Source:
Target: CD13 antigen (expressed on granulocytes, monocytes, and epidermal basal cells).
| Parameter | CTCLs | Benign Lesions |
|---|---|---|
| MY7+ CD4+ Cells | >50% | <10% |
| MY7+ Basal Cells | Absent | Present |
| Diagnostic Accuracy | High specificity | Confirmed via IHC/IF |
Mechanism: MY7 modulation may involve epidermal cytokine secretion affecting antigen expression.
Source:
Target: Myosin heavy chain 7 (MYH7), critical for cardiac/skeletal muscle contraction.
Pathological Role:
MYH7 mutations linked to hypertrophic cardiomyopathy (HCM).
Antibody enables study of MYH7’s role in muscle integrity and disease mechanisms.
| Conjugate Type | Catalog Number | Price (USD) |
|---|---|---|
| Unconjugated | sc-53089 | $316.00 |
| HRP-conjugated | sc-53089 HRP | $316.00 |
| Alexa Fluor® 647 | sc-53089 AF647 | $357.00 |
Sources: ,
Target: Matrix metalloproteinase-7 (MMP-7), implicated in cancer progression.
Function:
Blocks MMP-7 catalytic activity (IC50 = 132 ± 10 nM) via steric hindrance at the active site.
Induces apoptosis in pancreatic cancer cells by stabilizing Fas ligand.
Synergizes with chemotherapeutics (gemcitabine, oxaliplatin).
| Parameter | Value/Outcome |
|---|---|
| Binding Affinity | 132 ± 10 nM IC50 |
| Therapeutic Effect | Reduced migration |
| Diagnostic Use | Detects active MMP-7 in PDAC biopsies |
Applications: Flow cytometry, intracellular staining.
Cross-Reactivity: Human, rat, rabbit.
Storage: -20°C to -70°C; avoid freeze-thaw cycles.
Source:
Target: HIV-1 CD4-binding site.
Neutralization Breadth: 98% of HIV-1 isolates.
Mechanism: Avoids glycan steric clashes via unique light-chain orientation.
| Antibody | Neutralization % | IC50 (ng/mL) |
|---|---|---|
| N6 | 98% | <100 |
| VRC01 | 78% | ~500 |
Source:
Target: SARS-CoV-2 spike protein epitopes.
| Antibody | Target Region | Neutralization IC50 (ng/mL) |
|---|---|---|
| 2-15 | RBD | 9 |
| 2-17 | NTD | 12 |
KEGG: spo:SPBC16A3.13
STRING: 4896.SPBC16A3.13.1
MY7 is a monoclonal antibody that recognizes CD13 (aminopeptidase N), a surface antigen normally expressed on peripheral granulocytes and monocytes. Interestingly, it also cross-reacts with an antigen expressed on epidermal basal cells. The dual reactivity pattern of MY7 antibody in both hematopoietic cells and epidermal structures makes it particularly valuable for dermatopathological investigations. Under normal conditions, MY7 shows positive staining of basal cells in the epidermis while showing minimal reactivity with dermal CD4+ T-cells in benign conditions .
MY7 antibody demonstrates a unique dual modulation pattern that has significant diagnostic value. In cutaneous T-cell lymphomas (CTCLs), more than 50% of CD4+ tumoral cells in the dermis express MY7 antigen, while the epidermal basal cells become MY7-negative. This pattern directly contrasts with benign inflammatory conditions, where less than 10% of dermal CD4+ cells express MY7, and basal cells maintain normal MY7 expression. This inverse relationship between dermal and epidermal MY7 staining provides a valuable marker for differentiating malignant from benign cutaneous lymphoid infiltrates .
For optimal results with MY7 antibody, researchers should implement double labeling techniques. Indirect immunofluorescence with double labeling (MY7 and CD4) and immunoperoxidase techniques have both demonstrated efficacy in research studies. When performing immunohistochemistry, it's critical to assess both the epidermal basal cell layer and the dermal infiltrate to observe the characteristic modulation pattern. This dual assessment is essential as the diagnostic value comes from the relative expression patterns rather than absolute staining intensity .
The modulation of MY7 labeling in cutaneous T-cell lymphomas appears to be related to the secretion of epidermal cytokines. Research indicates that interferon-alpha can induce MY7 (CD13) expression in basal cells of CTCL. This suggests a complex immunomodulatory network where cytokines secreted by malignant T-cells or reactive immune cells influence the expression patterns of MY7 in both dermal and epidermal compartments. Researchers investigating this phenomenon should consider incorporating cytokine profiling alongside MY7 immunostaining to better understand these regulatory pathways .
Validation of MY7 antibody specificity should ideally employ genetic approaches using knockout or knockdown controls. Based on comprehensive antibody characterization studies, genetic validation strategies are significantly more reliable than orthogonal approaches, particularly for immunofluorescence applications. While orthogonal strategies (which rely on known information about the target protein) may be somewhat suitable for Western blot, they yield much less reliable results for immunofluorescence, where only 38% of antibodies validated through orthogonal approaches were confirmed using knockout controls .
The gold standard for MY7 antibody validation involves testing on both wild-type cells and isogenic CRISPR knockout versions of the same cells. This approach costs approximately $25,000 but provides definitive validation data that greatly exceeds the reliability of other methods. Researchers should consider these validation costs against the even higher costs of research conducted with unvalidated antibodies, which contributes to an estimated $1 billion in wasted research funding annually .
| Application | Success Rate for Validated Antibodies | Key Considerations |
|---|---|---|
| Immunofluorescence (IF) | 80% for genetically validated antibodies | Requires paired WT/KO controls in same field |
| Western Blot (WB) | 80-89% depending on validation method | More forgiving than IF, can detect denatured antigens |
| Immunoprecipitation (IP) | Variable; dependent on protein solubility | Requires non-denaturing conditions for many targets |
False results with MY7 antibody can stem from multiple sources. Insufficient antibody validation is a primary concern, as approximately 50% of commercial antibodies fail to meet basic standards for characterization. This problem leads to estimated financial losses of $0.4–1.8 billion annually in research funding in the United States alone. Common technical issues include improper tissue preparation (fixation affecting epitope accessibility), suboptimal antibody dilution, and inadequate blocking of non-specific binding sites .
For MY7 specifically, false negative results in CTCL diagnosis might occur if sampling is performed from areas with minimal tumor infiltration, while false positives might result from certain inflammatory conditions with activated monocytic infiltrates expressing CD13. Researchers should always include appropriate positive and negative controls, including known CTCL cases and benign inflammatory dermatoses .
At minimum, researchers should employ tissue-matched positive and negative controls when using MY7 antibody. For CTCL diagnosis, this includes:
Known CTCL cases with confirmed MY7+/CD4+ dermal infiltrate and MY7- basal cells
Benign inflammatory dermatoses showing MY7-/CD4+ dermal infiltrate and MY7+ basal cells
Normal skin to establish baseline MY7 expression in epidermal basal cells
For cell-based research, the gold standard control involves paired wild-type and CRISPR knockout cell lines tested in parallel. When using immunofluorescence, researchers should ideally employ a mosaic imaging approach that captures both wild-type and knockout cells in the same visual field to reduce imaging and analysis biases .
Researchers should prioritize antibodies with publicly available characterization data. Resources like the RRID Portal Community and Antibody Registry (containing over 2.5 million commercial antibodies) provide searchable databases of characterized antibodies. The YCharOS initiative (Antibody Characterization through Open Science) makes comprehensive antibody characterization data freely available through ZENODO, a data-sharing website operated by CERN .
When selecting MY7 antibody, researchers should look for:
Evidence of validation using genetic approaches (knockout/knockdown controls)
Application-specific validation data (not just general claims of reactivity)
Publication record showing successful use in similar experimental systems
Clear documentation of clone number, host species, and immunogen information
The clonality of MY7 antibody significantly impacts its performance characteristics. Large-scale antibody characterization studies have shown that recombinant antibodies generally perform better than monoclonal antibodies, which in turn outperform polyclonal antibodies. When selecting MY7 antibody preparations, researchers should consider this hierarchy of performance reliability .
Emerging technologies that could enhance MY7 antibody applications include multiplexed imaging techniques that allow simultaneous visualization of multiple markers alongside MY7, providing better context for interpretation of MY7 expression patterns. Advanced validation technologies, such as genome-wide CRISPR knockout libraries for antibody screening, hold promise for more comprehensive validation of antibodies like MY7 .
Additionally, proteome-wide approaches targeting the human proteome will benefit research using MY7 antibody. Creation of broadly accessible biobanks of bespoke knockout cells for each human gene should be a priority for the research community, as this would dramatically simplify antibody validation processes. Such resources would allow researchers to definitively validate MY7 antibody performance across different experimental systems .
Single-cell technologies offer powerful complements to traditional MY7 antibody-based studies. Single-cell RNA sequencing can correlate MY7/CD13 protein expression with transcript levels and broader gene expression patterns, potentially revealing new insights into the biology of cutaneous T-cell lymphomas. Mass cytometry (CyTOF) allows simultaneous detection of dozens of markers alongside MY7, enabling more comprehensive immunophenotyping of lymphoid infiltrates .
These approaches could help researchers better understand the heterogeneity within CTCL populations and potentially identify new diagnostic markers or therapeutic targets. Combining traditional MY7 immunohistochemistry with these advanced technologies may reveal new aspects of CD13 biology in both normal and pathological skin conditions .