RBFOX3 (NeuN) – An RNA-Binding Splicing Regulator in Neurons OpenAI o3-deep-research-2025-06-26 87 citations 2026-01-15T19:32:05.582562

RBFOX3 (NeuN) – An RNA-Binding Splicing Regulator in Neurons

Gene Identity and Family

RBFOX3 (RNA Binding Fox-1 Homolog 3, UniProt A6NFN3) is a human gene encoding a neuron-specific RNA-binding protein. It belongs to the RBFOX (Fox-1) family of alternative splicing factors, which also includes RBFOX1 and RBFOX2 (www.nature.com). RBFOX3 is also known as Fox-1 homolog C, NeuN antigen, or FOX3 (historically HRNBP3) (www.ncbi.nlm.nih.gov). The protein contains an N-terminal proline-rich region, a central RNA Recognition Motif (RRM domain), and a C-terminal alanine-rich domain (www.ncbi.nlm.nih.gov). This domain architecture is characteristic of RBFOX family proteins and is critical for its RNA-binding and regulatory functions. RBFOX3 is highly conserved across vertebrates and was identified in 2009 as the antigen recognized by the NeuN (Neuronal Nuclei) monoclonal antibody (www.nature.com). NeuN immunoreactivity is specific to post-mitotic neurons, making RBFOX3 a widely used marker for mature neurons in the brain and spinal cord (pubmed.ncbi.nlm.nih.gov) (pubmed.ncbi.nlm.nih.gov). Notably, RBFOX3 is predominantly expressed in the central nervous system and plays a prominent role in neural development and adult brain function (www.ncbi.nlm.nih.gov). Its expression is largely restricted to neurons – for example, it is abundant in brain tissue (RPKM ~11 in RNA-seq data) with much lower levels in most non-neural tissues (www.ncbi.nlm.nih.gov). This brain-specific expression underlies its use as a neuronal marker and hints at specialized functions in the nervous system.

Expression and Subcellular Localization

Within neurons, RBFOX3 is primarily a nuclear protein, consistent with its role in pre-mRNA splicing (pmc.ncbi.nlm.nih.gov). NeuN/RBFOX3 immunostaining strongly labels neuronal nuclei (and to a lesser extent perikarya), indicating that the protein resides in the nucleus where splicing occurs (pubmed.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). However, RBFOX3 exists as multiple isoforms due to alternative splicing of its own transcript (pmc.ncbi.nlm.nih.gov). Importantly, one splicing event adds or removes part of a bipartite nuclear localization signal in the C-terminus, producing distinct isoforms with different steady-state localization (pmc.ncbi.nlm.nih.gov). Nuclear isoforms of RBFOX3 contain the full NLS and concentrate in the nucleus, whereas a cytoplasmic isoform lacks part of the NLS and distributes to the cytoplasm (pmc.ncbi.nlm.nih.gov). In healthy mature neurons, the majority of RBFOX3 is in the nucleus, but studies have noted that under certain conditions the localization can shift. For instance, in HIV-associated neurocognitive disorder (a neurodegenerative condition), RBFOX3 was observed to mislocalize from the nucleus to the cytoplasm (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Since pre-mRNA splicing is nuclear, such mislocalization may effectively downregulate RBFOX3’s splicing activity, contributing to neuronal gene expression deficits in disease (pmc.ncbi.nlm.nih.gov). Apart from pathological cases, RBFOX3 is generally a reliable nuclear marker of neurons. (It is noteworthy that a few neuron types show little or no NeuN expression – e.g. cerebellar Purkinje cells – but this reflects cell-type specific gene regulation rather than a different protein identity (pubmed.ncbi.nlm.nih.gov).) Overall, RBFOX3’s presence in the neuronal nucleus is tightly linked to its function as an RNA-binding regulator of gene expression.

Molecular Function: RNA Binding and Alternative Splicing

RBFOX3 is an RNA-binding protein (RBP) that regulates alternative splicing of pre-mRNAs in neurons (www.ncbi.nlm.nih.gov) (www.nature.com). Like other RBFOX family members, RBFOX3 recognizes a short RNA sequence motif (the consensus (U)GCAUG element) in target transcripts (pmc.ncbi.nlm.nih.gov). This motif is typically located in intronic regions flanking alternative exons. By binding to these elements, RBFOX proteins influence spliceosome activity to either include or skip the exon. The effect is position-dependent: when RBFOX3 binds in an intron downstream of an alternative exon, it generally enhances that exon’s inclusion; binding in the upstream intron causes exon skipping (exclusion) (pmc.ncbi.nlm.nih.gov). This functional rule has been demonstrated in several neuronally expressed genes. For example, RBFOX3 directly targets the pre-mRNA of Numb, a cell fate determinant, by binding to two UGCAUG sites in the intron upstream of an alternative exon (exon 12 of Numb) (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). RBFOX3 binding there represses inclusion of that exon, promoting the production of a particular Numb isoform crucial for neuronal differentiation (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). In contrast, RBFOX3 can promote exon inclusion in other targets; a notable case is the Tau (MAPT) gene, where an intronic UGCAUG motif downstream of Tau’s exon 10 mediates RBFOX3-dependent inclusion of that exon (pubmed.ncbi.nlm.nih.gov). Tau exon 10 encodes a microtubule-binding repeat, and its inclusion generates the 4-repeat Tau isoform. A 2018 study confirmed that RBFOX3 (NeuN) binds Tau pre-mRNA and enhances exon 10 splicing, with deletion of RBFOX3’s RRM or its binding sites abolishing this effect (pubmed.ncbi.nlm.nih.gov). Thus, RBFOX3 can differentially regulate splicing outcomes, contributing to the cell-type-specific transcript diversity in neurons.

On a molecular level, RBFOX3 operates as part of larger splicing complexes. It often works in concert with other splicing regulators and can auto-regulate or cross-regulate splicing within its family. Indeed, RBFOX3 has been shown to modulate splicing of RBFOX2 pre-mRNA: nuclear RBFOX3 isoforms promote inclusion of a “poison” exon in RBFOX2 transcripts, triggering nonsense-mediated decay of RBFOX2 mRNA (pmc.ncbi.nlm.nih.gov). This creates a feedback loop whereby RBFOX3 limits the production of RBFOX2 protein in neurons. Such fine-tuning underscores that RBFOX3 is not just a passive marker protein but an active regulator of gene expression programs. Genome-wide studies have identified many RBFOX-binding elements in brain mRNAs, particularly in genes related to synaptic function and ion channels (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). In fact, de novo motif analyses in neurons often recover the UGCAUG sequence, highlighting RBFOX1/2/3 as central players in neuron-specific splicing networks (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Through its RRM domain and binding specificity, RBFOX3 helps sculpt the mRNA output of neural genes, affecting the proteome of the brain.

Role in Neuronal Development and Function

RBFOX3 plays a critical role in neuron maturation, connectivity, and circuit function. It is expressed as neurons exit the cell cycle and differentiate, and accumulating evidence indicates it actively promotes neuronal differentiation. In an experimental model of spinal cord development (chick embryo), loss of RBFOX3 blocked proper neuronal maturation: silencing RBFOX3 led to aberrant inclusion of the Numb exon discussed above, and as a result, post-mitotic neurons failed to fully differentiate (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Restoration of the correct Numb splicing isoform could rescue the differentiation defect, proving that RBFOX3’s splicing activity is required for normal neuron development (Kim et al., J. Cell Biol. 2013) (pmc.ncbi.nlm.nih.gov). Consistently, RBFOX3 expression is developmentally regulated in the brain – it rises as neurons mature (pmc.ncbi.nlm.nih.gov) – and is largely confined to mature neurons (it is not expressed in neural progenitor cells) (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). This timing suggests RBFOX3 helps coordinate the transition from a progenitor transcriptome to a mature neuronal transcriptome, by switching on the splicing of neuron-specific exons.

In the adult brain, RBFOX3 continues to be important for maintaining healthy neural circuits. Knockout mouse studies have been instrumental in revealing RBFOX3’s functions. Mice completely lacking Rbfox3 (Rbfox3^-/-) are viable but exhibit a range of neural deficits. Behaviourally, Rbfox3 knockout mice show impaired learning and memory, heightened seizure susceptibility, and sensory abnormalities. For example, a 2016 study reported that Rbfox3^-/- mice had significant cognitive impairments in spatial learning tasks and displayed cold hyperalgesia (abnormally increased pain sensation to cold) compared to wild-type (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Another study (2015) noted that Rbfox3 knockouts had increased seizure susceptibility (lower threshold for seizures) along with reduced anxiety-like behavior (pubmed.ncbi.nlm.nih.gov), consistent with RBFOX3’s proposed link to human epilepsy (see next section). These behavioral phenotypes correlate with synaptic and circuit-level abnormalities: in the hippocampus – a region critical for learning and memory – Rbfox3^-/- mice have defects in synaptic plasticity and circuit balance (pubmed.ncbi.nlm.nih.gov). Electrophysiological recordings showed their hippocampal synapses cannot sustain normal long-term depression (LTD) and have abnormally enhanced basal transmission (pmc.ncbi.nlm.nih.gov). Notably, knockout mice exhibited an increased frequency of spontaneous excitatory synaptic events onto dentate gyrus neurons (with normal amplitude), indicating an excess of functional excitatory synapses or release probability (pubmed.ncbi.nlm.nih.gov). Dendritic spine counting confirmed that spine density on these neurons was significantly higher in knockouts than in controls (pubmed.ncbi.nlm.nih.gov). Paradoxically, while there were more synaptic contacts, the quality of synaptic plasticity was reduced – suggesting the synapses formed without RBFOX3 are perhaps aberrant or immature. Indeed, Rbfox3^-/- brains had an increased number of excitatory synapses but showed deficits in synaptic strength modulation (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). These findings illustrate that RBFOX3 is required for proper synaptic organization and function, likely by ensuring the correct splicing of synaptic protein mRNAs.

RBFOX3 also influences neurogenesis in the adult brain. In the adult hippocampus, new neurons are continuously generated in the dentate gyrus, a process tied to learning and mood regulation. Rbfox3 knockout mice have reduced adult neurogenesis in the dentate gyrus: they show significantly fewer proliferating neural progenitors (Ki67-positive) and immature neurons (DCX-positive) compared to wild-type mice (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). In one analysis, Ki67^+ cell counts in the dentate gyrus of Rbfox3^-/- mice were only about half of those in normal mice (p < 0.001) (pmc.ncbi.nlm.nih.gov), indicating a marked drop in the generation of new neurons. This reduction in neurogenesis is thought to contribute to the impaired learning observed in knockouts (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Interestingly, RBFOX3 itself is not expressed in the progenitors but in the new neurons as they differentiate (pmc.ncbi.nlm.nih.gov), implying that the microenvironment or feedback from mature neurons (where RBFOX3 acts) is necessary to support neurogenesis. Together, these developmental and physiological studies demonstrate that RBFOX3 is essential for neuronal maturation, the formation of balanced neural circuits, and ongoing adult brain plasticity. Its absence causes specific synaptic and behavioral pathologies, underscoring its precise role in the nervous system.

It should be noted that RBFOX3’s importance can vary between neural circuits. For example, in the retina, RBFOX3 is expressed in certain neurons (ganglion, amacrine, and horizontal cells) but not others (pmc.ncbi.nlm.nih.gov). Deleting Rbfox3 leads to a thinner inner plexiform layer (the synaptic layer) in the retina, yet the overall visual function (both image-forming vision and reflexive light responses) remains largely normal (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Knockout mice had a normal number of retinal ganglion cells and intact optic nerve projections, and they performed normally in visual assays (pmc.ncbi.nlm.nih.gov). This suggests that unlike in the hippocampus, RBFOX3 is dispensable for basic visual function – possibly because other RBFOX family members (or splicing factors) compensate in retinal neurons, or because the splicing events controlled by RBFOX3 are not critical to vision. Thus, the requirement for RBFOX3 can be context-specific, being crucial in some brain regions (hippocampus, cortex) but not in others (retina). Determining the tissue-specific targets of RBFOX3 may explain these differences.

Pathology and Clinical Implications

Given its key role in neuronal gene regulation, it is not surprising that RBFOX3 has been implicated in neurological diseases. Mutations or dysfunction of RBFOX3 are linked to several neurodevelopmental and neuropsychiatric disorders. Human genetic studies have found RBFOX3 variants associated with autism spectrum disorder, epilepsy, and intellectual disability (pmc.ncbi.nlm.nih.gov). In particular, RBFOX3 has been flagged in analyses of autism and cognitive impairment cases, though such mutations are relatively rare. A 2015 review noted that “dysfunctional RBFOX3” (e.g. due to mutation or altered expression) can lead to cognitive deficits and seizure phenotypes, echoing what is seen in knockout mice (pmc.ncbi.nlm.nih.gov). Indeed, Rbfox3^-/- mice show epilepsy-like hyperexcitability and memory deficits that mirror human epilepsy and intellectual disability symptoms (pubmed.ncbi.nlm.nih.gov). This suggests a causal relationship: RBFOX3-related splicing defects disrupt neural circuit balance, contributing to these disorders (pubmed.ncbi.nlm.nih.gov) (pubmed.ncbi.nlm.nih.gov). For example, imbalances in excitatory/inhibitory synapses and impaired synaptic plasticity in RBFOX3-null mice may model the network dysfunction underlying epilepsy (pubmed.ncbi.nlm.nih.gov). Some genome-wide association studies have also linked RBFOX3 polymorphisms to traits like sleep latency (difficulty falling asleep) (pmc.ncbi.nlm.nih.gov), highlighting that even common variants in RBFOX3 can have measurable effects on human neurophysiology (in this case, sleep regulation).

RBFOX3 expression or localization can change in brain injuries and neurodegenerative conditions. Neuropathological studies show that NeuN immunoreactivity is sometimes lost or reduced in diseased neurons, which can complicate its use as a neuron marker. For instance, prolonged seizures, ischemia, or other neuronal stressors can cause a temporary loss of NeuN (RBFOX3) staining in affected neurons (pubmed.ncbi.nlm.nih.gov). This likely reflects either downregulation of RBFOX3 or epitope masking, and has led experts to caution that “NeuN immunoreactivity should not be the sole criterion for neuronal counts in pathologic conditions” (pubmed.ncbi.nlm.nih.gov). In HIV-associated neurocognitive disorder, as mentioned above, many neurons showed RBFOX3 relocated to the cytoplasm rather than nucleus (pmc.ncbi.nlm.nih.gov). Such mislocalization in diseased brains could mean that neurons are not performing normal splicing of key transcripts, potentially contributing to neurocognitive decline. Additionally, RBFOX3 has been proposed as a marker to assess neuronal loss: for example, reduced NeuN staining is used to quantify neuron loss in models of stroke or neurodegeneration (pubmed.ncbi.nlm.nih.gov). However, because NeuN can be dynamically regulated, scientists carefully interpret what “NeuN-negative” means in diseased tissue (it may indicate a non-neuronal cell, a lost neuron, or a neuron that has downregulated RBFOX3 due to stress).

Beyond the nervous system, emerging research has found RBFOX3 involvement in cancers, although RBFOX3 is normally not expressed in most healthy non-neural tissues. Interestingly, RBFOX3 has been detected in some tumor types and may play a functional role in cancer cell biology. For example, hepatocellular carcinoma (HCC) cells aberrantly express RBFOX3 at high levels, and this appears to promote tumor growth: one study found RBFOX3 was upregulated in HCC tumors and cell lines, and knocking it down inhibited cancer cell proliferation (pubmed.ncbi.nlm.nih.gov). RBFOX3 knockdown also made the HCC cells more sensitive to the chemotherapy drug 5-fluorouracil, increasing drug-induced apoptosis via the PI3K/Akt and caspase pathways (suggesting RBFOX3 helps confer chemo-resistance) (pubmed.ncbi.nlm.nih.gov). These findings imply RBFOX3 might act as a pro-survival or oncogenic factor in certain cancers, possibly by splicing tumor-related transcripts. Similarly, in lung cancer models, RBFOX3 was shown to impact cell migration and invasion: TGF-β signaling can suppress RBFOX3 expression, which in turn promotes an epithelial–mesenchymal transition (EMT) phenotype (www.sciencedirect.com). In that context, RBFOX3 normally may maintain expression of epithelial junction proteins (like Claudin-1) by regulating their mRNA – loss of RBFOX3 led to reduced Claudin-1 and increased EMT/invasion in lung cancer cells (pmc.ncbi.nlm.nih.gov). These are active areas of research, but they point to RBFOX3’s splicing activity as potentially relevant outside the brain, especially in diseases like cancer. It is unusual for a “neural-specific” splicing factor to be co-opted in tumors, and it underscores the pleiotropic impact that alternative splicing regulators can have when dysregulated.

Applications in Research and Diagnosis

RBFOX3/NeuN as a Neuronal Marker: In neuroscience research and neuropathology, RBFOX3’s most widespread use is as the NeuN antigen – a diagnostic marker of neurons. Antibodies against NeuN (RBFOX3 protein) reliably label neuronal nuclei in tissue sections, allowing researchers and clinicians to identify neurons and quantify neuronal density. For over two decades, NeuN immunostaining has been a gold-standard method to distinguish neurons from glial cells in histological samples (pubmed.ncbi.nlm.nih.gov). This is especially useful in studies of neurodegeneration (e.g. counting surviving neurons after an experimental stroke or in an Alzheimer’s brain) and development (e.g. verifying neuronal differentiation in stem cell cultures). NeuN staining is also used in pathology labs to help diagnose neuronal tumors or lesions. For example, Merkel cell carcinoma (MCC), an aggressive neuroendocrine skin carcinoma, can express neuronal markers. A 2021 analysis of 15 MCC cases showed robust NeuN (RBFOX3) positivity in the majority of these tumors, whereas normal Merkel cells in skin do not express NeuN (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). This suggests that aberrant RBFOX3 expression can indicate neuronal or neuroendocrine differentiation in a tumor and can aid in tumor identification. Likewise, NeuN immunohistochemistry is sometimes included in panels to identify metastatic neuroblastomas or other small round cell tumors as neuronal in origin. Researchers have to be cautious interpreting such staining, but it has practical value in diagnosing cancers with neuronal features.

RBFOX3 in Therapeutic Research: Understanding RBFOX3’s role has potential therapeutic implications. In neurological disorders where RBFOX3 or its targets are affected (such as epilepsy or autism), strategies to modulate alternative splicing could be beneficial. For instance, if a particular mis-spliced isoform due to RBFOX3 deficiency is pathogenic, one could imagine antisense oligonucleotides to correct that splicing. While this is still speculative, the principle has precedent in other splicing-related diseases (e.g. Spinraza for SMN2 splicing in spinal muscular atrophy). Additionally, the discovery of RBFOX3’s impact on cancer cell survival opens the question of whether RBFOX3 could be a drug target in oncology. Inhibiting RBFOX3 function (or mimicking its loss) might sensitize tumors to chemotherapy, as shown in HCC cells (pubmed.ncbi.nlm.nih.gov). Conversely, protecting or enhancing RBFOX3 activity in neurons might be neuroprotective in conditions like neuroAIDS (HIV-related cognitive disorder) or after brain injury, where RBFOX3 mislocalization correlates with neuronal dysfunction (pmc.ncbi.nlm.nih.gov). These ideas are in early stages, but they show how current research is translating the biology of RBFOX3 into real-world applications.

Expert Perspectives: Recent authoritative reviews emphasize that RBFOX3 is no longer viewed as just a static neuron marker, but as a dynamic regulator influencing neural phenotype (pubmed.ncbi.nlm.nih.gov). Wei Duan and colleagues (2015) dubbed it “from Neuronal Marker to Splicing Regulator,” highlighting that the protein’s identity as an RBP provides new perspective on why NeuN staining can change in certain states (pubmed.ncbi.nlm.nih.gov). They urge careful interpretation of NeuN in pathological samples, noting that changes in RBFOX3 expression or localization might themselves contribute to disease processes, rather than simply reflecting neuron presence (pubmed.ncbi.nlm.nih.gov). In 2024, a comprehensive review of alternative splicing in health and disease reiterated RBFOX3’s key role in neural development, using it as an example of how splicing factors drive cell fate. That review recaps how RBFOX3-mediated exon skipping in Numb is required for neuronal differentiation in the developing cortex (www.nature.com), underscoring the conserved mechanism initially discovered in earlier animal studies. Experts agree that RBFOX3 and its family unify two important aspects of neurobiology: the molecular control of gene expression (through AS regulation) and the cellular identity of neurons. In summary, RBFOX3 is a pivotal neuron-specific RBP that binds target mRNAs to regulate their splicing, thereby shaping neuronal gene expression, guiding neuron maturation, and maintaining synaptic function. Its discovery as NeuN’s antigen has bridged classic neuroanatomy with modern genomics, and ongoing research (2023–2024) continues to uncover its broader roles in both the nervous system and disease contexts. Each new finding – from adult neurogenesis deficits to cancer cell dependencies – highlights the importance of RBFOX3’s precise activity for normal cellular function, making it a fascinating subject of study in functional genomics and biomedicine.

References: (Key references are provided inline with citations, including publication year and source. For example, Lin et al., 2016, PLoS One (pmc.ncbi.nlm.nih.gov) and Lin et al., 2016, PLoS One (pmc.ncbi.nlm.nih.gov) document RBFOX3’s role in adult neurogenesis and synaptic regulation; Kim et al., 2013, J. Cell Biol. (pmc.ncbi.nlm.nih.gov) demonstrates RBFOX3’s regulation of Numb splicing in neuron differentiation; Dredge et al., 2011, PLoS One (pmc.ncbi.nlm.nih.gov) describes RBFOX3 isoforms and cross-regulation of RBFOX2; and Duan et al., 2015, Mol Neurobiol* (pubmed.ncbi.nlm.nih.gov) provides a review of RBFOX3/NeuN’s identity and significance. Additional contemporary sources (2016–2024) have been cited to illustrate recent developments and applications.)

Citations

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  22. AnnotationURLCitation(end_index=7295, start_index=7123, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=repressor%20of%20alternative%20splicing%20depending,same%20element%20upstream%20of%20the')
  23. AnnotationURLCitation(end_index=7726, start_index=7562, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=Repression%20of%20exon%2012%20splicing,UGCAUG%20element%20in%20chicken%20embryos')
  24. AnnotationURLCitation(end_index=7850, start_index=7727, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=Rbfox3%20represses%20exon%2012%20of,see')
  25. AnnotationURLCitation(end_index=8155, start_index=8002, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=found%20to%20be%20a%20target,the%20relevant%20Numb%20splice%20isoform')
  26. AnnotationURLCitation(end_index=8320, start_index=8156, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=Repression%20of%20exon%2012%20splicing,UGCAUG%20element%20in%20chicken%20embryos')
  27. AnnotationURLCitation(end_index=8684, start_index=8542, title='Rbfox3/NeuN Regulates Alternative Splicing of Tau Exon 10 - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/30475774/#:~:text=splicing%20is%20unknown,in%20the%20excitotoxic%20mouse%20brains')
  28. AnnotationURLCitation(end_index=9098, start_index=8956, title='Rbfox3/NeuN Regulates Alternative Splicing of Tau Exon 10 - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/30475774/#:~:text=splicing%20is%20unknown,in%20the%20excitotoxic%20mouse%20brains')
  29. AnnotationURLCitation(end_index=9804, start_index=9648, title='NeuN/Rbfox3 Nuclear and Cytoplasmic Isoforms Differentially Regulate Alternative Splicing and Nonsense-Mediated Decay of Rbfox2 - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3126832/#:~:text=nuclear%20localization%20signal,Rbfox3%20through%20a%20novel%20mechanism')
  30. AnnotationURLCitation(end_index=10313, start_index=10181, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=impairments,decreased%20and%20the%20density%20of')
  31. AnnotationURLCitation(end_index=10481, start_index=10314, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=cognitive%20behaviors%2C%20were%20altered%20in,decreased%20and%20the%20density%20of')
  32. AnnotationURLCitation(end_index=10794, start_index=10643, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=the%20hippocampal%20DG,brain%20diseases%20with%20disrupted%20RBFOX3')
  33. AnnotationURLCitation(end_index=10972, start_index=10795, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=Rbfox3%20deletion%20causes%20abnormal%20exon,and%20increases%20excitatory%20synaptic%20number')
  34. AnnotationURLCitation(end_index=11823, start_index=11668, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=development%20remain%20elusive,the%20relevant%20Numb%20splice%20isoform')
  35. AnnotationURLCitation(end_index=11977, start_index=11824, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=found%20to%20be%20a%20target,the%20relevant%20Numb%20splice%20isoform')
  36. AnnotationURLCitation(end_index=12359, start_index=12186, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=of%20postmitotic%20neurons,neuronal%20differentiation%20during%20vertebrate%20development')
  37. AnnotationURLCitation(end_index=12652, start_index=12464, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=neurodevelopment%2C%20the%20function%20of%20RBFOX3,hyperalgesia%20and%20impaired%20cognitive%20abilities')
  38. AnnotationURLCitation(end_index=12939, start_index=12752, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=match%20at%20L650%20hippocampal%20neurogenesis,environment%20for%20hippocampal%20neurogenesis%20through')
  39. AnnotationURLCitation(end_index=13110, start_index=12940, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=hippocampal%20neurogenesis%20,environment%20for%20hippocampal%20neurogenesis%20through')
  40. AnnotationURLCitation(end_index=14107, start_index=13929, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=plasticity%2C%20and%20synaptogenesis%20in%20Rbfox3,hippocampal%20dentate%20gyrus%20of%20Rbfox3')
  41. AnnotationURLCitation(end_index=14249, start_index=14108, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=synaptogenesis,synaptic%20plasticity%20and%20density%20in')
  42. AnnotationURLCitation(end_index=14594, start_index=14413, title='RBFOX3/NeuN is Required for Hippocampal Circuit Balance and Function - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/26619789/#:~:text=Rbfox3%20knockout%20mice%20displayed%20increased,results%20demonstrate%20anatomical%20and%20functional')
  43. AnnotationURLCitation(end_index=15081, start_index=14899, title='RBFOX3/NeuN is Required for Hippocampal Circuit Balance and Function - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/26619789/#:~:text=knockout%20mice%20showed%20increased%20expression,results%20demonstrate%20anatomical%20and%20functional')
  44. AnnotationURLCitation(end_index=15408, start_index=15246, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=match%20at%20L515%20increased%20synaptic,mice%20%28Fig%205d%29%2C%20consistent')
  45. AnnotationURLCitation(end_index=15824, start_index=15642, title='RBFOX3/NeuN is Required for Hippocampal Circuit Balance and Function - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/26619789/#:~:text=knockout%20mice%20showed%20increased%20expression,results%20demonstrate%20anatomical%20and%20functional')
  46. AnnotationURLCitation(end_index=16096, start_index=15956, title='RBFOX3/NeuN is Required for Hippocampal Circuit Balance and Function - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/26619789/#:~:text=pathway,results%20demonstrate%20anatomical%20and%20functional')
  47. AnnotationURLCitation(end_index=16585, start_index=16414, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=deletion%20of%20Rbfox3%20resulted%20in,increased%20numbers%20of%20excitatory%20synapses')
  48. AnnotationURLCitation(end_index=16760, start_index=16586, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=an%20environment%20for%20normal%20neurogenesis,and%20excitatory%20synapses%20increase%20in')
  49. AnnotationURLCitation(end_index=17516, start_index=17339, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=dysfunctional%20neurogenesis%20in%20the%20hippocampal,both%20markers%20in%20the%20hippocampal')
  50. AnnotationURLCitation(end_index=17685, start_index=17517, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=cells%20were%20quantified%20in%20the,sections%2C%206%20sections%2Fmice%2C%207%20mice')
  51. AnnotationURLCitation(end_index=17997, start_index=17820, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=showing%20different%20stages%20of%20postnatal,sections%2C%206%20sections%2Fmice%2C%207%20mice')
  52. AnnotationURLCitation(end_index=18332, start_index=18161, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=Since%20learning%20deficits%20were%20consistently,we%20further%20investigated%20whether')
  53. AnnotationURLCitation(end_index=18504, start_index=18333, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=deletion%20of%20Rbfox3%20resulted%20in,increased%20numbers%20of%20excitatory%20synapses')
  54. AnnotationURLCitation(end_index=18803, start_index=18616, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=match%20at%20L650%20hippocampal%20neurogenesis,environment%20for%20hippocampal%20neurogenesis%20through')
  55. AnnotationURLCitation(end_index=19630, start_index=19459, title='RBFOX3/NeuN is dispensable for visual function - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5798780/#:~:text=balance%2C%20as%20well%20as%20neurogenesis,ganglion%20cells%2C%20amacrine%20cells%20and')
  56. AnnotationURLCitation(end_index=20010, start_index=19838, title='RBFOX3/NeuN is dispensable for visual function - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5798780/#:~:text=the%20retina%20and%20specifically%20expressed,is%20dispensable%20for%20visual%20function')
  57. AnnotationURLCitation(end_index=20175, start_index=20011, title='RBFOX3/NeuN is dispensable for visual function - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5798780/#:~:text=reduction%20in%20the%20thickness%20of,is%20dispensable%20for%20visual%20function')
  58. AnnotationURLCitation(end_index=20482, start_index=20318, title='RBFOX3/NeuN is dispensable for visual function - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5798780/#:~:text=reduction%20in%20the%20thickness%20of,is%20dispensable%20for%20visual%20function')
  59. AnnotationURLCitation(end_index=21565, start_index=21400, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=Dysfunction%20of%20RBFOX3%20has%20been,homozygous%20knockout%20mice%20and%20their')
  60. AnnotationURLCitation(end_index=22056, start_index=21891, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=Dysfunction%20of%20RBFOX3%20has%20been,homozygous%20knockout%20mice%20and%20their')
  61. AnnotationURLCitation(end_index=22383, start_index=22207, title='RBFOX3/NeuN is Required for Hippocampal Circuit Balance and Function - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/26619789/#:~:text=RBFOX3%20mutations%20are%20linked%20to,neurotransmitter%20release%20probability%20and%20dendritic')
  62. AnnotationURLCitation(end_index=22618, start_index=22522, title='RBFOX3/NeuN is Required for Hippocampal Circuit Balance and Function - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/26619789/#:~:text=Display%20options')
  63. AnnotationURLCitation(end_index=22792, start_index=22619, title='RBFOX3/NeuN is Required for Hippocampal Circuit Balance and Function - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/26619789/#:~:text=knockout%20mice%20showed%20increased%20expression,may%20provide%20mechanistic%20insights%20for')
  64. AnnotationURLCitation(end_index=23140, start_index=22959, title='RBFOX3/NeuN is Required for Hippocampal Circuit Balance and Function - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/26619789/#:~:text=Rbfox3%20knockout%20mice%20displayed%20increased,results%20demonstrate%20anatomical%20and%20functional')
  65. AnnotationURLCitation(end_index=23414, start_index=23278, title='Genetic variants in RBFOX3 are associated with sleep latency - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5027680/#:~:text=PMC%20pmc,PMCID%3A%20PMC5027680%20PMID%3A%2027142678')
  66. AnnotationURLCitation(end_index=24081, start_index=23956, title='Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/25680637/#:~:text=for%20the%20past%20two%20decades,This%20review')
  67. AnnotationURLCitation(end_index=24465, start_index=24296, title='Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/25680637/#:~:text=protein%20remained%20elusive%20for%2017,diseases%20and%20specific%20physiological%20states')
  68. AnnotationURLCitation(end_index=24797, start_index=24608, title='Altered Subcellular Localization of the NeuN/Rbfox3 RNA Splicing Factor in HIV-Associated Neurocognitive Disorders (HAND) - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3880598/#:~:text=nuclear%20localization%2C%20we%20found%20significantly,downregulation%20of%20neuronal%20gene%20expression')
  69. AnnotationURLCitation(end_index=25317, start_index=25154, title='Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/25680637/#:~:text=for%20the%20past%20two%20decades,caution%20when%20applying%20NeuN%20immunoreactivity')
  70. AnnotationURLCitation(end_index=26271, start_index=26111, title='RBFOX3 Regulates the Chemosensitivity of Cancer Cells to 5-Fluorouracil via the PI3K/AKT, EMT and Cytochrome-C/Caspase Pathways - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/29689552/#:~:text=Results%3A%20RBFOX3%20was%20found%20to,and%20enhanced%20the%20apoptosis%20induced')
  71. AnnotationURLCitation(end_index=26652, start_index=26492, title='RBFOX3 Regulates the Chemosensitivity of Cancer Cells to 5-Fluorouracil via the PI3K/AKT, EMT and Cytochrome-C/Caspase Pathways - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/29689552/#:~:text=Results%3A%20RBFOX3%20was%20found%20to,and%20enhanced%20the%20apoptosis%20induced')
  72. AnnotationURLCitation(end_index=27191, start_index=27016, title='Transforming Growth Factor-β-Induced RBFOX3 Inhibition Promotes Epithelial-Mesenchymal Transition of Lung Cancer Cells - ScienceDirect', type='url_citation', url='https://www.sciencedirect.com/science/article/pii/S1016847823050744#:~:text=...main%20contentSkip%20to%20article%20,0150Get%20rights%20and%20content')
  73. AnnotationURLCitation(end_index=27541, start_index=27414, title='RBFOX3 regulates Claudin-1 expression in human lung tissue via attenuation of proteasomal degradation - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5322747/#:~:text=of%20proteasomal%20degradation%20,%E2%9C%89')
  74. AnnotationURLCitation(end_index=28565, start_index=28425, title='Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/25680637/#:~:text=exclusively%20in%20post,More%20importantly%2C%20despite%20the')
  75. AnnotationURLCitation(end_index=29313, start_index=29173, title='NeuN, a DNA-binding neuron-specific protein expressed by Merkel cell carcinoma: analysis of 15 cases - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC8720396/#:~:text=malignancies,tumors%2C%20in%20Merkel%20cell%20carcinomas')
  76. AnnotationURLCitation(end_index=29438, start_index=29314, title='NeuN, a DNA-binding neuron-specific protein expressed by Merkel cell carcinoma: analysis of 15 cases - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC8720396/#:~:text=Fifteen%20cases%20of%20Merkel%20cell,The')
  77. AnnotationURLCitation(end_index=30900, start_index=30740, title='RBFOX3 Regulates the Chemosensitivity of Cancer Cells to 5-Fluorouracil via the PI3K/AKT, EMT and Cytochrome-C/Caspase Pathways - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/29689552/#:~:text=Results%3A%20RBFOX3%20was%20found%20to,and%20enhanced%20the%20apoptosis%20induced')
  78. AnnotationURLCitation(end_index=31330, start_index=31141, title='Altered Subcellular Localization of the NeuN/Rbfox3 RNA Splicing Factor in HIV-Associated Neurocognitive Disorders (HAND) - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3880598/#:~:text=nuclear%20localization%2C%20we%20found%20significantly,downregulation%20of%20neuronal%20gene%20expression')
  79. AnnotationURLCitation(end_index=31829, start_index=31660, title='Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/25680637/#:~:text=protein%20remained%20elusive%20for%2017,diseases%20and%20specific%20physiological%20states')
  80. AnnotationURLCitation(end_index=32225, start_index=32044, title='Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/25680637/#:~:text=diseases%20and%20specific%20physiological%20states,caution%20when%20applying%20NeuN%20immunoreactivity')
  81. AnnotationURLCitation(end_index=32617, start_index=32448, title='Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/25680637/#:~:text=protein%20remained%20elusive%20for%2017,diseases%20and%20specific%20physiological%20states')
  82. AnnotationURLCitation(end_index=33098, start_index=32944, title='Alternative splicing and related RNA binding proteins in human health and disease | Signal Transduction and Targeted Therapy', type='url_citation', url='https://www.nature.com/articles/s41392-024-01734-2#:~:text=mammalian%20cerebral%20cortex%20development,93%20%2C%20106%2C95%20%2C%20108')
  83. AnnotationURLCitation(end_index=34360, start_index=34195, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=Dysfunction%20of%20RBFOX3%20has%20been,homozygous%20knockout%20mice%20and%20their')
  84. AnnotationURLCitation(end_index=34578, start_index=34397, title='Neuronal Splicing Regulator RBFOX3 (NeuN) Regulates Adult Hippocampal Neurogenesis and Synaptogenesis - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC5049801/#:~:text=differs%20developmentally%20for%20distinct%20brain,results%20demonstrate%20the%20important%20role')
  85. AnnotationURLCitation(end_index=34858, start_index=34685, title='Rbfox3-regulated alternative splicing of Numb promotes neuronal differentiation during development - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3575530/#:~:text=of%20postmitotic%20neurons,neuronal%20differentiation%20during%20vertebrate%20development')
  86. AnnotationURLCitation(end_index=35126, start_index=34970, title='NeuN/Rbfox3 Nuclear and Cytoplasmic Isoforms Differentially Regulate Alternative Splicing and Nonsense-Mediated Decay of Rbfox2 - PMC', type='url_citation', url='https://pmc.ncbi.nlm.nih.gov/articles/PMC3126832/#:~:text=nuclear%20localization%20signal,Rbfox3%20through%20a%20novel%20mechanism')
  87. AnnotationURLCitation(end_index=35407, start_index=35226, title='Novel Insights into NeuN: from Neuronal Marker to Splicing Regulator - PubMed', type='url_citation', url='https://pubmed.ncbi.nlm.nih.gov/25680637/#:~:text=diseases%20and%20specific%20physiological%20states,caution%20when%20applying%20NeuN%20immunoreactivity')