CLEC4M Antibody, FITC conjugated

What is CLEC4M and what are its primary functions in human physiology?

CLEC4M (C-type lectin domain family 4 member M) is a calcium-dependent mannose-specific receptor primarily expressed on endothelial cells in liver sinusoids and lymph nodes. It consists of an N-terminal cytoplasmic region, a polymorphic neck region containing variable numbers of tandem repeats (VNTR), and a carbohydrate recognition domain (CRD) . The protein functions include:

• Binding and internalizing ligands with mannose-exposed N-linked glycans

• Clearance of von Willebrand factor (VWF) and factor VIII (FVIII) from circulation

• Recognition of various pathogens, including viruses such as SARS-CoV

• Potential tumor suppression in hepatocellular carcinoma through inhibition of the JAK1/STAT3 pathway

The neck region stabilizes CLEC4M on the endothelial surface through tetramerization of monomers and influences the conformation of the carbohydrate recognition domain, affecting its binding capabilities .

How do FITC-conjugated CLEC4M antibodies differ from other fluorescent conjugates for flow cytometry?

FITC-conjugated CLEC4M antibodies provide specific advantages and limitations compared to other fluorescent conjugates:

• FITC (Fluorescein isothiocyanate) has an excitation maximum at 488 nm and emission at approximately 520 nm, making it compatible with standard flow cytometers with 488 nm lasers

• Unlike PE/Cy7 conjugates (excitation = 488 nm, emission = 778 nm), FITC has less compensation needs with PE channels but may show lower sensitivity

• FITC-conjugated antibodies may be more susceptible to photobleaching compared to more photostable fluorophores like Alexa Fluor dyes

• For multicolor panels, FITC can be paired effectively with PE, APC and far-red fluorochromes

• Storage requirements are similar to other conjugates (4°C in the dark), but FITC may be more sensitive to pH changes than some alternatives

When designing multicolor flow cytometry panels, consider that FITC works best for abundantly expressed targets due to its moderate brightness compared to PE or APC conjugates.

What controls should be included when using FITC-conjugated CLEC4M antibodies in flow cytometry?

A comprehensive experimental design for flow cytometry with FITC-conjugated CLEC4M antibodies should include:

• Unstained control: Cells with no antibody to establish autofluorescence baseline

• Isotype control: Matched isotype (IgG2 for clones like MM0241-2U25) conjugated to FITC to assess non-specific binding

• Single-color controls: For compensation when performing multicolor analysis

• Fluorescence Minus One (FMO) control: All antibodies in your panel except CLEC4M-FITC

• Positive control: Cells known to express CLEC4M (e.g., liver sinusoidal endothelial cells or transfected HEK293 cells)

• Negative control: Cells known not to express CLEC4M

• Viability dye: Include a fixable viability dye (e.g., eFluor 780) in a non-overlapping channel to exclude dead cells

For optimal results, include blockers for Fc receptors if analyzing cells that may express them, and validate antibody performance using both positive and negative cell populations before conducting full experiments.

How can CLEC4M polymorphisms affect antibody binding, and what strategies can overcome these challenges?

CLEC4M contains a polymorphic neck region with variable numbers of tandem repeats (VNTR), ranging from 3 to 9 repeats of a conserved 23-amino-acid sequence . This polymorphism presents several research challenges:

Impact on antibody binding:

• Different VNTR lengths alter the spatial organization of the carbohydrate recognition domain (CRD)

• Homozygous vs. heterozygous VNTR status affects oligomerization and binding capacity

• The neck region stabilizes CLEC4M tetramers on the cell surface, affecting epitope accessibility

Strategies to address polymorphism challenges:

• Epitope selection: Use antibodies targeting conserved regions outside the VNTR domain

• Genotyping: Perform CLEC4M VNTR genotyping of samples before antibody studies to stratify results

• Multiple clone approach: Compare binding patterns of different antibody clones (e.g., MM0241-2U25, 120604, OTI7D12)

• Domain-specific controls: Include recombinant CLEC4M variants with defined VNTR lengths as controls

• Cross-validation: Combine flow cytometry with immunoblotting to verify specificity across VNTR variants

When studying populations with known VNTR distribution differences, consider the potential impact of these polymorphisms on antibody recognition patterns and interpret data accordingly.

What are the optimal fixation and permeabilization protocols for CLEC4M detection in different cell types?

The optimal protocols for CLEC4M detection vary based on experimental goals and cell types:

For surface CLEC4M detection (recommended protocol):

• Harvest cells using gentle methods (e.g., EDTA rather than trypsin) to preserve surface epitopes

• Incubate with viability dye (e.g., eFluor 780) for 20 minutes at 4°C

• Wash cells in calcium-containing buffer (e.g., TSM: 20 mM Tris HCl, 150 mM NaCl, 2 mM CaCl₂, 2 mM MgCl₂)

• Block with 5% normal serum matched to secondary antibody species

• Incubate with FITC-conjugated CLEC4M antibody at validated concentration for 30 minutes at 4°C

• Wash twice with buffer and analyze immediately or fix in 1-2% paraformaldehyde

For intracellular trafficking studies:

• Perform surface staining as above

• Fix cells in 4% paraformaldehyde for 15 minutes at room temperature

• Permeabilize with 0.1% saponin or commercial permeabilization buffer

• Re-stain with antibodies against intracellular markers (e.g., early endosomal antigen-1)

• Use confocal microscopy with z-stack analysis to distinguish surface from internalized CLEC4M

Special considerations:

• For liver sinusoidal endothelial cells, gentle isolation techniques are critical as these cells are sensitive to mechanical stress

• When studying CLEC4M-mediated internalization, compare 4°C (binding only) versus 37°C (binding and internalization) conditions

• For dual staining with other markers (e.g., stabilin-2), optimize antibody concentrations to prevent cross-interference

How can researchers effectively analyze CLEC4M-mediated ligand internalization using FITC-conjugated antibodies?

CLEC4M-mediated internalization can be effectively studied using the following methodological approach:

Experimental design for internalization assays:

• Establish CLEC4M-expressing cell system:

  • Use stably transfected cell lines (e.g., HEK293 cells expressing CLEC4M)

  • Compare with control cells lacking CLEC4M expression

  • Consider using cells expressing defined VNTR variants (homozygous vs. heterozygous)

• Dual fluorescence labeling strategy:

  • Label target ligand (e.g., VWF, FVIII) with one fluorophore

  • Use FITC-conjugated anti-CLEC4M antibody to track receptor localization

  • Include early endosomal markers (EEA1) with a third fluorophore

• Time-course analysis protocol:

  • Incubate cells with ligand at 4°C (binding only)

  • Shift cells to 37°C for various time intervals (5-60 minutes)

  • Fix cells at each timepoint with 4% paraformaldehyde

  • Perform immunofluorescence with anti-CLEC4M-FITC and endosomal markers

• Z-stack confocal microscopy analysis:

  • Acquire z-stacks to distinguish membrane-bound from internalized signals

  • Perform quantitative colocalization analysis using appropriate software

  • Compare 4°C control (membrane only) with 37°C samples (internalization)

• Flow cytometry-based internalization assay:

  • Label ligand with pH-sensitive fluorophore (quenched in acidic endosomes)

  • Track surface CLEC4M with FITC-conjugated antibody at different timepoints

  • Quantify receptor internalization by measuring surface CLEC4M reduction over time

Data analysis considerations:

• Calculate percent colocalization between CLEC4M, ligand, and endosomal markers

• Compare internalization rates between different CLEC4M VNTR variants

• For inhibition studies, pretreat cells with mannan (1 mg/mL) to block CLEC4M binding

How can CLEC4M antibodies be used to study hepatocellular carcinoma progression and prognosis?

Research indicates that CLEC4M plays a tumor-suppressive role in hepatocellular carcinoma (HCC), making it a valuable target for prognostic and mechanistic studies:

Experimental approaches for HCC research:

• Tissue expression analysis:

  • Compare CLEC4M expression between HCC and paired non-tumor tissues using FITC-conjugated antibodies for immunohistochemistry

  • Correlate expression levels with clinicopathological features and patient outcomes

  • Develop a standardized scoring system for CLEC4M immunostaining intensity

• Prognostic marker assessment:

  • Analyze CLEC4M expression in patient cohorts with known survival data

  • Create Kaplan-Meier survival curves stratified by CLEC4M expression levels

  • Perform multivariate analysis to determine if CLEC4M is an independent prognostic factor

• Mechanistic investigations:

  • Study JAK1/STAT3 pathway activity in relation to CLEC4M expression using phospho-specific antibodies

  • Perform flow cytometry on HCC cell lines (e.g., Huh7, PLC/PRF/5) with CLEC4M-FITC to track expression changes during experimental manipulation

  • Use CLEC4M overexpression models to study effects on cell proliferation, apoptosis, and signaling pathways

Data analysis framework:

• Compare CLEC4M expression between different HCC stages and grades

• Correlate CLEC4M levels with established HCC biomarkers

• Analyze the relationship between CLEC4M polymorphisms and HCC risk/progression

• Develop multiparameter flow cytometry panels combining CLEC4M-FITC with markers for cell cycle, apoptosis, and JAK/STAT signaling

The experimental data from Huang et al. demonstrated that CLEC4M overexpression inhibited proliferation and enhanced apoptosis in HCC cell lines while suppressing the JAK1/STAT3 pathway, suggesting its potential utility as both a prognostic marker and therapeutic target .

What methodology should be used when studying CLEC4M's role in viral binding and infection processes?

CLEC4M's role in viral binding and infection can be comprehensively studied using the following methodological approach:

Experimental design for viral studies:

• Viral binding assays:

  • Express CLEC4M in suitable cell lines (HEK293 cells) with defined VNTR genotypes

  • Incubate cells with fluorescently labeled virus particles at 4°C (binding only)

  • Quantify binding by flow cytometry using CLEC4M-FITC antibodies to confirm receptor expression

  • Include mannan competition (1 mg/mL) to determine specificity of interactions

• Viral internalization studies:

  • Compare cells expressing homozygous versus heterozygous CLEC4M VNTR variants

  • Track virus internalization using confocal microscopy with immunofluorescence for viral proteins

  • Monitor CLEC4M-virus colocalization in early endosomes and lysosomes over time

  • Use proteasome inhibitors to assess viral degradation pathways

• Trans-infection assays:

  • Incubate CLEC4M-expressing cells with virus, then co-culture with susceptible target cells

  • Quantify viral transfer and infection of target cells

  • Compare trans-infection efficiency between different CLEC4M VNTR variants

• Genetic association studies:

  • Analyze CLEC4M VNTR polymorphisms in infection-exposed versus non-infected populations

  • Perform Hardy-Weinberg equilibrium testing for genotype distributions

  • Calculate odds ratios for infection risk based on homozygous versus heterozygous status

Key methodological considerations:

• Maintain calcium in all buffers (2 mM CaCl₂) to preserve CLEC4M binding capacity

• Include appropriate controls to distinguish specific from non-specific binding

• For SARS-CoV or other BSL-3 pathogens, use pseudotyped viral particles or isolated spike proteins for initial studies

• When comparing VNTR variants, ensure equivalent surface expression levels by titrating transfection conditions

Chan et al. demonstrated that homozygosity for CLEC4M VNTR was associated with protection against SARS-CoV infection, and CLEC4M-expressing cells showed increased viral binding but enhanced proteasome-dependent viral degradation, highlighting the importance of studying both binding and post-binding events .

How can researchers effectively study the interaction between CLEC4M and coagulation factors using antibody-based approaches?

CLEC4M binds both von Willebrand factor (VWF) and factor VIII (FVIII), making it an important regulator of coagulation factor clearance. The following methodological framework enables detailed investigation of these interactions:

Comprehensive experimental approach:

• Solid-phase binding assays:

  • Coat microplates with purified coagulation factors (VWF, FVIII, or VWF-FVIII complex)

  • Detect binding using recombinant CLEC4M-Fc chimera proteins

  • Quantify binding affinity (Kd) through dose-response curves

  • Perform competitive inhibition with mannose polymers (mannan) to confirm specificity

• Flow cytometry analysis:

  • Express CLEC4M in cell lines with defined VNTR genotypes

  • Incubate with fluorescently labeled coagulation factors

  • Use FITC-conjugated CLEC4M antibodies to confirm receptor expression

  • Compare binding at 4°C (surface only) versus 37°C (internalization)

• Glycan dependency studies:

  • Perform enzymatic deglycosylation of coagulation factors:

    • PNGase F for N-glycan removal

    • O-glycosidase for O-glycan removal

  • Compare binding of native versus deglycosylated factors

  • Use lectin blotting to confirm effective deglycosylation

• Internalization and trafficking analysis:

  • Track coagulation factor internalization using confocal microscopy

  • Co-stain for endosomal markers (EEA1) and lysosomal markers (LAMP1)

  • Perform time-course analysis to follow the degradation pathway

  • Use pharmacological inhibitors to identify specific endocytic routes

Experimental data table from literature:

Advanced research considerations:

• Study the impact of CLEC4M VNTR polymorphisms on coagulation factor clearance rates

• Investigate how VWF glycoform variations affect CLEC4M binding affinity

• Explore the potential competition between different CLEC4M ligands in physiological settings

• Examine how CLEC4M-mediated clearance is affected by pathological states

These methodological approaches have revealed that CLEC4M binds to VWF through N-glycan-dependent mechanisms and can internalize both VWF alone and VWF-FVIII complexes, potentially regulating their plasma levels .

How should researchers address inconsistent CLEC4M staining results in primary liver sinusoidal endothelial cells?

Primary liver sinusoidal endothelial cells (LSECs) present unique challenges for CLEC4M detection. A systematic troubleshooting approach includes:

Problem: Low or variable CLEC4M signal intensity

Potential causes and solutions:

• Cell isolation issues:

  • LSECs are fragile and may lose surface markers during harsh isolation

  • Use gentle, optimized isolation protocols with collagenase perfusion

  • Verify LSEC purity using multiple markers (stabilin-2, FcγRIIb2/SE-1)

  • Prepare fresh isolates as LSEC phenotype changes rapidly in culture

• Antibody selection issues:

  • Test multiple antibody clones as epitope accessibility may vary

  • Titrate antibody concentration using positive control cells

  • Consider using signal amplification for low-abundance detection

• Buffer composition problems:

  • Ensure calcium presence (2 mM) in all buffers as CLEC4M is calcium-dependent

  • Avoid detergents that may disrupt membrane integrity

  • Include protease inhibitors to prevent receptor degradation

• Technical variables:

  • Standardize fixation time and temperature (4% paraformaldehyde, 15 min, RT)

  • Block Fc receptors to reduce background on isolated liver cells

  • Use freshly prepared antibody dilutions for each experiment

Validation strategy:

• Use double-staining with established LSEC markers (stabilin-2, SE-1)

• Include rat LSECs as biological controls with known CLEC4M expression

• Perform parallel RNA analysis (RT-PCR) to confirm CLEC4M expression

• Compare staining patterns between fresh isolates and cultured LSECs

Flow cytometry data from Elvevold et al. demonstrates that LSECs express both CLEC4M and other scavenger receptors, which can be used for co-staining validation approaches .

What are the critical factors affecting CLEC4M antibody performance in different experimental applications?

Multiple factors can significantly impact the performance of FITC-conjugated CLEC4M antibodies across different applications:

Critical performance factors:

• Epitope accessibility factors:

  • CLEC4M's oligomeric state affects epitope exposure

  • Neck region VNTR polymorphisms alter protein conformation

  • Calcium-dependent conformational changes influence antibody binding

  • Ligand binding may induce epitope masking

• Technical optimization parameters:

  • Flow cytometry: Optimal concentrations are typically 2-5 μg/mL

  • Immunohistochemistry: Antigen retrieval methods critically affect staining

  • Western blotting: Reducing vs. non-reducing conditions impact detection

  • Immunoprecipitation: Buffer composition affects complex stability

• Sample-specific considerations:

  • Tissue fixation methods impact epitope preservation (fresh-frozen vs. FFPE)

  • Cell surface CLEC4M may be cleaved by proteases during sample processing

  • Expression levels vary significantly between liver, lymph nodes, and other tissues

  • Pathological conditions can alter glycosylation and expression patterns

• Clone-specific characteristics:

  • Clone MM0241-2U25: Optimal for flow cytometry and immunohistochemistry

  • Clone 120604: Used to establish CD designation, works well in multicolor panels

  • Clone OTI7D12: Validated for western blotting applications

Performance optimization matrix:

Validation approach:

• Include both positive controls (CLEC4M-transfected cells) and negative controls

• Perform parallel staining with multiple CLEC4M antibody clones

• Validate results with complementary detection methods (flow + microscopy)

• Consider genetic verification of CLEC4M VNTR status in heterogeneous samples

How can researchers distinguish between specific and non-specific binding when using FITC-conjugated CLEC4M antibodies?

Distinguishing specific from non-specific binding is crucial for accurate CLEC4M analysis. A systematic verification approach includes:

Comprehensive validation strategy:

• Essential control samples:

  • Positive control: CLEC4M-transfected HEK293 cells with confirmed expression

  • Negative control: Non-transfected parent cell line

  • Tissue controls: Liver sinusoidal endothelial cells (positive) vs. hepatocytes (negative)

  • Blocking controls: Pre-incubation with unconjugated antibody to demonstrate specificity

• Molecular validation techniques:

  • siRNA knockdown: Demonstrate signal reduction following CLEC4M silencing

  • CRISPR knockout: Generate CLEC4M-null cells as definitive negative controls

  • Recombinant expression: Create dose-dependent expression models for calibration

  • Domain deletion mutants: Express CLEC4M lacking specific domains to map epitopes

• Signal verification methods:

  • Dual-antibody approach: Use two antibodies targeting different CLEC4M epitopes

  • Fluorescence minus one (FMO): Include all antibodies except anti-CLEC4M-FITC

  • Isotype control: Match isotype (IgG2) and fluorophore concentration

  • Dilution series: Perform antibody titration to identify optimal signal-to-noise ratio

• Technical optimization approaches:

  • Fc receptor blocking: Use commercial Fc blockers before antibody incubation

  • Filtering strategy: Apply hierarchical gating to exclude debris and aggregates

  • Live/dead discrimination: Include viability dye to exclude nonspecific binding to dead cells

  • Autofluorescence correction: Apply spectral unmixing for tissues with high autofluorescence

Data interpretation framework:

• Calculate signal-to-noise ratio between positive and negative controls

• Define positivity thresholds based on isotype control staining

• Consider using fluorescence intensity (MFI) ratios rather than absolute values

• For tissues, compare staining patterns with known CLEC4M expression in literature

When studying CLEC4M in heterogeneous cell populations like non-parenchymal liver cells, dual staining with established cell-type specific markers (stabilin-2 for LSECs, CD68 for Kupffer cells) can help distinguish specific CLEC4M expression from background .

How can FITC-conjugated CLEC4M antibodies be integrated into single-cell analysis workflows?

CLEC4M detection can be effectively integrated into advanced single-cell analysis workflows:

Comprehensive single-cell strategy:

• Single-cell suspension preparation protocol:

  • For liver tissue: Optimize enzymatic digestion to preserve CLEC4M epitopes

  • For cell lines: Use non-enzymatic dissociation methods when possible

  • Include calcium (2 mM) in all buffers to maintain CLEC4M conformation

  • Maintain cells at 4°C to prevent receptor internalization

• Multi-parametric flow cytometry panel design:

  • Include CLEC4M-FITC as a key marker for endothelial cell subtyping

  • Pair with additional markers: CD31 (pan-endothelial), stabilin-2 (LSEC-specific)

  • Add functional markers: scavenger receptors, mannose receptor

  • Include lineage markers to exclude other cell types

• Cell sorting parameters for single-cell applications:

  • Use 100 μm nozzle for gentle sorting of endothelial cells

  • Collect in media containing calcium and serum to maintain viability

  • Sort directly into lysis buffer for immediate RNA/protein analysis

  • Include index sorting to retain fluorescence intensity data

• Integration with transcriptomic/proteomic platforms:

  • CITE-seq: Conjugate CLEC4M antibodies to DNA barcodes for simultaneous protein and RNA analysis

  • Single-cell RNA-seq: Use flow-sorted CLEC4M+ populations for transcriptomic profiling

  • Imaging mass cytometry: Combine CLEC4M-FITC with metal-tagged antibodies for spatial analysis

  • Spatial transcriptomics: Correlate CLEC4M protein expression with local gene expression patterns

Advanced analytical approaches:

• Perform trajectory analysis to identify CLEC4M expression dynamics during cell differentiation

• Create dimensional reduction visualizations (UMAP, t-SNE) incorporating CLEC4M as a key parameter

• Develop automated classification algorithms to identify CLEC4M+ cell subtypes

• Correlate CLEC4M expression levels with transcriptional signatures

These advanced workflows enable researchers to identify novel CLEC4M-expressing cell populations and characterize their functional states with unprecedented resolution.

What are the most effective strategies for studying CLEC4M's roles in tumor microenvironments using imaging approaches?

CLEC4M's role in tumor microenvironments can be effectively investigated using advanced imaging strategies:

Comprehensive imaging methodology:

• Multiplex immunofluorescence protocol:

  • Optimize CLEC4M-FITC staining on frozen or FFPE tumor sections

  • Combine with markers for: endothelial cells (CD31), tumor cells, immune cells

  • Include functional markers: JAK1/STAT3 pathway components, proliferation/apoptosis markers

  • Employ tyramide signal amplification for detecting low-abundance epitopes

• Spatial analysis framework:

  • Quantify CLEC4M+ vessel density in tumor regions vs. adjacent normal tissue

  • Measure distances between CLEC4M+ vessels and tumor invasion fronts

  • Analyze colocalization of CLEC4M with markers of tumor progression

  • Create spatial maps of CLEC4M expression across tumor microenvironments

• Live cell imaging approaches:

  • Generate tumor cell lines expressing fluorescent reporters for JAK/STAT activity

  • Co-culture with CLEC4M+ endothelial cells labeled with membrane dyes

  • Perform time-lapse imaging to track interactions and signaling dynamics

  • Use FRET-based biosensors to monitor CLEC4M-mediated signaling events

• Intravital microscopy applications:

  • Develop fluorescently labeled anti-CLEC4M Fab fragments for in vivo imaging

  • Create window chamber models to visualize CLEC4M+ vessels in live tumors

  • Track tumor cell interactions with CLEC4M+ endothelium in real-time

  • Monitor effects of CLEC4M-targeting interventions on tumor vasculature

Data analysis considerations:

• Employ machine learning algorithms for automated identification of CLEC4M+ structures

• Develop spatial statistics to quantify CLEC4M distribution patterns

• Correlate CLEC4M expression patterns with clinical outcome data

• Integrate imaging data with molecular profiles from the same tumor regions

In hepatocellular carcinoma research, these imaging approaches can reveal how CLEC4M expression in tumor-associated endothelium influences cancer cell proliferation and apoptosis through JAK1/STAT3 signaling, potentially explaining the favorable prognosis associated with CLEC4M overexpression .

How can CLEC4M antibodies be used in developing novel therapeutic targeting strategies?

CLEC4M's unique expression pattern and functional properties make it a promising therapeutic target, which can be explored using the following research strategies:

Therapeutic research framework:

• Target validation approaches:

  • Characterize CLEC4M expression across normal and diseased tissues using FITC-conjugated antibodies

  • Evaluate the safety profile based on restricted expression pattern (primarily liver and lymph node endothelium)

  • Determine the functional consequences of CLEC4M modulation in different pathological contexts

  • Assess the role of CLEC4M polymorphisms in predicting therapeutic responses

• Antibody-based therapeutic development:

  • Generate and screen anti-CLEC4M antibodies with agonist vs. antagonist properties

  • Develop antibody-drug conjugates targeting CLEC4M+ cells in specific diseases

  • Create bispecific antibodies linking CLEC4M to immune effector cells

  • Design antibodies targeting specific CLEC4M epitopes to modulate ligand binding

• Ligand-directed approaches:

  • Identify high-affinity mannose-containing glycan structures for CLEC4M targeting

  • Develop glycan-modified nanoparticles for liver-specific drug delivery

  • Create chimeric molecules combining CLEC4M ligands with therapeutic payloads

  • Design competitive inhibitors of pathogen binding to CLEC4M

• Therapeutic applications by disease area:

  • Hepatocellular carcinoma: Enhance CLEC4M expression or signaling to suppress JAK1/STAT3 pathway

  • Viral infections: Block viral binding sites on CLEC4M to prevent pathogen entry

  • Coagulation disorders: Modulate CLEC4M-mediated clearance of VWF and FVIII

  • Liver-targeted drug delivery: Exploit CLEC4M for hepatic targeting of therapeutics

Target assessment considerations:

• Evaluate the impact of CLEC4M VNTR polymorphisms on therapeutic targeting

• Consider potential competition between therapeutic agents and endogenous ligands

• Assess the risk of altering physiological clearance functions of CLEC4M

• Develop biomarkers to identify patients likely to respond to CLEC4M-targeted therapies

These research approaches can guide the development of novel therapeutic strategies leveraging CLEC4M's unique properties, while FITC-conjugated antibodies provide essential tools for target validation and patient stratification studies.