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
Working Concentration
This isotype control antibody should be used at the same concentration as the primary antibody.
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.
Description
Specificity
This Rat IgG2a isotype control (anti-Trinitrophenol + KLH) antibody has been tested against selected species' cells and tissues to assure minimal cross reactivity.
Leinco Antibody Advisor
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Clone 1-1 is most commonly associated with the anti-mouse NK1.1 antibody, used extensively in in vivo applications in mice to study the role and function of natural killer (NK) cells. Its primary purpose is in vivo NK cell depletion, where researchers inject the antibody into mice to selectively deplete NK1.1+ cells, allowing the study of immune responses and disease processes in the absence of NK cells.
Common in vivo applications of clone 1-1 in mice include:
NK cell depletion: Researchers use clone 1-1 to deplete NK cells in models of infection, cancer, transplantation, and autoimmunity, enabling them to assess the functions and importance of NK cells within these contexts.
Assessing immune regulation: By observing the effects of NK cell removal, studies have identified regulatory roles for cytokine-stimulated NK cells in preventing pathogenic immune responses.
Functional studies: Clone 1-1 is used in combination with other antibodies or experimental treatments to clarify the contributions of NK1.1+ cells to immune surveillance, tumor rejection, and tissue homeostasis.
Additional uses:
Flow cytometry and immunophenotyping: Clone 1-1 is commonly used for cell surface staining to confirm NK cell depletion or identify NK cell populations during or after in vivo experiments.
Mechanism: Clone 1-1 targets the NK1.1 antigen, a surface marker expressed on NK cells in certain mouse strains (e.g., C57BL/6). When administered in vivo, the antibody binds these cells, leading to their depletion predominantly through antibody-dependent mechanisms.
Limitations:
NK1.1 expression varies among mouse strains; not all strains express this antigen, so clone 1-1-mediated depletion is only effective in NK1.1+ strains like C57BL/6.
In some contexts, clone 1-1 may affect other NK1.1-expressing populations, such as subsets of NKT cells.
In summary, the most common in vivo application of clone 1-1 in mice is the selective depletion of NK cells to study their role in immunity, with broad use in tumor, infection, and transplantation models.
Commonly used antibodies or proteins that are frequently paired with 1-1 (commonly referencing clone PK136, the anti-NK1.1 antibody used to identify and manipulate NK cells in mice) include markers for immune cell populations and functional assays in immunology research.
Key context:
NK1.1 (clone PK136) is routinely used with other antibodies to analyze mouse NK cells via flow cytometry, immunoprecipitation, and depletion studies.
Common markers and proteins used alongside NK1.1/PK136:
CD3: Used to distinguish NK cells (NK1.1⁺ CD3⁻) from NKT cells (NK1.1⁺ CD3⁺) or T cells, since T cells express CD3 whereas NK cells do not.
CD19/B220: B-cell markers, added to panels to exclude B cells and to gate on pure NK populations.
CD4/CD8: To identify T cell subsets, often used in broader lymphocyte profiling.
CD11b and CD27: NK cell maturation markers, useful in studying NK cell subsets and their development.
Granzyme B, Perforin, IFN-γ: Functional proteins tested by intracellular staining during NK cell activation studies.
Thy-1 (CD90): Sometimes included to characterize T cell subsets, as Thy-1 is a T cell marker.
Annexin V or 7-AAD: Apoptosis/viability dyes to assess NK cell survival or response to depletion.
Additional details:
These combinations are employed in cytotoxicity assays, depletion experiments, adoptive transfer, and detailed phenotyping protocols.
Some commercial protocols explicitly recommend using anti-NK1.1 (PK136) with antibodies against CD3 and CD19 for gating strategies.
Researchers may also use isotype controls to distinguish specific binding from background.
For depletion, anti-NK1.1 (PK136) is often administered with complement in vivo or ex vivo to confirm NK cell-specific effects.
When working with anti-NK1.1 (PK136), the most common panel consists of CD3, NK1.1, CD19, and CD4/CD8; for functional studies, granzyme B, perforin, and IFN-γ are added.
If you meant a different "1-1" antibody (such as human Fas APO-1-1 or HO-1-1), panels would differ: for Fas (APO-1-1), it is often paired with CD95, apoptosis markers, or T cell surface proteins. For HO-1-1, co-staining with markers of oxidative stress or myeloid lineage is frequent.
If you clarify the species or cell type, I can provide a tailored panel. The above information is focused on the common context of mouse NK1.1 (PK136) research.
Key findings from "clone 1-1" citations in the scientific literature predominantly address two distinct areas: synthetic code clone research in software engineering and issues concerning cloned (fake) scientific journals.
1. Synthetic Code Clone Research in Software Engineering
Studies systematically review and analyze code clone detection techniques, particularly leveraging machine learning models such as Recurrent Neural Networks (RNNs).
RNN-based approaches have shown notable improvements in detecting complex code clones (specifically Type-III and Type-IV clones), with recent methods achieving high precision and recall (up to 99.8% precision in ASTNN and ~99.5% on other benchmarks).
Comparative analyses highlight specific techniques:
ASTNN: Exceptional in precision on benchmarks like BigCloneBench.
DFS Technique: Excels in both precision and recall, especially on OJClone datasets, surpassing other methods for challenging clone types.
Progress over time is clear, as deep learning advancements have driven F1-scores higher for clone detection tasks.
2. Cloned (Fake) Scientific Journals
"Clone journals" refer to fraudulent or imitation journals that mimic legitimate publications, undermining the integrity of scientific publishing.
These journals pose risks to the credibility of peer review and the quality assurance that underpins scientific literature.
Their proliferation has increased concern about academic integrity and the potential erosion of trust in legitimate scholarly communication.
In summary, "clone 1-1" citations most frequently appear in:
Software engineering literature: Addressing state-of-the-art progress in detecting code clones using deep learning and benchmarking key techniques for accuracy and robustness.
Academic publishing discussions: Highlighting the dangers and prevalence of fake or clone journals that threaten research quality and trust.
Dosing regimens for clone 1-1 in mouse models are not explicitly detailed in the available search results. General dosing guides for monoclonal antibodies in mice suggest that dose, route, and frequency are highly dependent on both the antibody specificity and mouse disease model.
Key context from available sources:
Standard practice for function-blocking or depleting antibodies (such as those targeting cell surface proteins) typically involves doses ranging from 100–500 μg per mouse, administered intraperitoneally or intravenously, at intervals of every 3–4 days or 2–3 times per week, but regimens vary depending on the targeted molecule and the experimental context.
Specificity to the mouse strain, immune status, and disease model (e.g., tumor model, infection, baseline immune activation) may alter the optimal dosing regimen substantially.
Some antibody clones, when xenogeneic (from another species), can provoke hypersensitivity in certain mouse models after repeated dosing, emphasizing the importance of antibody origin and host compatibility.
Directly related detail: According to a commercial antibody supplier, "dosing regimens of clone 1-1 in mouse models are not explicitly detailed" in general literature or in their published technical data. This suggests a lack of standardized or widely-reported dosing regimens for clone 1-1 specifically.
Relevant general practice (when direct detail is missing):
If clone 1-1 is similar in type (isotype, target, species) to commonly used depletion or blocking antibodies, an initial dosing regimen of 200–500 μg per mouse, administered intraperitoneally every 3–4 days is typically used as a starting point in pilot experiments, with titrations to optimize for effect and minimize toxicity.
Dosing schedules and quantities should always be optimized in pilot studies for each combination of clone, mouse strain, and disease model due to potential differences in pharmacokinetics and immune response.
In summary: There is no standardized published dosing regimen for clone 1-1 across mouse models. Researchers typically refer to dosing regimens for similar antibody types and adjust based on experimental needs. Pilot titration studies are necessary, and consultation of clone-specific supplier data or primary literature (when available) is strongly advised.
References & Citations
1. Gubin, M. et al. (2018) Cell.175(4):1014–1030.e19 Journal Link
2. Wurster S. et al. (2020) The Journal of Infectious Diseases 222 , 6:1989–994 Journal Link
3. Tzetzo, S. L., Kramer, E. D., Mohammadpour, H., Kim, M., Rosario, S. R., Yu, H., Dolan, M., Oturkar, C. C., Morreale, B., Bogner, P. N., Stablewski, A., Benavides, F., Brackett, C. M., Ebos, J. M., Das, G. M., Opyrchal, M., Nemeth, M. J., Evans, S. S., & Abrams, S. I. (2024). Downregulation of IRF8 in alveolar macrophages by G-CSF promotes metastatic tumor progression. iScience, 109187. https://doi.org/10.1016/j.isci.2024.109187