MEN1 Antibody

What is MEN1 and why is it significant in endocrine research?

MEN1 (Multiple Endocrine Neoplasia Type 1) is a rare autosomal dominant inherited tumor syndrome affecting approximately 1 in 30,000 individuals. It is characterized by the development of tumors in multiple endocrine organs, primarily the parathyroid glands, anterior pituitary, and enteropancreatic tissues . The condition results from mutations in the MEN1 tumor suppressor gene, which encodes the protein menin .

The significance of MEN1 in endocrine research extends beyond its clinical manifestations. Menin acts as a tumor suppressor by regulating critical cellular functions including DNA replication and repair, apoptosis, and transcriptional regulation . Understanding menin's molecular functions provides insights into fundamental tumor suppressor mechanisms and potential therapeutic targets for both MEN1-related tumors and other cancers.

What is the molecular structure and function of menin protein?

Menin is a 68-70 kDa nuclear protein encoded by the MEN1 gene . It acts as a tumor suppressor by:

• Regulating cell proliferation and apoptosis

• Interacting with transcription factors to control gene expression

• Playing a role in DNA repair and genome stability

• Contributing to chromatin remodeling through interactions with histone methyltransferase complexes

Structurally, menin is predominantly localized in the nucleus of cells and is ubiquitously expressed across tissues . The protein interacts with numerous binding partners, most notably components of the MLL histone methyltransferase complex that methylates histone H3 at lysine 4 (H3K4) . This interaction is crucial for its role in transcriptional regulation.

Research has demonstrated that menin influences the expression of key proteins including p53 and retinoblastoma protein (Rb), which are critical cell cycle regulators . Menin knockout studies have revealed its complex roles in different cellular contexts, where it can show both tumor-suppressive and oncogenic functions depending on the tissue microenvironment .

What types of MEN1 antibodies are available for research?

There is a diverse array of MEN1 antibodies available for research purposes, which can be categorized based on several characteristics:

Selection of the appropriate antibody depends on the specific research application, target species, and experimental design. For instance, a researcher studying protein-protein interactions might prefer a monoclonal antibody for immunoprecipitation, while someone examining tissue expression patterns might opt for a polyclonal antibody with strong IHC capability .

How do I select the appropriate MEN1 antibody for my specific application?

Selecting the optimal MEN1 antibody requires consideration of multiple factors:

• Experimental Application: Different applications require different antibody properties:

  • For Western blot: Choose antibodies validated for WB with appropriate dilution ranges (e.g., 1:500-1:2000 for polyclonal or 1:5000-1:50000 for high-affinity monoclonal antibodies)

  • For IHC/IF: Select antibodies specifically validated for these applications with proper epitope exposure (e.g., antibodies requiring TE buffer pH 9.0 for antigen retrieval)

  • For IP: Use antibodies specifically validated for immunoprecipitation with recommended amounts (e.g., 0.5-4.0 μg for 1.0-3.0 mg of total protein lysate)

• Species Reactivity: Ensure the antibody has been validated in your species of interest:

  • For human samples: Most commercial antibodies react with human menin

  • For mouse/rat models: Verify cross-reactivity with rodent menin (e.g., Bethyl Laboratories antibody reacts with both human and mouse)

• Epitope Consideration: Depending on your research question, target region matters:

  • C-terminal epitopes may be masked in certain protein complexes

  • If studying a specific MEN1 mutation, ensure the antibody's epitope is not affected by the mutation

• Validation Evidence: Review published literature and validation data:

  • Citation records (e.g., Bethyl Laboratories antibody with 110 citations)

  • Validation data gallery showing expected banding patterns

  • Published validation in applications similar to yours

Always perform appropriate controls when using a new antibody, such as positive control lysates from cells known to express menin (e.g., HeLa, HepG2, Jurkat cells) and negative controls using MEN1 knockout samples or siRNA-mediated knockdown.

What are the optimal protocols for Western blot detection of menin?

For optimal Western blot detection of menin, follow these methodological considerations:

Sample Preparation:

• Extract nuclear proteins preferentially, as menin is predominantly a nuclear protein

• Use a lysis buffer containing protease inhibitors to prevent degradation

• Standard RIPA or NP-40 buffers supplemented with protease inhibitors work well for menin extraction

SDS-PAGE and Transfer:

• Use 8-10% polyacrylamide gels to adequately resolve the 68-70 kDa menin protein

• Transfer to PVDF membrane at 100V for 90 minutes or 30V overnight at 4°C

Blocking and Antibody Incubation:

• Block with 5% non-fat dry milk or BSA in TBST (based on antibody specifications)

• Primary antibody dilutions:

  • For polyclonal antibodies: 1:500-1:2000 dilution

  • For monoclonal antibodies: 1:5000-1:50000 dilution

• Incubate with primary antibody overnight at 4°C

• Wash 3-5 times with TBST, 5-10 minutes each

• Use appropriate HRP-conjugated secondary antibody (1:5000-1:10000)

Detection:

• Enhanced chemiluminescence (ECL) detection systems work well for menin

• Expected molecular weight: 63-70 kDa

Controls:

• Positive controls: HepG2, HeLa, Jurkat, or HEK-293 cell lysates

• Negative controls: MEN1 knockout cell lines or siRNA-mediated knockdown samples

• Loading control: β-actin, GAPDH, or nuclear proteins like HDAC1 or Lamin B1

Troubleshooting Tips:

• If detecting multiple bands, optimize primary antibody concentration

• For weak signals, extend exposure time or increase protein loading

• For high background, increase washing steps or reduce antibody concentration

How can I use MEN1 antibodies to study protein-protein interactions?

MEN1 antibodies can be valuable tools for studying protein-protein interactions involving menin through several methodological approaches:

Immunoprecipitation (IP):

• Use 0.5-4.0 μg of anti-MEN1 antibody per 1.0-3.0 mg of total protein lysate

• Cross-linking antibodies to protein A/G beads can reduce heavy chain interference in subsequent Western blot analysis

• Include appropriate controls (IgG control, input lysate)

• After IP, analyze co-precipitated proteins by mass spectrometry or Western blot

Co-immunoprecipitation (Co-IP) Strategy:

• Forward approach: IP with anti-MEN1 antibody and blot for potential interacting proteins

• Reverse approach: IP with antibodies against suspected interacting proteins and blot with anti-MEN1 antibody

• This approach has been successfully used to identify menin interactions with transcription factors and components of histone modification complexes

Proximity Ligation Assay (PLA):

• Use two antibodies targeting menin and its potential interaction partner

• Secondary antibodies with oligonucleotide probes generate a signal only when proteins are in close proximity

• This technique allows visualization of protein interactions in situ

Chromatin Immunoprecipitation (ChIP):
MEN1 antibodies have been effectively used for ChIP to study menin's association with chromatin and interaction with other chromatin-associated proteins:

• Use formaldehyde to cross-link protein-DNA complexes

• Sonicate chromatin to appropriate fragment sizes (200-500 bp)

• Immunoprecipitate with anti-menin antibody (e.g., Bethyl Laboratories BL342)

• Analyze co-occupancy with other factors such as MLL1 (BL1289) and Rbbp5 (BL766)

• ChIP-seq analysis has revealed menin's binding across the genome, particularly at H3K4me3-marked regions

These approaches have helped identify menin's interactions with various proteins including MLL histone methyltransferase complexes, which has been critical for understanding menin's role in chromatin regulation and gene expression .

How do I design experiments to study menin's dual function in tumor suppression and oncogenesis?

Recent research has revealed that menin exhibits context-dependent functions that can be either tumor-suppressive or oncogenic . To investigate this duality, consider these experimental approaches:

In Vitro vs. In Vivo Comparative Analysis:

• Set up parallel in vitro and in vivo experiments with the same cell lines

• Use CRISPR/Cas9 to knockout MEN1 in cancer cell lines (e.g., A549 lung cancer cells)

• Compare proliferation rates in vitro (2D and 3D cultures) with tumor growth in mouse models

• Include both immunodeficient (e.g., NOD/SCID) and immunocompetent mouse models

• As demonstrated in recent research, MEN1 knockout may show minimal effects in vitro but significant and opposing effects in different in vivo models

Microenvironment Investigation:

• Co-culture MEN1-knockout and wild-type cells with different stromal or immune cells

• Use transwell assays to examine paracrine effects

• Analyze cytokine and chemokine production profiles using multiplex assays

• Monitor immune cell infiltration in tumors using flow cytometry and immunohistochemistry

• Research has shown MEN1 knockout can affect cytokine gene expression and immune cell recruitment

Molecular Mechanism Exploration:

• Perform RNA-seq and ChIP-seq in various conditions to identify context-dependent gene regulation

• Compare chromatin occupancy patterns of menin and associated factors (e.g., MLL1) in different cell types

• Investigate H3K4me3 distribution, particularly at repetitive genomic regions

• Examine double-stranded RNA expression and downstream signaling pathways

Therapeutic Response Testing:

• Evaluate menin-MLL inhibitors in different tumor models

• Compare responses in immunodeficient vs. immunocompetent settings

• Test combinations with immunotherapy agents

• Assess CD8+ T cell-dependent mechanisms

Data Table: Contrasting Effects of MEN1 Knockout in Different Contexts:

This experimental framework addresses the complex roles of menin in different contexts and provides a systematic approach to understanding its dual functions in cancer .

What methods are available for studying MEN1 mutations and their functional consequences?

Studying MEN1 mutations and their functional impacts requires a multi-faceted approach:

Genetic Analysis Techniques:

• Next-Generation Sequencing (NGS): Use targeted sequencing panels or whole exome sequencing to identify MEN1 mutations

• Multiplex Ligation-dependent Probe Amplification (MLPA): Detect large deletions or duplications that may be missed by sequencing

• RNA-seq: Identify potential splicing defects and expression changes associated with mutations

• Digital droplet PCR: Quantify allelic ratios in samples with suspected mosaicism

Loss of Heterozygosity (LOH) Analysis:

• Compare germline DNA with tumor DNA to detect second-hit events

• Use microsatellite markers or SNP arrays for LOH detection

• Perform laser capture microdissection to isolate tumor cells for precise analysis

• Studies have shown that LOH at the MEN1 locus (11q13) is a critical event in MEN1-associated tumors

Functional Characterization Systems:

• CRISPR/Cas9 Gene Editing:

  • Create isogenic cell lines with specific MEN1 mutations

  • A recent study successfully used CRISPR/Cas9 to generate an isogenic iPSC line from a MEN1 patient and correct the mutation, creating a valuable experimental system

  • Develop knock-in mouse models of specific mutations

• Patient-Derived Models:

  • Generate induced pluripotent stem cells (iPSCs) from patients with MEN1 mutations

  • Differentiate iPSCs into relevant cell types (e.g., endocrine cells)

  • Establish patient-derived xenografts from MEN1 tumor samples

• Protein Function Assays:

  • Protein stability and half-life measurements

  • Protein-protein interaction analyses (co-IP, mammalian two-hybrid)

  • Subcellular localization studies using fluorescently tagged mutant proteins

  • DNA binding and transcriptional regulation assays

Phenotypic Assessment:

• Cell proliferation and apoptosis assays

• Colony formation assays

• Soft agar growth for anchorage-independent growth

• In vivo tumorigenicity studies

• Differentiation capacity analysis, particularly for endocrine lineages

Data Table: Examples of MEN1 Mutations and Their Functional Impacts:

These comprehensive approaches enable researchers to connect specific MEN1 mutations with their molecular and cellular consequences, potentially revealing genotype-phenotype correlations that could inform clinical management .

How can I use MEN1 antibodies in a temporal conditional knockout system to study acute effects of MEN1 deletion?

To study the immediate consequences of MEN1 deletion, researchers can implement temporal conditional knockout systems paired with appropriate antibody-based detection methods:

Experimental System Design:

• Inducible Cre-loxP System:

  • Use mice with floxed MEN1 alleles (Men1^fl/fl)

  • Employ tamoxifen-inducible CreERT2 under tissue-specific promoters

  • This approach allows temporal control of MEN1 deletion in specific tissues

• Alternative Temporal Control Systems:

  • Tetracycline-regulated gene expression systems (Tet-On/Tet-Off)

  • Degradation domain fusion proteins with small molecule-induced stabilization

  • CRISPR interference (CRISPRi) with inducible promoters

Time-Course Analysis Protocol:

• Establish baseline measurements before MEN1 deletion

• Induce MEN1 deletion via tamoxifen or doxycycline administration

• Collect samples at multiple time points (e.g., 24h, 48h, 72h, 7 days, 14 days post-induction)

• Research has shown that effects on cell proliferation can be detected as early as 7 days post-MEN1 excision

Antibody-Based Detection Methods:

• Western Blot:

  • Track menin protein levels using anti-MEN1 antibodies (1:500-1:2000 dilution)

  • Quantify relative protein abundance at each time point

  • Include appropriate loading controls

• Immunohistochemistry:

  • Process tissue sections at each time point

  • Use anti-MEN1 antibodies (1:250-1:1000 dilution)

  • Perform antigen retrieval with TE buffer pH 9.0 or citrate buffer pH 6.0

  • Quantify percentage of cells with menin expression

• Co-staining for Proliferation and Differentiation Markers:

  • Combine anti-MEN1 antibodies with proliferation markers (Ki67, BrdU)

  • Include tissue-specific differentiation markers

  • Particularly useful for pancreatic islet studies, where increased proliferation has been observed within 7 days of Men1 excision

Molecular and Cellular Analysis:

• ChIP-seq Time Course:

  • Track changes in menin occupancy across the genome

  • Monitor H3K4me3 redistribution following menin loss

  • Examine recruitment of interacting factors

• Transcriptome Analysis:

  • RNA-seq at multiple time points to identify immediate-early response genes

  • Focus on cell cycle regulators and tissue-specific functional genes

  • Pathway analysis to identify biological processes affected acutely by menin loss

• Cell Cycle Analysis:

  • Flow cytometry for cell cycle phase distribution

  • EdU incorporation to measure S phase entry

  • Phospho-histone H3 staining for mitotic index

  • Previous research has shown that acute effects of Men1 mutation include accelerated S phase entry and enhanced cell proliferation

This temporal approach allows researchers to distinguish primary effects of menin loss from secondary adaptations or compensatory mechanisms, providing crucial insights into menin's direct functions in cellular processes and tumor suppression.

How do I troubleshoot inconsistent results in MEN1 antibody-based experiments?

Inconsistent results with MEN1 antibodies can arise from multiple sources. Here's a systematic troubleshooting approach:

Antibody-Related Issues:

• Epitope Masking: Menin interacts with numerous proteins which may obscure antibody recognition sites

  • Solution: Try antibodies targeting different epitopes of menin

  • Compare results from C-terminal vs. N-terminal targeting antibodies

• Antibody Specificity: Some antibodies may cross-react with similar proteins

  • Solution: Validate specificity using MEN1 knockout samples or siRNA knockdown

  • Compare results across multiple antibodies from different manufacturers

• Antibody Sensitivity: Detection thresholds vary between antibodies

  • Solution: Test different antibody concentrations and detection methods

  • Consider signal amplification techniques for low-abundance samples

Sample Preparation Issues:

• Protein Extraction Efficiency: Nuclear proteins like menin require efficient extraction

  • Solution: Compare different lysis buffers optimized for nuclear protein extraction

  • Include phosphatase and protease inhibitors to prevent degradation

• Post-translational Modifications: These may affect antibody recognition

  • Solution: Test samples with phosphatase treatment before analysis

  • Consider using antibodies that recognize modified forms if available

Experimental Design Considerations:

• Tissue Heterogeneity: Menin expression varies across cell types

  • Solution: Use laser capture microdissection for specific cell populations

  • Employ single-cell techniques when possible

• Developmental Timing: Menin function may vary temporally

  • Solution: Carefully control for developmental stage in your experiments

  • Include age-matched controls and time-course analyses

Data Interpretation Framework:
When faced with inconsistent results, consider these potential biological explanations:

As demonstrated in research, MEN1 can have differential effects in vitro versus in vivo , highlighting the importance of experimental context in data interpretation.

What controls should I include when studying MEN1 in different experimental systems?

Rigorous controls are essential for reliable MEN1 research across various experimental systems:

General Controls for MEN1 Antibody Use:

• Positive Controls:

  • Cell lines with confirmed menin expression (HepG2, HEK-293, HeLa, Jurkat)

  • Tissues known to express menin (e.g., pancreatic islets, parathyroid)

  • Recombinant menin protein for Western blot standardization

• Negative Controls:

  • MEN1 knockout cell lines or tissues

  • siRNA/shRNA-mediated MEN1 knockdown samples

  • Secondary antibody-only controls for immunostaining

  • IgG isotype controls for immunoprecipitation

Genetic Modification Experiments:

• For CRISPR/Cas9 MEN1 Editing:

  • Non-targeting sgRNA controls

  • Verification of on-target editing by sequencing

  • Analysis of potential off-target effects at predicted sites

  • Inclusion of isogenic control lines

• For Conditional Knockout Models:

  • Cre-negative controls with same floxed alleles

  • Vehicle-treated controls for inducible systems

  • Wild-type tissues processed identically to experimental samples

  • Time-matched sampling for temporal studies

Functional Studies:

• For Proliferation/Growth Assays:

  • Parallel in vitro and in vivo assessments

  • Multiple cell/tissue types to account for context-dependency

  • Both immunodeficient and immunocompetent models for in vivo studies

• For Gene Expression Analysis:

  • Multiple reference genes for normalization (e.g., GAPDH, β-actin)

  • Samples across different time points to capture dynamics

  • Independent validation using alternative methods (e.g., qPCR confirming RNA-seq findings)

Disease Model Controls:

• For MEN1 Syndrome Models:

  • Age-matched controls for each time point

  • Single-organ affected controls to understand tissue interactions

  • Comparison of heterozygous vs. homozygous models

  • Inclusion of clinical samples when available

• For Tumor Studies:

  • Adjacent normal tissue controls

  • Comparison of familial vs. sporadic cases

  • Analysis of multiple tumor regions to account for heterogeneity

  • MEN1 wildtype tumors of the same histological type

Example Control Strategy for CRISPR/Cas9 MEN1 Correction:
A study creating an isogenic cell system for MEN1 syndrome exemplifies comprehensive controls :

Implementing these control strategies ensures reproducibility and robust interpretation of results across different experimental contexts.

How can MEN1 antibodies be used to explore the dual role of menin in cancer and the tumor microenvironment?

Recent research has revealed that menin plays context-dependent roles in cancer, showing both tumor-suppressive and oncogenic functions depending on the tumor microenvironment . MEN1 antibodies can be instrumental in exploring this duality through several innovative approaches:

Spatial Transcriptomics and Proteomics:

• Combine anti-MEN1 immunostaining with spatial transcriptomics to correlate menin expression with spatial gene expression patterns

• Use multiplexed immunofluorescence with anti-MEN1 and immune cell markers to map menin expression relative to the immune microenvironment

• This approach can reveal associations between menin expression and specific microenvironmental niches

Single-Cell Analysis:

• Perform single-cell Western blot or CyTOF with anti-MEN1 antibodies to quantify menin levels in individual cells

• Correlate with other proteins like cytokine receptors or immune checkpoint molecules

• This can identify cell populations where menin levels correlate with specific functional states

In Situ Interaction Mapping:

• Use proximity ligation assays with anti-MEN1 and antibodies against potential interacting partners

• Compare interaction patterns between in vitro cultures and tumor tissues

• Research has shown that menin's interactions may differ between controlled in vitro environments and complex in vivo settings

Chromatin Occupancy in Different Contexts:

• Perform ChIP-seq with anti-MEN1 antibodies in:

  • In vitro cultured cancer cells

  • Tumor cells isolated from immunodeficient mouse xenografts

  • Tumor cells from immunocompetent syngeneic models

• Compare menin genomic occupancy and H3K4me3 patterns

• Recent work has shown that MEN1 knockout redistributes MLL1 chromatin occupancy and increases H3K4me3 at repetitive genomic regions

Cytokine-Mediated Regulation:

• Treat cells with various cytokines and assess menin levels and localization using anti-MEN1 antibodies

• Examine how menin regulates cytokine gene expression in different immune contexts

• Research has identified "cytokine-cytokine receptor interaction" as a top enriched term in MEN1-low patients, suggesting a key role for menin in immune signaling

Experimental Approaches to Study MEN1's Dual Role:

These approaches leverage MEN1 antibodies to understand the molecular basis for menin's context-dependent functions, potentially informing therapeutic strategies that target menin in specific tumor microenvironments.

What are the emerging applications of MEN1 antibodies in therapeutic development and precision medicine?

MEN1 antibodies are becoming increasingly valuable in therapeutic development and precision medicine approaches for MEN1-related disorders and beyond:

Target Validation and Drug Discovery:

• Use MEN1 antibodies to validate molecular targets downstream of menin

• Screen compound libraries for molecules that modulate menin protein levels or interactions

• Evaluate effects of menin-MLL interaction inhibitors using co-immunoprecipitation with MEN1 antibodies

• Recent research has shown that pharmacological inhibition of menin-MLL interaction reduces tumor growth in a CD8+ T cell-dependent manner, highlighting therapeutic potential

Biomarker Development:

• Develop immunoassays using MEN1 antibodies to quantify menin levels in liquid biopsies

• Correlate menin expression patterns with treatment responses

• Create multiplexed assays combining menin with other markers for patient stratification

• Research has identified aggressive tumor phenotypes associated with specific MEN1 mutations, suggesting potential for biomarker-guided approaches

Companion Diagnostics:

• Use immunohistochemistry with MEN1 antibodies to identify patients likely to respond to menin-targeting therapies

• Develop algorithms combining menin expression with other molecular features

• Create standardized scoring systems for clinical implementation

Therapeutic Monitoring:

• Apply MEN1 antibodies in longitudinal studies to track changes in menin expression during treatment

• Correlate with clinical outcomes and treatment resistance mechanisms

• Use in combination with functional assays to assess dynamic changes in menin activity

Novel Therapeutic Approaches:

• Immunotherapy Combinations:

  • Use MEN1 antibodies to identify tumors where menin inhibition might enhance immunotherapy responses

  • Recent findings showing MEN1's role in tumor immune microenvironment suggest potential synergy

• Targeted Protein Degradation:

  • Develop menin-targeting PROTACs (Proteolysis Targeting Chimeras)

  • Use MEN1 antibodies to monitor degradation efficiency and selectivity

• Cell-Based Therapies:

  • Engineer CAR-T cells targeting MEN1-mutated cells expressing aberrant menin

  • Use antibodies to validate target specificity

Implementation in Precision Medicine Paradigms:

These emerging applications of MEN1 antibodies demonstrate their potential value beyond basic research, extending into translational medicine and clinical practice. The dual nature of menin function revealed in recent research suggests that menin-targeted therapies may have applications in both MEN1-related tumors and other cancer types where menin plays a context-dependent role .

How can advanced genetic engineering techniques be combined with MEN1 antibodies to develop better disease models?

Integrating advanced genetic engineering with MEN1 antibody technologies enables the development of sophisticated disease models that more accurately recapitulate MEN1 syndrome and related disorders:

CRISPR/Cas9-Based Precision Models:

• Knock-in of Patient-Specific Mutations:

  • Generate exact mutations identified in MEN1 patients

  • Use MEN1 antibodies to verify protein expression and localization

  • A recent study successfully used CRISPR/Cas9 to correct a pathogenic MEN1 mutation (c.1252G>T) in patient-derived iPSCs, creating isogenic cell lines for comparative analysis

• Base Editing and Prime Editing:

  • Introduce precise point mutations without double-strand breaks

  • Use anti-MEN1 antibodies to assess effects on protein expression and function

  • This approach minimizes unwanted on-target indels and off-target effects

• Inducible Degradation Systems:

  • Integrate degron tags into endogenous MEN1

  • Use anti-MEN1 antibodies to monitor temporal control of protein levels

  • This allows studying acute effects of menin loss, similar to conditional knockout systems

Advanced Organoid and iPSC Models:

• Patient-Derived Organoids:

  • Develop 3D cultures from MEN1 patient tissues

  • Characterize menin expression patterns using immunostaining

  • Use for drug screening and personalized medicine approaches

• Directed Differentiation of iPSCs:

  • Generate endocrine cell types affected in MEN1 syndrome

  • Track menin expression during differentiation using anti-MEN1 antibodies

  • Research has shown successful differentiation of MEN1 patient-derived iPSCs into endodermal cells, demonstrating the feasibility of this approach

• Multi-Lineage Organoids:

  • Create complex organoid systems containing multiple cell types

  • Study cell-cell interactions in MEN1 deficiency

  • Use multiplexed antibody staining to track menin in different cell populations

Humanized Mouse Models:

• Conditional Tissue-Specific Models:

  • Generate mice with human MEN1 variants in specific tissues

  • Use antibodies to verify human menin expression patterns

  • Compare with existing mouse Men1 models for translational relevance

• Patient-Derived Xenografts:

  • Implant MEN1 patient tumor samples in immunodeficient mice

  • Characterize menin expression and function using antibodies

  • Test therapeutic approaches targeting menin or downstream pathways

Experimental Matrix for Comprehensive MEN1 Modeling:

Validation and Characterization Strategies:

• Combine genetic engineering verification (sequencing, digital PCR) with protein-level confirmation using MEN1 antibodies

• Use antibodies against modified histone marks (H3K4me3) to assess functional consequences of MEN1 mutations

• Perform multi-omics characterization (transcriptomics, proteomics, epigenomics) to comprehensively profile model systems

• Compare engineered models with patient samples using standardized antibody-based assays

These integrated approaches enable the development of more accurate and clinically relevant MEN1 disease models, facilitating both mechanistic studies and therapeutic development efforts.