FOXR1 Antibody

What is FOXR1 and why is it significant in biological research?

FOXR1 (Forkhead Box R1) is a member of the FOX family of transcription factors, which are characterized as monomeric, helix-turn-helix proteins with a core DNA-binding domain of approximately 110 amino acids . Unlike many other FOX family members, FOXR1 lacks the C-terminal basic region that is commonly found in this protein family .

The significance of FOXR1 in biological research has been highlighted by several findings. First, FOXR1 is located within the 11q23.3 chromosomal region, which is frequently deleted in neuroblastomas, suggesting a potential role in tumor suppression . More critically, recent research has identified FOXR1 as a transcription factor that regulates numerous genes involved in protein folding pathways and stress response mechanisms . The discovery of a de novo missense variant in FOXR1 associated with severe neurological symptoms including postnatal microcephaly, progressive brain atrophy, and global developmental delay has further elevated interest in this protein .

What types of FOXR1 antibodies are available for research purposes?

Several types of FOXR1 antibodies are available to researchers, designed to target different regions of the protein and optimized for various experimental applications. These include:

• C-terminal targeting antibodies: These antibodies are designed to recognize the C-terminal region of human FOXR1 protein . They are particularly useful for detecting full-length FOXR1.

• N-terminal targeting antibodies: These recognize epitopes in the N-terminal region of FOXR1 and can be used with samples from various species including human, mouse, and rat .

• Mid-region targeting antibodies: Antibodies targeting specific amino acid sequences within the FOXR1 protein, such as AA 38-87 or AA 231-280 .

Most commercially available FOXR1 antibodies are polyclonal, produced in rabbits, and available in unconjugated forms for maximum flexibility in experimental design .

What are the primary applications for FOXR1 antibodies?

FOXR1 antibodies have been validated for several key applications in molecular and cellular biology research:

• Western Blotting (WB): FOXR1 antibodies can be used at dilutions ranging from 1:500 to 1:2000 to detect endogenous levels of FOXR1 protein in cell and tissue lysates .

• Immunohistochemistry (IHC): At dilutions of 1:100 to 1:300, these antibodies can visualize FOXR1 expression patterns in tissue sections, including formalin-fixed paraffin-embedded (FFPE) samples .

• Enzyme-Linked Immunosorbent Assay (ELISA): FOXR1 antibodies can be used in ELISAs at approximately 1:20000 dilution for quantitative detection of the protein .

• Immunofluorescence (IF) and Immunocytochemistry (ICC): Some FOXR1 antibodies have been validated for these applications, allowing for subcellular localization studies .

These applications enable researchers to investigate FOXR1 expression, localization, and function in various experimental contexts relevant to development, disease, and cellular stress responses.

How should researchers validate the specificity of FOXR1 antibodies?

Validating FOXR1 antibody specificity is crucial for generating reliable research data. A comprehensive validation approach should include:

• Positive and negative controls: Use cell lines or tissues known to express FOXR1 as positive controls. For negative controls, use FOXR1 knockout samples, if available, or tissues known not to express the protein based on transcriptomic data .

• Western blot analysis: Verify that the antibody detects a band of the expected molecular weight (~37-45 kDa for human FOXR1). Multiple bands may indicate non-specific binding or protein isoforms .

• Competitive peptide blocking: Pre-incubate the antibody with the immunizing peptide before application to samples. This should abolish specific binding, confirming antibody specificity .

• siRNA or CRISPR knockout validation: Knockdown or knockout FOXR1 expression and confirm reduced or absent antibody signal in treated samples compared to controls .

• Subcellular localization comparison: Verify that the antibody detects FOXR1 predominantly in the nucleus, consistent with its function as a transcription factor. Compare this pattern with subcellular fractionation results or published localization data .

Data from search result shows that both wild-type FOXR1 and the M280L mutant localize primarily to the nuclear fraction in Western blot analysis, though the mutant shows reduced expression levels. This information provides a useful benchmark for antibody validation experiments.

What are the optimal sample preparation methods for FOXR1 antibody applications?

For optimal results with FOXR1 antibodies, sample preparation should be tailored to the specific application and research question:

• For Western blotting:

  • Extract proteins using RIPA or NP-40 buffer supplemented with protease inhibitors.

  • Include phosphatase inhibitors if investigating potential post-translational modifications.

  • Nuclear extraction protocols may be preferable given FOXR1's nuclear localization.

  • When comparing WT and mutant FOXR1 (like M280L), equal loading is critical as expression levels differ substantially .

• For immunofluorescence/immunocytochemistry:

  • Fix cells with 4% paraformaldehyde for 10-15 minutes at room temperature.

  • Permeabilize with 0.1-0.5% Triton X-100 to allow antibody access to nuclear FOXR1.

  • Blocking with 5% normal serum from the same species as the secondary antibody reduces background.

  • For detection of nuclear aggregates (as seen with the M280L mutant), confocal microscopy is recommended for optimal resolution .

• For immunohistochemistry:

  • Use FFPE tissue sections with antigen retrieval methods, typically heat-induced epitope retrieval in citrate buffer (pH 6.0).

  • Endogenous peroxidase blocking may be necessary if using HRP-based detection systems.

  • For brain tissue sections where FOXR1 is expressed at low levels, signal amplification methods may enhance detection sensitivity .

• For chromatin immunoprecipitation (ChIP):

  • Cross-link protein-DNA complexes with 1% formaldehyde.

  • Sonicate chromatin to fragments of ~200-500 bp.

  • Pre-clear lysates with protein A/G beads before immunoprecipitation with FOXR1 antibody.

  • Include IgG control and input samples for normalization and specificity assessment.

When studying FOXR1 nuclear aggregates, as described in the M280L mutant, careful fixation and visualization techniques are essential to preserve and accurately detect these structures .

How can researchers effectively optimize antibody concentration for specific applications?

Optimizing FOXR1 antibody concentration is essential for achieving the best signal-to-noise ratio across different applications:

• Titration approach:

  • Begin with the manufacturer's recommended dilution range (e.g., 1:500-1:2000 for WB, 1:100-1:300 for IHC) .

  • Perform a dilution series experiment with 3-4 concentrations spanning this range.

  • Select the dilution that provides sufficient specific signal with minimal background.

• Application-specific considerations:

  • For Western blotting: If detecting endogenous FOXR1, which is expressed at low levels in most tissues, start with higher antibody concentrations (1:500) and adjust based on results .

  • For immunohistochemistry/immunofluorescence: Background is often more problematic, so begin with a more dilute antibody (1:200) and increase concentration if signal is insufficient .

  • For detecting FOXR1 mutants with reduced expression (like M280L): Consider using less diluted antibody to enhance sensitivity, while ensuring specificity is maintained .

• Sample-specific adjustments:

  • When working with tissues known to have low FOXR1 expression, use higher antibody concentrations.

  • For overexpression systems or samples with high FOXR1 expression, more dilute antibody can prevent signal saturation.

  • When analyzing both wild-type and mutant FOXR1 simultaneously, optimize for the lower-expressing protein to ensure detection of both forms .

• Visualization system impact:

  • If using enhanced chemiluminescence (ECL) for Western blotting, standard antibody dilutions are typically sufficient.

  • For fluorescent secondary antibodies, sometimes higher primary antibody concentrations are needed.

  • When using signal amplification systems (e.g., TSA for IHC), more dilute primary antibody can be used.

Research from study demonstrates that detection of the M280L FOXR1 mutant protein requires careful optimization as it shows significantly reduced expression levels compared to wild-type FOXR1.

How can FOXR1 antibodies be utilized to study stress response pathways?

FOXR1 antibodies can be powerful tools for investigating stress response pathways, particularly given FOXR1's role in regulating genes involved in protein folding and stress responses:

• Stress-induced translocation studies:

  • Use immunofluorescence with FOXR1 antibodies to track potential changes in subcellular localization following various cellular stressors (heat shock, oxidative stress, ER stress).

  • Compare localization patterns between wild-type FOXR1 and stress-responsive mutants like M280L .

• Chromatin immunoprecipitation (ChIP) analysis:

  • Use FOXR1 antibodies for ChIP experiments to identify direct genomic binding sites under normal and stress conditions.

  • Combine with sequencing (ChIP-seq) to generate genome-wide binding profiles and identify stress-responsive target genes.

  • Research has shown that FOXR1 regulates expression of stress-responsive genes including heat shock proteins like HSPA6, HSPA1A, and oxidative stress response genes like DHRS2 .

• Co-immunoprecipitation for protein interaction networks:

  • Employ FOXR1 antibodies to pull down FOXR1 and its interacting partners from cells under normal and stressed conditions.

  • Mass spectrometry analysis of immunoprecipitates can reveal stress-dependent changes in the FOXR1 interactome.

  • This approach can help identify how FOXR1 connects to broader stress response networks.

• Monitoring stress-dependent expression changes:

  • Western blotting with FOXR1 antibodies can track changes in FOXR1 protein levels in response to different stressors.

  • Complementary analysis of FOXR1 target genes like HSPA6 and HSPA1A can provide functional readouts of FOXR1 activity .

Research has demonstrated that FOXR1 regulates multiple heat shock proteins and stress response genes, with the M280L mutant showing impaired regulation of these targets . FOXR1 antibodies can help dissect these pathways and identify therapeutic targets for stress-related disorders.

What methods are recommended for studying the role of FOXR1 in neurodevelopmental processes?

Given FOXR1's emerging role in neurodevelopment and its association with neurological disorders, these specialized approaches using FOXR1 antibodies are recommended:

• Developmental expression profiling:

  • Use immunohistochemistry with FOXR1 antibodies on brain tissue sections from different developmental stages to map temporal and spatial expression patterns.

  • Combine with markers for neural progenitors, neurons, and glia to identify FOXR1-expressing cell populations.

  • Research shows that Foxr1 is expressed in mouse embryonic brain tissue, suggesting a developmental role .

• Neural differentiation studies:

  • Employ immunofluorescence and Western blotting with FOXR1 antibodies to track expression changes during in vitro differentiation of neural stem cells.

  • Correlate FOXR1 expression with differentiation markers and morphological changes.

  • This approach can reveal stage-specific functions of FOXR1 during neurogenesis.

• Brain organoid analysis:

  • Apply FOXR1 antibodies in immunostaining of cerebral organoids derived from control and FOXR1-mutant iPSCs.

  • Assess changes in cortical layering, ventricle size, and cellular organization.

  • This method models the cortical thinning and ventricular enlargement observed in Foxr1 knockout mice .

• Comparative analysis of normal versus pathological samples:

  • Use immunohistochemistry to compare FOXR1 expression and localization between normal brain tissue and samples from patients with neurodevelopmental disorders.

  • Look for correlation between FOXR1 expression patterns and specific neuropathological features.

• Co-localization with neuronal stress markers:

  • Perform double immunofluorescence with FOXR1 antibodies and markers of neuronal stress or protein misfolding.

  • This can help establish connections between FOXR1 dysfunction and cellular stress in neurological contexts.

Evidence from mouse models shows that Foxr1 knockout leads to reduced cortical thickness and enlarged ventricles, resembling features seen in the human patient with FOXR1 mutation . FOXR1 antibodies are essential tools for translating these findings to human neurodevelopmental research.

How can researchers effectively study FOXR1 nuclear aggregates seen in mutant proteins?

The M280L FOXR1 mutant forms distinctive nuclear aggregates, a feature that requires specialized techniques for proper characterization:

• High-resolution imaging techniques:

  • Confocal microscopy is essential for accurate visualization of nuclear puncta formed by mutant FOXR1.

  • Super-resolution methods (STED, STORM, SIM) can provide detailed structural information about these aggregates.

  • Research has shown that approximately 13% of cells transfected with the M280L mutant form discrete nuclear puncta, with nuclei containing >15 puncta showing an average individual puncta size of <2 μm .

• Co-localization analysis:

  • Use dual immunofluorescence with FOXR1 antibodies and markers for nuclear bodies (PML bodies, splicing speckles, etc.) to determine if mutant FOXR1 localizes to known nuclear compartments.

  • Co-staining with protein misfolding markers can help establish if these aggregates represent misfolded protein.

  • In study , the researchers co-localized FOXR1 with DAPI to confirm nuclear localization of these aggregates.

• Biochemical fractionation approach:

  • Use differential detergent extraction to separate soluble and insoluble nuclear fractions.

  • Western blotting with FOXR1 antibodies can then quantify the distribution of wild-type versus mutant FOXR1 in these fractions.

  • This approach can confirm whether nuclear aggregates represent insoluble protein deposits.

• Live-cell imaging strategies:

  • Use GFP-tagged FOXR1 constructs together with immunofluorescence validation using FOXR1 antibodies.

  • Time-lapse imaging can track the formation and dynamics of nuclear aggregates in real-time.

  • Study used both GFP-tagged and untagged FOXR1 constructs to verify the nuclear aggregate phenotype.

• Quantitative image analysis:

  • Develop standardized protocols for counting nuclear puncta, measuring their size, and calculating the percentage of cells displaying this phenotype.

  • This allows for statistical comparison between wild-type and various FOXR1 mutants or between different experimental conditions.

The research demonstrates that both HEK293T and COS7 cells can be used to study the M280L mutant's nuclear aggregate phenotype, providing flexible experimental systems for investigating this pathological feature .

What are common challenges in detecting endogenous FOXR1 and how can they be addressed?

Detecting endogenous FOXR1 presents several challenges due to its typically low expression levels. Here are solutions to common issues:

• Low signal intensity:

  • Increase antibody concentration by using less diluted antibody (1:500 instead of 1:2000 for Western blots) .

  • Implement signal enhancement methods like HRP-conjugated polymers or tyramide signal amplification for immunohistochemistry.

  • Use more sensitive detection reagents for Western blotting (e.g., femto-level ECL substrates).

  • Increase protein loading for Western blots (50-100 μg of total protein).

  • Research shows that FOXR1 is expressed at low levels in most tissues, making detection challenging .

• High background:

  • Extend blocking time (overnight at 4°C) with 5% milk or BSA.

  • Increase washing duration and number of wash steps.

  • Try different blocking agents (BSA vs. milk vs. normal serum).

  • Pre-adsorb antibody with tissues/cells known not to express FOXR1.

  • Use more stringent antibody dilution buffer (e.g., include 0.1% Tween-20 or 0.1% Triton X-100).

• Non-specific bands in Western blots:

  • Optimize transfer conditions (time, voltage, buffer composition) for proteins in the 37-45 kDa range.

  • Try different membrane types (PVDF vs. nitrocellulose).

  • Perform membrane stripping and reprobing with another FOXR1 antibody targeting a different epitope for confirmation .

  • Include peptide competition controls to identify specific bands.

• Tissue-specific issues:

  • For brain tissue, where FOXR1 has been detected in embryonic stages, optimize antigen retrieval methods for fixed tissue (try both citrate and EDTA-based buffers) .

  • For reproductive tissues, consider the maternal-effect role of foxr1 observed in zebrafish when designing experiments and interpreting results .

• Species-specific considerations:

  • Verify antibody cross-reactivity with your species of interest (many antibodies react with human and mouse FOXR1) .

  • For zebrafish studies, specialized antibodies may be needed as standard mammalian antibodies may not cross-react .

How should researchers interpret differences in FOXR1 detection between various experimental conditions?

Interpreting variations in FOXR1 detection requires careful consideration of multiple factors:

• Expression level differences:

  • Wild-type vs. Mutant: Research demonstrates that the M280L FOXR1 mutant shows significantly reduced protein levels compared to wild-type, requiring adjustment of detection parameters .

  • Developmental stages: Consider that FOXR1 expression may vary during development, particularly in brain tissue .

  • Cellular stress: Evaluate whether changes in FOXR1 detection reflect actual expression changes or altered antibody accessibility due to protein modifications or interactions.

• Subcellular localization shifts:

  • Nuclear vs. Cytoplasmic: While FOXR1 is predominantly nuclear, both wild-type and M280L mutant FOXR1 have been detected in cytoplasmic fractions at lower levels .

  • Aggregation phenomena: Changes in detection pattern (diffuse vs. punctate) may indicate protein aggregation rather than expression changes, as seen with the M280L mutant .

  • Extraction efficiency: Different lysis buffers may extract nuclear proteins with varying efficiency, affecting detection.

• Technical variables:

  • Antibody batch variation: Compare results using the same antibody lot when possible, or validate new lots against previous ones.

  • Protocol modifications: Document all procedural changes that might affect detection sensitivity.

  • Image acquisition parameters: Standardize exposure times, gain settings, and post-processing for accurate comparisons.

• Biological context interpretation:

  • Cell type specificity: Consider whether detection differences reflect cell type-specific expression patterns rather than technical issues.

  • Functional state: Correlate FOXR1 detection with functional readouts (e.g., target gene expression) to interpret biological significance.

  • Protein modification: Consider whether post-translational modifications might affect antibody binding and detection.

Research from study provides an important comparative benchmark: wild-type FOXR1 shows diffuse nuclear localization, while approximately 13% of cells expressing the M280L mutant display discrete nuclear puncta aggregates.

What specialized techniques can help validate FOXR1 antibody results in challenging research contexts?

When standard approaches yield ambiguous results, these specialized validation techniques can enhance confidence in FOXR1 antibody findings:

• Multiple antibody validation:

  • Use antibodies targeting different FOXR1 epitopes (N-terminal, C-terminal, and mid-region) to corroborate findings .

  • Compare polyclonal and monoclonal antibodies when available to balance sensitivity and specificity.

  • Establish that multiple antibodies yield consistent detection patterns.

• Genetic validation approaches:

  • CRISPR/Cas9 knockout: Generate FOXR1 knockout controls for definitive antibody validation.

  • siRNA/shRNA knockdown: Create partial knockdown samples to establish signal correlation with expression level.

  • Overexpression systems: Use tagged FOXR1 constructs to compare antibody detection with tag-specific antibodies .

• Mass spectrometry validation:

  • Perform immunoprecipitation with FOXR1 antibody followed by mass spectrometry.

  • Confirm the presence of FOXR1 peptides in the immunoprecipitated material.

  • This approach validates both antibody specificity and can identify potential interacting proteins.

• Proximity ligation assay (PLA):

  • Use two antibodies targeting different FOXR1 epitopes in PLA to generate signal only when both antibodies bind in close proximity.

  • This approach dramatically increases specificity for true FOXR1 detection.

• Genomic footprinting correlation:

  • Combine ChIP-seq using FOXR1 antibodies with motif analysis.

  • Enrichment of FOXR1 consensus binding motifs in immunoprecipitated regions supports antibody specificity.

  • Integration with RNA-seq data to correlate binding with gene expression changes further validates findings.

• Combined protein-RNA detection:

  • Perform immunofluorescence for FOXR1 together with RNA FISH for FOXR1 mRNA.

  • Correlation between protein and mRNA detection supports antibody specificity.

  • This is particularly valuable in tissues with low or variable FOXR1 expression.

Research from study utilized both untagged and GFP-tagged FOXR1 constructs to validate antibody detection and cellular localization patterns, demonstrating the value of complementary detection approaches.

How can FOXR1 antibodies contribute to understanding neurodevelopmental disorders?

FOXR1 antibodies offer valuable tools for investigating neurodevelopmental disorders, particularly given the association between FOXR1 mutation and severe neurological symptoms:

• Patient-derived sample analysis:

  • Use FOXR1 antibodies for immunohistochemistry on postmortem brain tissue from patients with neurodevelopmental disorders.

  • Compare FOXR1 expression patterns and subcellular localization with age-matched controls.

  • Evidence suggests that FOXR1 dysfunction may contribute to postnatal microcephaly, brain atrophy, and developmental delay .

• iPSC-based disease modeling:

  • Apply FOXR1 antibodies to study protein expression and localization in patient-derived induced pluripotent stem cells (iPSCs) and their neural derivatives.

  • Compare wild-type and mutant FOXR1 behavior during neural differentiation and maturation.

  • Track correlation between FOXR1 aggregation and cellular stress responses in neural cells.

• Histopathological correlation:

  • Perform immunohistochemistry with FOXR1 antibodies on brain sections from mouse models of neurodevelopmental disorders.

  • Correlate FOXR1 expression patterns with neuropathological features like cortical thinning and ventricular enlargement that were observed in Foxr1 knockout mice .

  • Analyze co-expression with markers of neural development and cellular stress.

• Therapeutic target validation:

  • Use FOXR1 antibodies to monitor protein levels and aggregation in response to candidate therapeutics that might modulate protein folding or degradation pathways.

  • Assess whether treatments can normalize FOXR1 expression or prevent aggregate formation in cellular models of FOXR1 mutation.

• Diagnostic biomarker development:

  • Evaluate whether FOXR1 antibodies can detect disease-specific patterns in accessible patient samples (e.g., fibroblasts, lymphoblasts).

  • Determine if FOXR1 protein patterns correlate with disease severity or progression.

Research has shown that Foxr1 knockout mice exhibit brain pathology consistent with observations in a human patient carrying a FOXR1 mutation, suggesting conservation of its neurodevelopmental function across species .

What approaches combine FOXR1 antibodies with transcriptomic analysis for comprehensive pathway studies?

Integrating FOXR1 antibody-based methods with transcriptomic techniques creates powerful approaches for understanding FOXR1's regulatory networks:

• ChIP-seq and RNA-seq integration:

  • Use FOXR1 antibodies for chromatin immunoprecipitation followed by sequencing (ChIP-seq) to identify genome-wide binding sites.

  • Perform RNA-seq on the same samples to correlate binding events with gene expression changes.

  • Research has identified 2,644 differentially expressed genes regulated by FOXR1, with the M280L mutant showing impaired regulation of stress-responsive genes .

• CUT&RUN with transcriptome profiling:

  • Apply FOXR1 antibodies in Cleavage Under Targets and Release Using Nuclease (CUT&RUN) for higher resolution mapping of binding sites.

  • Combine with RNA-seq to create high-resolution maps of FOXR1 regulatory networks.

  • This approach can identify direct versus indirect FOXR1 targets with greater precision.

• Single-cell multi-omics:

  • Use FOXR1 antibodies for protein detection in single-cell protocols (e.g., CITE-seq).

  • Combine with single-cell RNA-seq to correlate FOXR1 protein levels with transcriptional profiles at single-cell resolution.

  • This approach can reveal cell type-specific FOXR1 functions in heterogeneous tissues like brain.

• Inducible systems with temporal analysis:

  • Employ FOXR1 antibodies to validate inducible FOXR1 expression or degradation systems.

  • Perform time-series RNA-seq following FOXR1 induction/depletion to identify primary versus secondary transcriptional responses.

  • This approach can establish the temporal dynamics of FOXR1-regulated pathways.

• Comparative analysis of wild-type versus mutant FOXR1:

  • Use antibodies to confirm expression of wild-type and mutant FOXR1 constructs.

  • Perform differential transcriptomic analysis to identify pathways specifically disrupted by mutations.

  • Research has shown that the M280L mutant fails to properly regulate stress-responsive genes like HSPA6, HSPA1A, and DHRS2 .

A heat map analysis in study revealed five coherent clusters of differentially expressed genes regulated by FOXR1, demonstrating the power of integrating protein-level and transcriptomic approaches.

How should researchers approach studying FOXR1's role in maternal-effect gene regulation?

FOXR1's identification as a maternal-effect gene in fish requires specialized approaches for studying its role in early development:

• Oocyte-specific analysis:

  • Use FOXR1 antibodies for immunolocalization in oocytes and early embryos to track protein distribution before and after fertilization.

  • Compare with in situ hybridization for foxr1 mRNA to distinguish maternal protein from new synthesis.

  • Research in zebrafish has established foxr1 as a maternal-effect gene essential for early embryonic development .

• Transgenerational experimental design:

  • Apply FOXR1 antibodies to study protein expression in female germline cells across generations.

  • Compare embryos from wild-type versus foxr1-mutant females to correlate maternal FOXR1 levels with developmental outcomes.

  • Analysis of embryos from foxr1 mutant females can reveal phenotypes resulting from maternal FOXR1 deficiency .

• Cell cycle regulation analysis:

  • Use FOXR1 antibodies in combination with cell cycle markers to investigate FOXR1's role in early cell divisions.

  • Correlate FOXR1 expression with levels of cell cycle regulators like p21, which shows dramatically increased expression in foxr1 mutant eggs .

  • This approach can clarify FOXR1's function as a transcriptional repressor in cell cycle regulation.

• Comparative approaches across species:

  • Apply FOXR1 antibodies in studies comparing mammalian and fish models to determine conservation of maternal effect functions.

  • Evaluate whether findings from zebrafish models translate to mammalian systems.

  • Cross-species comparison can identify evolutionarily conserved versus divergent functions of FOXR1.

• Molecular pathway reconstruction:

  • Use FOXR1 antibodies for immunoprecipitation from oocytes and early embryos to identify stage-specific interaction partners.

  • Integrate with transcriptomic data to build comprehensive models of FOXR1's role in maternal-to-zygotic transition.

  • Research has connected foxr1 to the regulation of rictor, a component of the mTOR complex involved in cell growth and proliferation .

Research has demonstrated that foxr1 regulates expression of cell cycle inhibitors and mTOR pathway components in zebrafish, suggesting a role in coordinating early cell divisions after fertilization .