Anti-Mouse CD96 – Purified in vivo GOLD™ Functional Grade
Anti-Mouse CD96 – Purified in vivo GOLD™ Functional Grade
Product No.: C781
Clone 3.3 Target CD96 Formats AvailableView All Product Type Monoclonal Antibody Alternate Names Tactile (T cell-activated increased late expression) Isotype Rat IgG1 κ Applications B , FC , in vivo |
Antibody DetailsProduct DetailsReactive Species Mouse Host Species Rat Recommended Isotype Controls Recommended Dilution Buffer Immunogen Not available or unknown 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 in vitro 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. Country of Origin USA Shipping Next Day 2-8°C RRIDAB_2829606 Applications and Recommended Usage? Quality Tested by Leinco FC The suggested concentration for anti-mouse CD96 antibody for staining cells in flow cytometry is ≤ 1.0 μg per 106 cells in a volume of 100 μl. Titration of the reagent is recommended for optimal performance for each application. Additional Applications Reported In Literature ? B Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change. DescriptionDescriptionSpecificity Clone 3.3 recognizes an epitope on mouse CD96.
Background CD96 is a single pass type I transmembrane glycoprotein in the immunoglobulin superfamily that is heavily N-glycosylated1. Murine (m) CD96 is present at the surface of most lymphocytes, including NK, CD4+ T, CD8+ T, NKT, and γδ T cells, but not B lymphocytes, neutrophils, macrophages, or dendritic cells2. mCD96 interacts with mCD155 and nectin-1 (CD111)1. A V-like domain mediates binding of mCD96 to mCD155 via interaction between amino acids of the FG loop of one binding partner with residues in the C’C’’-loop of the other. CD96 is a member of an interaction network that includes adhesion, activation, and inhibition activities.
CD96 contains three Ig-like domains that are separated from the transmembrane domain by a long proline, serine, and threonine rich stalk that undergoes extensive O-linked glycomodification1. The stalk may play a role in orientation or presentation of the Ig-like domains. mAb 3.3 binds to the first Ig domain and competes with CD155 for binding3. Human CD96 has a mild boosting effect on 2B4- and NKp30-mediated killing, but a direct role in the activation of NK cell-mediated cytotoxicity in vitro has not been observed 1. In contrast, mCD96 suppresses NK cells in vivo2. Blocking studies show that mCD96 competes with CD226 for CD155 binding and limits NK cell function by direct inhibition2. Additionally, blocking mCD96 in vivo with mAb 3.3 protects against metastasis in three different tumor models. The antimetastatic effect of mAb 3.3 is independent of antibody-dependent cell-mediated cytotoxicity and activating Fc receptors3,4 and is enhanced by anti-PD-1 and anti-CTLA-4 mAbs4. Suppression of metastasis by mAb 3.3 is dependent on NK cells, CD226 (DNAM-1), and IFN-γ4. Additionally, mAb 3.3 loses its antimetastatic function in CD155- and IL-12p35-deficient mice3. Antigen Distribution Mouse CD96 is mainly expressed by cells of hematopoietic origin, particularly T cells and NK cells.
Ligand/Receptor CD155, nectin 1 NCBI Gene Bank ID Research Area Immunology . Inhibitory Molecules Leinco Antibody AdvisorPowered 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 3.3 is a monoclonal antibody specific for mouse CD96 (also known as TACTILE) and is primarily used for in vivo experiments investigating the function and biology of CD96 in mice. Common in vivo applications of clone 3.3 in mice include:
CD96 is mainly expressed by hematopoietic cells, particularly T cells and NK cells, making clone 3.3 a valuable tool for dissecting the function of these immune cell subsets in vivo. Key supporting details:
In summary, clone 3.3 is most commonly used to block or study CD96 in the regulation of the mouse immune system in vivo, with a focus on T cell and NK cell function, tumor immunity, and general immune responses. The query concerns commonly used antibodies or proteins paired with "3.3" in the literature. The most probable interpretation is that "3.3" refers to the 14-3-3 protein family, which are key scaffold/adaptor proteins involved in many cellular pathways and extensively studied in biomedical research. Other interpretations might include antibody clone numbers (e.g., RMT3-23 for Tim-3), but the context here strongly suggests the 14-3-3 proteins. Commonly used antibodies/proteins with 14-3-3:
For reference, a typical experimental antibody/protein setup might include:
If you intended another meaning by "3.3," such as a clone number for a specific antibody (e.g., RMT3-23 for Tim-3), please clarify for a more targeted answer. Key findings from scientific literature citing clone 3.3 highlight its primary role in boosting diagnostic accuracy when used with large-scale clinical AI models. This is the most explicitly documented result in available research referencing this specific clone.
Currently, the search yields no evidence of broader or alternative uses for clone 3.3 beyond this application. If you are referencing a different scientific domain, antibody, or technology with the label "clone 3.3," further specificity may be required to provide additional insights or identify alternative findings. Dosing regimens of clone 3.3 can vary significantly depending on the specific mouse model used, the experimental goal (such as cell depletion or immune modulation), and the research context. However, the available information does not provide specific details about the exact dosing protocols, frequencies, or amounts used for clone 3.3 across different mouse models. General Principles of Dosing Variation in Mouse ModelsIn preclinical studies, dosing regimens typically vary based on several factors that influence how antibodies and therapeutic agents are administered. Drug-dosing regimens in mouse models can include multiple doses per day, such as twice daily for six doses (BID×6), or dosing at multi-day intervals, such as every 4 days for three doses (Q4D×3). The length of drug treatment varies based on the agent and specific regimen being tested. Context-Dependent Dosing ConsiderationsThe variation in dosing regimens across mouse models reflects the need to optimize for specific experimental endpoints. For instance, when testing antibodies for cancer immunotherapy or immune cell modulation, researchers must consider factors such as the tumor model being used, the desired level of target engagement, and the pharmacokinetic properties of the antibody in different strain backgrounds. To obtain specific dosing information for clone 3.3 in your particular mouse model and experimental context, it would be advisable to consult the primary literature specific to your application or contact the antibody manufacturer directly for detailed dosing recommendations based on published studies using this clone. References & Citations1. Georgiev H, Ravens I, Papadogianni G, et al. Front Immunol. 9:1072. 2018.
2. Chan CJ, Martinet L, Gilfillan S, et al. Nat Immunol. 15(5):431-438. 2014. 3. Roman Aguilera A, Lutzky VP, Mittal D, et al. Oncoimmunology. 7(5):e1424677. 2018. 4. Blake SJ, Stannard K, Liu J, et al. Cancer Discov. 6(4):446-459. 2016. Technical ProtocolsCertificate of Analysis |
Formats Available
