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
- The RhoBTB1-Cullin3 (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 labelling coupled with mass spectrometry in A7R5 SMCs, we identified proteins which bound to the C-terminal half of RhoBTB1 which functions as an adapter to deliver substrates to CUL3. We examined the physiological relevance of one of these substrates, RbFox2. Co-immunoprecipitation 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 SMC from RbFox2Flox/Flox (RbFox2F/F) mice and decreased the levels of globular and filamentous actin. ANG increased BP and arterial stiffness of RbFox2F/F 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 - SCNα genes encode components of voltage-gated sodium channels that are crucial for generating electrical signals. Humans have ten paralogous SCNα genes, some of which contain duplicated mutually exclusive exons 5a and 5b. In reconstructing their evolutionary history, we found multiple unannotated copies of exon 5 in distant species and showed that exon 5 duplication goes back to a common ancestor of the SCNα gene family. We characterized splicing patterns of exons 5a and 5b across tissues, tumors, and developmental stages, and demonstrated that the nonsense mediated decay (NMD) system is not the major factor contributing to their mutually exclusive choice. Comparison of SCN2A, SCN3A, SCN5A, and SCN9A intronic nucleotide sequences revealed multiple Rbfox2 binding sites and two highly conserved intronic splicing regulatory elements (ISRE) that are shared between paralogs. Minigene mutagenesis and blockage by antisense oligonucleotides showed that the formation of RNA structure between ISRE promotes exon 5b skipping in SCN9A. The inclusion of exon 5b is also suppressed in siRNA-mediated knockdown of Rbfox2, which makes the collective action of RNA structure and Rbfox2 compatible with the model of a structural RNA bridge. ISRE sequences are conserved from human to elephant shark and may represent an ancient, evolutionarily conserved regulatory mechanism. Our results demonstrate the power of comparative sequences analysis in application to paralogs for elucidating splicing regulatory programs. - Source: PubMed
Publication date: 2026/02/19
Chernyavskaya EkaterinaVorobeva MargaritaSpirin Sergei ASkvortsov Dmitry APervouchine Dmitri - Colorectal cancer (CRC) is the second most lethal cancer and metastatic dissemination of CRC cells, which predominantly occurs to the liver, is the principal cause of death. Many studies have highlighted the role of CRC-derived small extracellular vesicles (CRC-sEVs) in priming the pre-metastatic niche (PMN) in the liver, promoting morpho-functional alterations which pave the way for the establishment of a favourable microenvironment for future organ colonization by metastatic cells. Our research group demonstrated the effects of CRC-sEVs in promoting the epithelial-to-mesenchymal transition (EMT) of healthy human hepatocytes. In this study, we focused our attention on the long non-coding RNA H19 (lncH19), an oncogenic non-coding RNA whose role in CRC progression has been widely documented. Our data demonstrated that lncH19 is specifically loaded inside CRC-sEVs, carrying with it the RNA binding Fox-1 Homolog 2 (RBFOX2). The treatment of healthy human hepatocytes with CRC-sEVs allows the horizontal transfer of the complex that conveys a pro-EMT post-transcriptional modulation of RBFOX2 target genes. - Source: PubMed
Publication date: 2026/02/17
Loria MarcoAnello DeniseCordaro AuroraZichittella ChiaraFontana SimonaAlessandro RiccardoConigliaro Alice - Cardiac hypertrophy represents a complex remodeling process involving extensive reprogramming of gene expression. While transcriptional regulation has been well characterized, post-transcriptional RNA processing has recently emerged as a crucial determinant of cardiac homeostasis. This review summarizes current knowledge of RNA modifications, alternative splicing, mRNA stability, and RNA editing in physiological and pathological hypertrophy. We highlight key epitranscriptomic marks such as N6-methyladenosine (mA), 5-methylcytosine (mC), and 7-methylguanosine (mG), as well as the functions of RNA-binding proteins and adenosine deaminases acting on RNA (ADAR1/2). In exercise-induced hypertrophy, RNA processing contributes to adaptive remodeling by supporting sarcomere organization, calcium handling, and survival pathways, exemplified by RBFOX2-dependent splicing of CACNA1C, RBM20-directed regulation of titin isoforms, and METTL14-mediated mA signaling that enhances Akt activity. Conversely, pathological stress leads to dysregulated RNA programs that promote maladaptive remodeling through aberrant splice variants, perturbation of circular RNAs, and persistent pro-inflammatory signaling, thereby facilitating contractile dysfunction and progression to heart failure. Context-dependent regulators, including METTL3, YTHDF2, RBM24, and ADAR2, orchestrate the balance between adaptive and maladaptive responses. Targeting specific nodes, such as METTL3-driven mA methylation or RBM24-dependent splicing fidelity, may provide innovative therapeutic strategies. Advances in RNA-targeted interventions, including ADAR-mediated editing and small molecule inhibitors of methyltransferases, highlight the translational potential of RNA processing as a novel avenue for precision cardiovascular therapy. - Source: PubMed
Peng MenglingFu YuQin CongJin JingpengZhou Shanshan