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

- -
- -
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

- -
- -
Select Product Size
- -
- -

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
.
Immunology
.
Neuroinflammation
.
Neuroscience
.
CD Molecules
.
Stem Cells

Leinco Antibody Advisor

Powered by AI: AI is experimental and still learning how to provide the best assistance. It may occasionally generate incorrect or incomplete responses. Please do not rely solely on its recommendations when making purchasing decisions or designing experiments.

Clone M/K-2.7 is a rat monoclonal antibody that specifically targets mouse CD106 (VCAM-1), and it is commonly used in vivo for VCAM-1 neutralization studies in mice.

Key in vivo applications in mice include:

  • VCAM-1 neutralization: The primary use is blocking VCAM-1’s function, which interrupts leukocyte adhesion, migration (transmigration), and immune cell interactions within inflamed tissues.

  • Modulation of inflammation models: It is frequently employed in models of inflammatory diseases such as arthritis and hepatitis to test the role of VCAM-1 in disease progression, leukocyte recruitment, and tissue injury. For example, M/K-2.7 antibody administration has been reported to modulate joint inflammation in collagen-induced arthritis and exacerbate liver injury by affecting NK cell depletion.

  • Immunological studies: The antibody is applied to study T cell proliferation and co-stimulation pathways mediated by VCAM-1, and to investigate immune cell trafficking in various tissues (including vasculature, brain, heart, kidney, and others).

  • Vascular biology research: It is used to assess endothelial cell activation, vascular permeability, and the molecular mechanisms underlying cardiovascular conditions such as hypertensive heart condition and subretinal fibrosis.

Additional relevant details:

  • M/K-2.7 is effective for in vivo administration due to its high purity, low endotoxin, and validated neutralizing activity.
  • It is also utilized for flow cytometry applications (when conjugated to fluorescent dyes), enabling detection and quantification of VCAM-1 expression on different cell types.
  • Experimental readouts may include immunofluorescence (IF), ELISA, and functional assays for pathway analysis.

In summary, clone M/K-2.7 is primarily used for VCAM-1 neutralization and to dissect the role of VCAM-1 in immune cell trafficking, inflammation, and cardiovascular or tissue injury models in mice.

The M/K-2.7 antibody targets mouse CD106 (VCAM-1), and in published research, it is frequently used with other antibodies and proteins related to immune cell markers, endothelial cell markers, and adhesion molecules, depending on specific study aims.

Commonly co-used antibodies/proteins include:

  • CD49d (VLA-4) and CD29 (β1 integrin): These are VCAM-1 ligands and are often studied together to explore leukocyte adhesion and transmigration.
  • CD45 and CD4/CD8: Markers for specific leukocyte (especially T cell) populations, used to characterize immune cell infiltration and tissue-resident memory T cells (TRM).
  • ICAM-1 (CD54): Another major adhesion molecule on endothelial cells, frequently examined alongside VCAM-1 in studies of inflammation and transmigration.
  • Endothelial cell markers (e.g., CD31/PECAM-1): Used to confirm endothelial cell identity when studying VCAM-1 expression or function.
  • NK cell markers (e.g., NK1.1 in mouse): In experiments depleting natural killer cells, M/K-2.7 for VCAM-1 may be paired with anti-NK1.1 antibodies.
  • Cytokines and stimulating agents: Recombinant TNF-α or IL-1β used to induce VCAM-1 expression on cells prior to antibody testing.

Experimental applications:

  • Flow cytometry (FACS): Frequently involves panels including M/K-2.7 with anti-CD45, anti-CD4, anti-CD8, anti-NK1.1, and anti-CD31.
  • Immunofluorescence and immunohistochemistry: M/K-2.7 is often paired with other cell type-specific or activation-specific antibodies.
  • Functional/neutralization assays: Anti-VCAM-1 used alongside blocking antibodies against ICAM-1, VLA-4, or other adhesion molecules to dissect specific pathways.

Summary Table: Common co-used targets/proteins

Antibody/ProteinResearch Context
CD49d (VLA-4), CD29Leukocyte adhesion studies
CD45, CD4, CD8Immune cell characterization
NK1.1NK cell depletion experiments
ICAM-1 (CD54)Endothelial function/inflammation
CD31 (PECAM-1)Endothelial cell identification
Cytokines (TNF-α, IL-1β)VCAM-1 induction assays

The panel composition may vary based on whether the study focuses on immunology, vascular biology, or in vivo cell trafficking. For additional details on experimental combinations, flow panels, or molecular interactions, review primary literature or specific protocols cited in the manufacturer datasheets.

The clone M/K-2.7 is a widely cited rat monoclonal antibody targeting mouse CD106 (VCAM-1), primarily used for research on vascular biology, inflammation, immune cell trafficking, and transplant immunology.

Key findings from scientific literature using clone M/K-2.7 include:

  • VCAM-1 Characterization and Detection: M/K-2.7 specifically binds to mouse VCAM-1 (aka CD106), a 110 kDa glycoprotein upregulated on vascular endothelium during inflammation. This property enables sensitive detection of VCAM-1 expression in various tissues under physiological and pathological conditions.

  • Mechanistic Studies in Inflammation and Transplantation:

    • Anti-inflammatory/protective effects: Functional use of M/K-2.7 to block VCAM-1 shows that VCAM-1 is critical for leukocyte adhesion, transmigration, and T cell co-stimulation. Blocking it reduces leukocyte infiltration in inflamed tissues.
    • Transplant rejection models: M/K-2.7 has been shown to prolong allograft survival in several mouse models, including islet and cardiac transplantation, correlating with decreased immune cell infiltration and attenuated rejection. For instance, treatment with M/K-2.7 extended islet graft survival by over 100 days and cardiac graft survival by five days in mice.
    • Domain specificity: M/K-2.7 binds specifically to Ig-like domains 1 and 4 of VCAM-1, providing key evidence for their role in leukocyte migration and immune cell trafficking during transplantation and inflammation.
  • Experimental Applications: The M/K-2.7 antibody is frequently cited for:

    • In vivo neutralization of VCAM-1 function in mouse models.
    • Immunofluorescence and immunohistochemistry to localize VCAM-1 expression in tissue sections and cell culture.
  • Molecular Interactions: Research using M/K-2.7 reinforces that VCAM-1 interacts with integrins α4β1 (VLA-4) and α4β7, which mediate immune cell adhesion and transmigration—pivotal processes in chronic inflammation and autoimmunity.

In summary: Clone M/K-2.7 has been foundational in demonstrating VCAM-1’s roles in endothelial activation, immune cell migration, graft rejection, and in providing a valuable tool for dissecting the molecular mechanisms of immune responses in mouse disease models.

Dosing regimens of clone M/K-2.7 (anti-mouse CD106/VCAM-1) vary by disease model, study aim, and can differ in frequency, dose, and administration route in mouse studies. The most frequently reported regimen is:

  • 0.1–0.2 mg (100–200 μg) per mouse, administered intraperitoneally every 2 days for 14 days.

Variations Across Mouse Models

  • Cardiac Dysfunction Model:
    In studies assessing cardiac function in mice, M/K-2.7 was administered at 0.1 or 0.2 mg per mouse, intraperitoneally, once every 2 days, for 14 days. This dosing led to dose-dependent improvement in cardiac dysfunction and reduction in myocardial fibrosis, indicating both a pharmacological and physiological effect at these typical doses.

  • Viral Infection/Immune Cell Depletion Models:
    For studies examining tissue-resident memory T cells (TRM), or in vivo natural killer (NK) cell depletion, M/K-2.7 was used to manipulate immune cell populations. The published sources do not specify the exact dose and interval for these models, but the use of "in vivo depletion" protocols commonly employs similar dosing (100–200 μg per dose, repeated over several days), consistent with immunology literature standards.

  • Other Disease Models:
    When used as a blocking or neutralizing antibody in research (e.g., inflammation, autoimmune, or cancer models), M/K-2.7's dosing is often adopted from prior literature, with 100–200 μg per mouse as the baseline, given every 2–3 days by intraperitoneal route for one to several weeks depending on experimental timeline.

Considerations

  • Route: The typical administration route is intraperitoneal injection, favored for good bioavailability and ease of repeat dosing in mice.
  • Duration and Frequency: Most protocols use dosing every 2–3 days to maintain adequate antibody levels, considering the mouse IgG clearance rate.
  • Dose Adjustment: Doses may be adjusted upward or downward based on preliminary titration experiments or according to the acute/chronic phase of the disease model.

Mechanistic Note

Clone M/K-2.7 is a rat IgG1 monoclonal antibody that binds and neutralizes mouse VCAM-1, potentially affecting immune cell adhesion and trafficking, so its use can influence results in various disease and immunological contexts.

Summary Table: Reported Regimens

ModelDose (μg/mouse)RouteFrequencyNotes
Cardiac100–200IntraperitonealEvery 2 days (14 d)Improves cardiac function/fibrosis
Immunology100–200IntraperitonealEvery 2–3 daysTRM, NK depletion, T cell trafficking
General use100–200IntraperitonealEvery 2–3 daysBlocking/neutralization in diverse models

Reported regimens for clone M/K-2.7 remain relatively consistent in dosing amount and frequency, with small adjustments for disease model or experimental goals. If highly specific regimens for other disease models or genetically modified mice are required, consult recent primary literature matching your research focus.

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

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