Ask about this productRelated genes to: RBM9 antibody
- Gene:
- RBFOX2 NIH gene
- Name:
- RNA binding fox-1 homolog 2
- Previous symbol:
- RBM9
- Synonyms:
- HNRBP2, FOX-2, HRNBP2
- Chromosome:
- 22q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-12
- Date modifiied:
- 2017-09-13
Related products to: RBM9 antibody
Related articles to: RBM9 antibody
- Neutrophil extracellular traps (NETs) are increasingly recognized as key regulators of tumor progression, yet the molecular circuitry that governs their induction in cancer remains elusive. Here, we identify the RNA-binding protein RBFOX2 as a tumor suppressor that curtails glioma growth by coordinately restraining tumor cell proliferation and NETosis. RBFOX2 expression is markedly reduced in glioma and positively correlates with patient survival. Mechanistically, RBFOX2 binds to 5-hydroxymethylcytidine (5hmC)-modified sites within PDGFB mRNA and promotes its decay, thereby dampening AKT-SP1 signaling and repressing CSF3 transcription. This repression limits neutrophil-mediated NET formation in the tumor microenvironment, as confirmed in PAD4 mice and upon CSF3 neutralization. Collectively, our study uncovers a 5hmC-dependent post-transcriptional mechanism linking RBFOX2 to NETosis control and glioma suppression, revealing RBFOX2 as a potential biomarker and therapeutic lever and establishing a broader paradigm in which RNA-binding proteins couple post-transcriptional RNA modification and immune regulation in tumor evolution. - Source: PubMed
Publication date: 2026/06/11
Chen XiDai WeiweiWang HanlinFang JianingYin BowenLiu ChangweiChen YulingWu RuixinCai YihengBian ShashaHai RihanLi JinZhu YiqianShu Minfeng - Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide. Aberrant expression of RNA binding fox-1 homolog 2 (RBFOX2) has been implicated in tumorigenesis and progression; however, its biological functions and clinical significance in CRC remain poorly understood. This study aimed to elucidate the role of RBFOX2 in CRC. - Source: PubMed
Publication date: 2026/05/31
Liu WenDongDai GuangMingLiao GuoLongOuyang PengHuang JinTuanXu Meng - Treatment-induced neuroendocrine prostate cancer (NEPC) represents an aggressive form of castration-resistant prostate cancer (CRPC) associated with lineage plasticity and therapeutic resistance. In this study, we investigated the role of the Hippo signaling axis in the transdifferentiation from androgen receptor-positive prostate cancer (ARPC) to NEPC. RNA sequencing analyses of CRPC metastases revealed coordinated alterations in Hippo pathway components, with decreased expression of YAP1, LATS2, and TEAD2 and increased expression of LATS1, TEAD1, and the RNA splicing regulator RBFOX2 in NEPC. These transcriptional alterations were consistently observed across multiple model systems and patient samples. Epigenetic analyses demonstrated that reduced expression of YAP1, TEAD2, and LATS2 was associated with increased DNA methylation, whereas elevated TEAD1 expression correlated with DNA hypomethylation in NEPC. NEPC selectively retained TEAD1 expression, including a spliced isoform not detected in ARPC. Proteomic interactome analyses revealed that TEAD1 associated with RNA splicing factors and DNA repair proteins. Functional studies showed that TEAD1 knockdown led to the reversion of gene programs associated with epithelial differentiation. These findings indicate that the conversion of ARPC to NEPC involves coordinated loss of AR, YAP1, and REST activity alongside sustained TEAD1 expression and altered RNA processing. Our data identify TEAD1 as a transcriptional regulator associated with the NEPC state and suggest a role for TEAD1-linked transcriptional and post-transcriptional mechanisms in prostate cancer lineage plasticity. - Source: PubMed
Publication date: 2026/05/30
Brown Lisha GColeman Ilsa MChu Tony L HSayar ErolcanPatel Radhika AHanratty BrianAdil MohamedLi DapeiLi YongtaoNguyen Holly MSessions Conner JSweeney Erin LAlumkal Joshi Jda Costa Rui M GilWang YuzhuoLin Daniel WTrue Lawrence DDumpit RuthCorey EvaLee John KNelson Peter SXin LiHaffner Michael CMorrissey Colm - The RhoBTB1/Cullin-3 (CUL3) pathway in smooth muscle cells (SMCs) controls the ubiquitination and proteasomal degradation of target proteins that regulate vasodilation, vasoconstriction, and the actin cytoskeleton and, through this, blood pressure (BP) and arterial stiffness. Using proximity labeling coupled with mass spectrometry in A7R5 SMCs, we identified proteins that bound to the C-terminal half of RhoBTB1, which functions as an adaptor to deliver substrates to CUL3. We examined the physiological relevance of one of these substrates, RbFox2. Coimmunoprecipitation validated the interaction of RbFox2 with RhoBTB1. RbFox2 expression was elevated in response to inhibition of the ubiquitination-proteasomal pathway, CUL3 deficiency, and RhoBTB1 inhibition by either siRNA or angiotensin II (ANG). RbFox2 was ubiquitinated in a RhoBTB1- and CUL3-dependent manner, suggesting its regulation through the RhoBTB1/CUL3-dependent ubiquitin-proteasome pathway. Inhibition of RbFox2 impaired the actin cytoskeleton in A7R5 cells and in primary SMCs from RbFox2fl/fl mice and decreased the levels of globular and filamentous actin. ANG increased BP and arterial stiffness of RbFox2fl/fl mice, but the progression of arterial stiffness was halted after SMC-specific RbFox2 deletion despite a continued rise in BP. We conclude that RhoBTB1 and RbFox2 are important regulators of arterial stiffness through a mechanism that influences cytoskeletal integrity. - Source: PubMed
Publication date: 2026/04/02
Kumar GauravChaihongsa NisitaBrozoski Daniel TGolosova DariaVazirabad IbrahimLu Ko-TingWackman Kelsey KSingh Ravi KSigmund Curt D - Alzheimer's disease (AD) is a progressive neurodegenerative age-related disorder characterized by widespread transcriptional deregulation across multiple brain regions. Among the molecular players involved, the transcription factors (TFs) can regulate the expression of AD-related peptides (β-amyloid and tau). We aim to unveil reconstructed TF-centered networks and their dynamics across multiple brain regions. In this study, we conducted an exhaustive differential gene expression analysis, reconstructed TF-TF-centered regulatory networks, and performed master-regulation analyses across multiple regions. We used bulk RNA-seq data from 2,229 post-mortem samples from the ROSMAP, MAYO, and MSBB cohorts. To place these regulatory programs in a disease-relevant context, we integrated protein-protein interaction (PPI) data, experimental TF-target data, and AD-associated genetic risk loci as a translational layer. We assessed TF-centered regulons for 1,605 TFs and identified 354 master-regulators (MR-TFs) across multiple brain regions, including the parahippocampal gyrus, temporal cortex, and cerebellum, which exhibited the highest numbers of regulons. Overall, regulons fell within a moderate size range (median 55 targets), rather than into extensive large networks. Novel MR-TFs, including ADCYAP1, TEAD2, BCL6, MAFF, NFKBIA, were consistently identified as MR-TFs across tissues in AD. Furthermore, GUCY1B1, RBFOX2, and MEF2C were found conserved in the parahippocampal gyrus, inferior frontal gyrus, and posterior cingulate cortex. Additionally, our work identified the well-known AD-related genes BIN1, EGFR, and SPI1 as MR-TFs, reinforcing their functional roles as susceptibility risk markers in AD. This work established an MR-TF-centered integrated regulatory network map of AD, revealing MR-TFs as factors that orchestrate gene deregulation in a region- and cell-context-dependent approach, and providing a robust foundation for mechanistic and translational investigations in neurodegeneration. - Source: PubMed
Publication date: 2026/02/23
Belém-Souza Marcella VitóriaBarra-Matos Gustavode Araújo Gilderlanio Santana