenuation with reduced viral replication, less weight loss, and limited immune pathology. Notably, infection with the YF/F17A mutant stimulated less interferon and inflammation. Despite these muted host responses, the YF/F17A mutant stimulated robust protection against subsequent challenge with WT SARS-CoV-2. Overall, the study highlights the importance of SG control for SARS-CoV-2 infection and offers a novel, interferon independent target for vaccination and therapeutic treatment going forward. - Source: PubMed
Publication date: 2026/06/18
Alvarado R EliasChen JenniferLokugamage Kumari GZhou YiyangEstes Leah KMorgan AngelicaAhearn YaniDeng XiangxueLai LilinMoayyed ArianMeyers WilliamPlante Jessica APlante Ken SWalker David HXie XupingSuthar Mehul SJohnson Bryan AMenachery Vineet D - The cytoplasm of vertebrate cells is compartmentalized into the cytosol and several messenger RNA (mRNA)-scaffolded condensates, present at steady-state conditions and in the absence of stress. They include TIS granules and the FXR1 network and act as translation, folding, and signaling environments. Therefore, in addition to serving as templates for protein synthesis, mRNAs play essential roles in cytoplasmic organization. However, not all mRNAs function as condensate scaffolds. Whereas mRNAs with short and structured 3' untranslated regions (UTRs) usually diffuse freely and localize to the cytosol, scaffold mRNAs are characterized by long and multivalent 3' UTRs. Scaffold mRNAs are responsible for the characteristic irregular, network-like morphology of mesh-like condensates and play active, functional roles during protein biosynthesis. For example, mesh-like condensates act as folding environments for proteins with long intrinsically disordered regions, where multivalent 3' UTRs act as cotranslational chaperones to prevent protein misfolding. The scaffold function of mRNAs is also important for post-translational processes, where the mRNA-mediated proximity of signaling factors promotes cellular signaling reactions. In this review, the discovery of cytoplasmic mRNA-scaffolded mesh-like compartments and their currently known assembly principles and biological roles are discussed. - Source: PubMed
Publication date: 2026/06/25
Mayr Christine - The precise assembly of the sperm flagellum is essential for male fertility and has long been ascribed to kinesin-2-driven intraflagellar transport (IFT) of protein cargoes. However, during late spermiogenesis, when transcription activity is largely silenced, how the spatiotemporally regulated delivery of flagellar components remains poorly understood. Here, we systematically screened kinesin genes in asthenozoospermic patients and identified two homozygous deleterious KIF6 variants in unrelated men characterized by complete sperm immotility. Mouse models carrying the corresponding mutations recapitulated the human infertility phenotypes. Multi-omics analyses revealed that most testicular mRNAs remained largely unchanged in Kif6 mice, whereas proteins involved in axonemal organization and energy metabolism were markedly reduced. Mechanistically, KIF6 interacts with the RNA-binding proteins (RBPs) FMRP and FXR1 to assemble mRNP transport complexes that ferry transcripts encoding flagellar structural proteins (e.g., DNALI1) and metabolic enzymes (e.g., HK1). Impaired KIF6 function compromises mRNP trafficking to the developing flagellum, reducing flagellar transcript levels and ultimately causing decreased protein abundance and defective flagellar function. Collectively, we identify KIF6 as a key regulator of mRNA transport during spermiogenesis. It interacts with RBPs through a novel IFT-like pathway to deliver mRNAs essential for flagellar biogenesis, redefining the traditional protein-centric IFT paradigm. - Source: PubMed
Publication date: 2026/06/25
Xie ChunboYi SibingLin XinleZhang ShenWang WeiliYuan ShiminMeng LanlanLi YongTan ChenWei ChunjiaYu YanyanLiang YaoqiongZhang HuanHu LiangLu GuangxiuHe WenbinZhang QianjunDu JuanLin GeTu ChaofengTan Yue-Qiu - Meningiomas are the most common primary intracranial tumors and the only brain tumors that are more common in females compared with males1. Progestin hormonal therapies increase the risk of meningioma, and progestin-induced or pregnancy-associated meningiomas can regress as serum progestogen levels normalize2. The mechanisms that underlie sex differences and progestogen signaling in meningioma are unknown. Here we show that sex hormone interaction with PGRMC1, a transmembrane progesterone binding protein, regulates the activity of RNA processing proteins FXR1 and RBM39 to drive meningioma sex differences. The genomic architecture and stem cells underlying meningiomas are conserved across vertebrate species3-5 and, using mass spectrometry-based proteomics to analyze 703 meningioma and meningeal samples, we demonstrate that meningiomas are enriched in RNA processing proteins in humans and dogs. Interactions between PGRMC1, FXR1, and RBM39 are inhibited by progestogens and stabilized by testosterone. After release from PGRMC1, FXR1 and RBM39 bind and stabilize progesterone receptor (PR) transcript to enable expression of PR protein, which induces cell cycle, membrane, and cytoskeleton remodeling genes that drive tumor growth. These findings reveal therapeutic strategies and a PR target gene biomarker that may improve outcomes for patients. More broadly, we elucidate an estrogen receptor-independent mechanism of PR expression that underlies sex differences in cancer. - Source: PubMed
Publication date: 2026/06/02
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