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
- Increasing evidence supports important roles of post-transcriptional regulation in brain development; however, the precise mechanism remains unclear. Here, we show that Fragile X autosomal homolog 1 (FXR1), a brain-enriched RNA-binding protein (RBP), is essential for human neurogenesis. FXR1-deficient human cortical neural progenitor cells (NPCs) have reduced proliferation and impaired cell cycle exit during differentiation, leading to impaired neuronal differentiation. Transcriptomic and co-expression network analyses revealed FXR1 as an orchestrator of stage-specific gene programs driving neural differentiation. High-mobility group protein B2 (HMGB2), a master transcriptional regulator in stem cells, is a direct target of FXR1. FXR1 and HuR co-regulate HMGB2 mRNA, and their opposing actions on mRNA stability maintain the levels of HMGB2 in human NPCs. Reducing HMGB2 levels in FXR1-deficient NPCs rescues NPC proliferation and neuronal differentiation. Together, these findings establish post-transcriptional regulation as a key mechanism that maintains neurogenic potency of human NPCs. - Source: PubMed
Publication date: 2026/09/17
Méndez-Albelo Natasha MZhang YajieSandoval Soraya OGuo YuGao YuPeters Lily ASirois Carissa LWidicus Anna BYang PaofueTrygstad Drew NEckholm Magnus TXu ZhiyanSmith Riley VDisher Rachel MJohnston Christian JZhao Xinyu - Viruses must subvert host responses to facilitate successful infection. While most antiviral responses are associated with interferons, stress granules (SGs) 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 compensates 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 interferon sensitivity, attenuation corresponds to increased induction of SGs. Importantly, the SARS-CoV-2 YF/F17A mutant attenuates significantly 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.IMPORTANCEThis study demonstrates that SARS-CoV-2 uses multiple mechanisms to block host stress granules during infection. Knocking out both N- and NSP3-mediated antagonism of stress granules attenuates viral replication and disease caused by SARS-CoV-2. Importantly, while most therapeutics target key viral processes or induce interferon pathways, this study shows stress granule activation as a novel approach to attenuate and treat coronavirus infection. - Source: PubMed
Publication date: 2026/09/08
Alvarado R EliasChen JenniferLokugamage Kumari GZhou YiyangEstes Leah KMorgan Angelica LAhearn YaniDeng XiangxueLai LilinMoayyed ArianMeyers WilliamPlante Jessica APlante Ken SWalker David HXie XupingSuthar Mehul SJohnson Bryan AMenachery Vineet D - This study aimed to explore the protective effect of Agaricus bisporus polysaccharide (ABP) against high-fat diet (HFD) induced cognitive impairment (CI), with a particular focus on gut-brain communication. ABP supplementation alleviated anxiety-like behavior and cognitive deficits in HFD-fed mice. These effects were associated with enhanced hippocampal synaptic plasticity and attenuated inflammatory responses, which were accompanied by the elevation of Bdnf levels and the upregulated expression of plasticity-related genes (e.g., Gria2, Grin2b, Tdp2, and Fxr1). Crucially, ABP supplementation was associated with alleviated HFD-induced morphological changes in microglia and reduced inflammatory factor mRNA levels (Tnf, Il1b). Meanwhile, ABP remodeled the gut microbiome, significantly enriching beneficial taxa including Akkermansia and Bacteroides and enhancing the production of short-chain fatty acids (SCFAs), mainly acetate and propionate. These findings suggest that ABP may serve as a promising nutritional component for alleviating diet-related CI with effect associated with modulation of the microbiota-gut-brain axis. - Source: PubMed
Publication date: 2026/08/07
Fu ChujingYe KaiQiu ZhichangHu XinyuWang XiaoxuanXiao Hang - 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