Anti-Mouse CD106 (VCAM-1) (Clone M/K-2.7) – Purified in vivo GOLD™ Functional Grade

Anti-Mouse CD106 (VCAM-1) (Clone M/K-2.7) – Purified in vivo GOLD™ Functional Grade

Product No.: C2491

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Clone
M/K-2.7
Target
CD106 (VCAM-1)
Formats AvailableView All
Product Type
Hybridoma Monoclonal Antibody
Alternate Names
VCAM-1, INCAM-110
Isotype
Rat IgG1 κ
Applications
IF
,
in vivo
,
N

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Antibody Details

Product Details

Reactive Species
Mouse
Host Species
Rat
Recommended Dilution Buffer
Immunogen
Stromal cells derived from mouse bone marrow
Product Concentration
≥ 5.0 mg/ml
Endotoxin Level
< 1.0 EU/mg as determined by the LAL method
Purity
≥95% monomer by analytical SEC
>95% by SDS Page
Formulation
This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.
Product Preparation
Functional grade preclinical antibodies are manufactured in an animal free facility using only in vitro protein free cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.
Storage and Handling
Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles.
Regulatory Status
Research Use Only
Country of Origin
USA
Shipping
2 – 8° C Wet Ice
Additional Applications Reported In Literature ?
IF,
in vivo,
N
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Description

Specificity
The M/K-2.7 activity is specifically directed against mouse CD106 also known as VCAM-1 and INCAM-110.
Background
CD106 is a single-chain type I glycoprotein with a molecular weight of 110 kDa. It is upregulated in response to inflammatory stimuli and cytokines, and it plays an important role in leukocyte adhesion, transmigration, and T-cell proliferation by binding to integrins CD49d/CD29 (VLA-4) and α4β71. It has implications in several pathologies, including heart diseases, inflammation, and cancer metastasis2. The regulation and function of CD106 in immune responses highlight its potential as a therapeutic target in treating these conditions.

The M/K-2.7 clone was developed using stromal cells derived from mouse bone marrow as the immunogen. It has been widely used in various research contexts, particularly in studies involving in vivo VCAM-1 neutralization, immunofluorescence techniques, and more. This clone demonstrates its versatility across a range of experimental setups and is a valuable tool for investigating vascular cell adhesion mechanisms and the inflammatory process. It is particularly useful for research focused on inflammatory processes, immune cell migration, and the study of vascular biology3-6.

Antigen Distribution
CD106 is predominantly expressed on activated vascular endothelial cells, as well as on various other cells including follicular and interfollicular dendritic cells, some macrophages, and bone marrow stromal cells. Its expression can also be found in non-vascular cells within joints, kidneys, muscles, the heart, the placenta, and the brain.
Ligand/Receptor
VLA-4 (α4/β1 integrin) and LPAM-1 (α4/β7 integrin)
NCBI Gene Bank ID
UniProt.org
Research Area
Cell Adhesion
.
Cell Biology
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Immunology
.
Neuroinflammation
.
Neuroscience
.
CD Molecules
.
Stem Cells

Leinco Antibody Advisor

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The monoclonal antibody clone M/K-2.7 is used in in vivo mouse studies primarily as a function-blocking antibody directed against mouse VCAM-1 (Vascular Cell Adhesion Molecule-1, also known as CD106). It is a rat IgG antibody that binds specifically and with high affinity to mouse VCAM-1, neutralizing its biological activity.

Key in vivo applications include:

  • Blocking VCAM-1 function in mouse models to assess the role of VCAM-1 in pathophysiological processes, such as inflammation, cancer progression, and vascular injury.

  • Targeted drug delivery and biodistribution studies: When conjugated to therapeutic agents or nanoparticles (such as immunoliposomes), M/K-2.7 enables specific targeting to VCAM-1–expressing endothelium, especially at sites of inflammation or injury. For example, in models of brain inflammation induced by TNF-? injection, M/K-2.7 facilitated highly specific and increased uptake of targeted agents in the inflamed brain regions.

  • Studying molecular function in disease models: M/K-2.7 has been used to evaluate VCAM-1’s role in diseases such as collagen-induced arthritis and ovarian cancer metastasis. In these studies, M/K-2.7 was administered (systemically, e.g., intravenous or intraperitoneal injection) to block VCAM-1-mediated interactions, resulting in measurable effects on disease progression, such as reduced inflammation or increased response to chemotherapy.

Administration and Dosing:
Typical protocols involve systemic (often intravenous or intraperitoneal) administration of M/K-2.7 to mice, either alone or conjugated to drug carriers. The antibody is selected for its ability to achieve efficient, high-specificity targeting and functional blockade of VCAM-1 in living animals.

Summary Table:| Application | How M/K-2.7 Is Used | Reference ||--------------------------------------|-------------------------------|------------------|| Blockade of VCAM-1 in vivo | Injected to neutralize VCAM-1 | || Targeted drug/nanoparticle delivery | Used as targeting ligand | || Cancer or inflammation models | Inhibits VCAM-1 binding | |

Mechanism:
By binding to mouse VCAM-1, M/K-2.7 prevents its interaction with ligands such as ?4?1 integrin (VLA-4), thereby interfering with leukocyte adhesion, transmigration, and related pathological processes.

Note:
M/K-2.7 is particularly valued for its high specificity and neutralizing activity in mouse models, enabling both target validation and proof-of-concept studies in VCAM-1–mediated disease mechanisms.

The correct storage temperature for sterile packaged clone M/K-2.7 is:

  • Short-term (1–2 weeks): +4°C
  • Long-term: -20°C

Before opening the vial, centrifuge it briefly. For extended preservation, aliquot the antibody to avoid repeated freeze/thaw cycles, which can degrade its stability. These practices are standard for monoclonal antibodies, ensuring maximum stability and activity.

If storage longer than a year is needed, ultra-low temperatures (e.g., -80°C) can offer even greater stability, though this is rarely necessary for standard applications.

Always avoid room temperature and temperature fluctuations, and consult the specific product datasheet if available to confirm any antibody-specific instructions.

Other commonly used antibodies or proteins used in combination or for comparison with M/K-2.7 (an anti-mouse VCAM-1 monoclonal antibody) in the literature include:

  • Anti-VCAM-1 Fab fragments: Used in parallel to M/K-2.7 to confirm specificity for VCAM-1 and to assess functional effects in adhesion assays.
  • Purified VCAM-1 specific polysera: Served as a positive control in detection assays of native VCAM-1 on various cell types (e.g., HUVECs, PAECs).
  • Anti-VCAM-1 IgG: Used for comparison of neutralizing effects along with Fab fragments and M/K-2.7, in assays measuring leukocyte binding to endothelial cells.
  • Secondary detection antibodies: Typically, anti-mouse IgG or IgM isotype-specific antibodies are used to detect primary binding of M/K-2.7 in flow cytometry or immunohistochemistry assays (not always explicitly stated, but standard for monoclonal detection workflows in the literature).

In adhesion and flow cytometry assays with M/K-2.7, common co-used antibodies/proteins include:

  • CSFE-labeled U937 cells: These serve as model leukocytes in binding assays to measure the effect of VCAM-1 inhibition.
  • Other endothelial cell markers or leukocyte integrins may be used as context-specific controls, but primary literature focuses on direct comparisons of different anti-VCAM-1 formats.

In summary, M/K-2.7 is most often used alongside other anti-VCAM-1 antibodies (e.g., Fab fragments, IgG forms, polysera) and standard detection reagents for validation, specificity, and functional studies targeting VCAM-1.

Clone M/K-2.7 is a monoclonal antibody targeting mouse VCAM-1 (Vascular Cell Adhesion Molecule-1), and its citations in scientific literature focus on its role in blocking VCAM-1's interaction with integrins, with key findings in transplant survival and inflammation reduction.

Key findings from M/K-2.7 citations:

  • Transplant Survival Enhancement:

    • Treatment with M/K-2.7 significantly prolongs allograft survival in animal models. In a mouse islet allograft study, M/K-2.7 prolonged survival by more than 100 days, with a graft survival rate of 75%.
    • In cardiac allograft mice, M/K-2.7 therapy extended survival by about five days compared to controls, suggesting efficacy in reducing acute rejection.
  • Mechanism:

    • M/K-2.7 specifically binds to Ig-like domains 1 and 4 of VCAM-1, thereby blocking its interaction with ?4?1 integrin, which is critical for leukocyte adhesion and migration during inflammatory and rejection processes.
    • VCAM-1 blockade by M/K-2.7 has been reported to reduce CD4^+ T cell and macrophage migration into grafts, contributing to decreased rejection and inflammation.
  • Experimental Findings:

    • In collagen-induced arthritis models, administration of M/K-2.7 results in reduced joint inflammation, indicating a broader potential for anti-VCAM-1 therapies in autoimmune and inflammatory diseases.
    • Biochemical studies demonstrate that M/K-2.7 and related Fab fragments can strongly block leukocyte–endothelial cell interactions in vitro.
    • The antibody exhibits cross-reactivity with VCAM-1 from multiple species (mouse, human, rat, porcine), making it a versatile tool in translational research.

Additional Notes:

  • Some studies emphasize the antibody's effect on transendothelial migration rather than merely adhesion, suggesting a nuanced mechanism of immune modulation.
  • The antibody has served as a benchmark for developing humanized or chimeric anti-VCAM-1 antibodies with enhanced therapeutic promise.

Summary Table: Main Effects of M/K-2.7 clone

EffectModel/ContextKey DetailsSource
Allograft survivalIslet/cardiac grafts>100 days in islet model; ~5 days cardiac; reduced rejection
Inflammation reductionArthritis modelsDecreased joint inflammation
Mechanism of actionIn vitro/in vivoBlocks VCAM-1/?4?1 integrin, affects migration not adhesion
Species cross-reactivityBiochemical analysisBinds VCAM-1 from mouse, human, rat, porcine

These findings position clone M/K-2.7 as an important research and potential therapeutic tool for studying and modulating VCAM-1-mediated immune and inflammatory processes in transplantation and autoimmune disease.

References & Citations

1. Tolstrup A, Hokland P, Nielsen B, Justesen J, Hokland M. J Interferon Res. 1993;13(6):433-441.
2. Salajegheh A, Salajegheh A. Springer International Publishing; 2016:375-379.
3. Hession C, Moy P, Tizard R, et al. Biochem Biophys Res Commun. 1992;183(1):163-169.
4. Osborn L, Hession C, Tizard R, et al. Cell. 1989;59(6):1203-1211.
5. Miyake K, Medina K, Ishihara K, Kimoto M, Auerbach R, Kincade PW. The Journal of cell biology. 1991;114(3):557-565.
6. Kumar AG, Dai XY, Kozak CA, Mims MP, Gotto AM, Ballantyne CM. The Journal of Immunology. 1994;153(9):4088-4098.
7. Yousef H, Czupalla CJ, Lee D, et al. Nat Med. 2019;25(6):988-1000.
8. de Juan A, Ince LM, Pick R, et al. Circulation. 2019;140(13):1100-1114.
9. He W, Holtkamp S, Hergenhan SM, et al. Immunity. 2018;49(6):1175-1190.e7.
10. Kapitsinou PP, Sano H, Michael M, et al. J Clin Invest. 2014;124(6):2396-2409.
11. Chow A, Huggins M, Ahmed J, et al. Nat Med. 2013;19(4):429-436.
12. Brinkman CC, Rouhani SJ, Srinivasan N, Engelhard VH. J Immunol. 2013;191(5):2412-2425.
13. Thomas SY, Scanlon ST, Griewank KG, et al. J Exp Med. 2011;208(6):1179-1188.

Formats Available

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Disclaimer AlertProducts are for research use only. Not for use in diagnostic or therapeutic procedures.