Anti-Mouse CD49d – Purified in vivo PLATINUM™ Functional Grade

Anti-Mouse CD49d – Purified in vivo PLATINUM™ Functional Grade

Product No.: C621

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Clone
R1-2
Target
CD49D
Formats AvailableView All
Product Type
Hybridoma Monoclonal Antibody
Alternate Names
VLA-4 α chain, integrin α4, ITGA4
Isotype
Rat IgG2b κ
Applications
FA
,
FC
,
IHC
,
IP

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Antibody Details

Product Details

Reactive Species
Mouse
Host Species
Rat
Recommended Isotype Controls
Recommended Dilution Buffer
Immunogen
AKR/Cum mouse Spontaneous T lymphoma line TK1
Product Concentration
≥ 5.0 mg/ml
Endotoxin Level
≤ 0.5 EU/mg as determined by the LAL method
Purity
≥95% by SDS Page
≥98% monomer by analytical SEC
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.
State of Matter
Liquid
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 ?
FA,
IHC-F,
IP,
FC
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
R1-2 activity is directed against mouse CD49d.
Background
Integrins are a large family of heterodimeric transmembrane molecules that mediate adhesion, migration, cell survival, and cell differentiation. CD49d is a single-pass type I membrane glycoprotein also known as integrin alpha-4 (Uniprot Accession P13612). CD49d is the α4 subunit of integrin heterodimers alpha-4/beta-1 (VLA-4; CD49d/CD29; α4β1 integrin) and alph-4/beta-7 (LPAM-1)1. These integrins act as receptors for fibronectin and VCAM1 (CD106). Integrin alpha-4/beta-7 is also a receptor for MADCAM1.

CD49d is expressed on most lymphocytes, granulocytes, monocytes, and thymocytes. CD49d/CD29 (VLA-4; α4β1) is expressed at high levels on the surface of lymphohematopoietic progenitors and is involved in their development and proliferation. CD49d/CD29 integrin/VCAM-1 interactions facilitate B cell adhesion to stromal cells and enhance B cell activation. In the absence of alpha-4 integrins, pre-B cells fail to transmigrate and proliferate.

R1-2 was generated by immunizing Fisher rats with TK1, a Peyer’s patch high endothelial venules (HEV) binding lymphoma line2. Spleen cells were subsequently fused with nonsecreting mouse myeloma P3x63Ag8.653 cells. Hybridomas producing antibodies reactive with TK1 cells, but not the HEV nonbinding lymphoma TK5, were cloned and screened for inhibition of lymphocyte binding to HEV of either peripheral nodes or Peyer’s patches.
Antigen Distribution
CD49d is expressed on T cells, B cells, NK cells, dendritic cells, thymocytes, monocytes, eosinophils, mast cells.
Ligand/Receptor
VCAM-1, MAdCAM-1, fibronectin
NCBI Gene Bank ID
UniProt.org
Research Area
Cell Adhesion
.
Immunology

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.

The clone R1-2 is a monoclonal antibody specific to the mouse integrin alpha 4, also known as CD49d. In mice, this antibody is commonly used for flow cytometric analysis of mouse splenocytes, which can involve studying cell populations such as T cells and their homing to specific tissues. One of the key applications of the R1-2 antibody is in blocking CD49d-mediated interactions, which can be significant in studying immune responses and cell adhesion processes.

Here are some common in vivo applications or potential uses related to this antibody:

  • Immune Response Studies: By blocking CD49d interactions, researchers can study the role of integrin alpha 4 in immune cell homing and adhesion, which is crucial for understanding immune responses.
  • Tissue-Specific Cell Tracking: While the R1-2 antibody itself is not used for cell tracking, its application in understanding cell adhesion can inform strategies for tracking immune cells in vivo.
  • In Vivo Functional Studies: The antibody can be used in in vivo settings to study the function of integrin alpha 4 in health and disease, including its role in inflammation, tissue repair, and immune cell migration.

Despite the specific focus on flow cytometry and blocking interactions, the R1-2 antibody contributes significantly to understanding the biological roles of CD49d in mice, which can guide broader in vivo applications in immunology and cell biology.

As of the provided search results, there is no specific or unambiguous reference to “R1-2” as a widely recognized protein or antibody in the biomedical literature[1–13]. However, interpreting the query broadly—perhaps as referring to TRAIL-R1 and TRAIL-R2 (apoptosis-inducing receptors involved in cancer research), or to an antibody/protein construct labeled R1–R12, or to syphilis antibodies—we can summarize relevant commonly associated antibodies and proteins as per current literature.

TRAIL-R1 and TRAIL-R2 in Cancer Research

  • TRAIL-R1 (DR4) and TRAIL-R2 (DR5): These are death receptors involved in apoptosis and are often targeted by agonists to induce cancer cell death.
  • Anti-TRAIL-R1 and Anti-TRAIL-R2 Antibodies: Monoclonal antibodies (mAbs) and single-chain variable fragments (scFv) specific for these receptors have been developed, with a diverse set of epitopes targeted for each receptor, indicating a broad potential for therapeutic combinations.
  • Recombinant TRAIL (Apo2L): Often used in combination with anti-TRAIL-R1 or anti-TRAIL-R2 antibodies to synergistically induce apoptosis, especially in cancer cell lines.
  • Chemotherapeutic Agents: Frequently combined with anti-TRAIL receptor antibodies to enhance apoptosis in both TRAIL-sensitive and resistant cell types.
  • Isotype Controls: In immunological assays, isotype-matched control antibodies (e.g., Rat IgG1 for mouse models) are commonly used with experimental antibodies to distinguish specific from non-specific binding.

SARS-CoV-2 Spike Protein and Neutralizing Antibodies

  • Spike (S) Protein: The SARS-CoV-2 spike protein is a primary target for neutralizing monoclonal antibodies (nAbs) such as REGN10987, 8H12, 3E2, and others, which are often tested in combinations (antibody cocktails) for broader neutralization and higher potency.
  • Antibody Cocktails: Combinations like 3E2/S2E12, S2X35/8H12, and 3E2/XMA01 have been shown to simultaneously bind the spike’s RBD and exhibit synergistic neutralization effects.
  • ACE2: Angiotensin-converting enzyme 2 is the receptor for SARS-CoV-2 and is used in blocking assays to evaluate antibody effectiveness.

General Research and Diagnostic Use

  • Common Research Antibodies: CD14, CD20, CD34 (for ELISA, immunocytochemistry, western blot, flow cytometry).
  • Therapeutic Antibodies: Examples include rituximab (anti-CD20), infliximab (anti-TNF), nivolumab (anti-PD-1), and panitumumab (anti-EGFR).
  • Recombinant Antibodies: Widely used due to consistency and purity, often in IgG format for various applications.

Confusion with “R1-2” Labeling

  • R1–R12: In one study, these refer to a set of 12 antibodies created by combinatorial heavy and light chain pairing, with no clear indication of widespread use outside that specific context.
  • Nonspecific Antibodies: In syphilis diagnostics, “nonspecific antibodies” are those not directed against Treponema pallidum, but this is unrelated to protein research.

Summary Table

ContextCommonly Used Proteins/AntibodiesPurpose/Target
Cancer/TRAIL PathwaysTRAIL-R1, TRAIL-R2, TRAIL (Apo2L), scFv/mAbs, chemoApoptosis induction, oncology research
SARS-CoV-2Spike protein, REGN10987, 8H12, 3E2, ACE2Neutralization, viral entry inhibition
Research/DiagnosticsCD14, CD20, CD34, TNF, PD-1, EGFR, IgG isotypeTarget detection, quantification

If “R1-2” refers to a very specific but obscure target or product, please clarify its context, as no direct evidence of its widespread use or co-usage with other antibodies/proteins appears in the current literature. If you meant TRAIL-R1/2 or the R1–R12 combinatorial set, the above summaries apply. If you have a different definition of “R1-2,” specifying the field or application would help provide a more precise answer.

The primary key findings from scientific citations specifically referencing clone R1-2 relate to studies of induced pluripotent stem cells (iPSCs) and genetic editing, particularly in the context of the KRAS gene.

  • Clone R1-2 is described as a patient-derived iPSC clone harboring a heterozygous KRAS G13C mutation.
  • Genome editing using CRISPR/Cas9 was applied to clone R1-2 to generate both gene-corrected wild-type homozygous clones (WT^ed^/WT) and heterozygous knockout clones (Δ^ed^/WT) from the same genetic background.
  • Western blotting confirmed that KRAS protein expression in gene-corrected clones was similar to that of non-edited mutant clones, while in knockout clones, KRAS protein was reduced as expected for haploinsufficiency.
  • Observations from clone R1-2 and similarly edited clones support the interpretation that the phenotypes are directly attributable to the specific KRAS genotype, not off-target effects or clonal variation.

These findings highlight clone R1-2 as:

  • A reference model for validating CRISPR/Cas9 editing in human iPSCs.
  • A control for dissecting KRAS function and the impact of gene dosage on self-renewal and differentiation in patient-derived stem cells.

No evidence was found from the results that clone R1-2 pertains to plasmids, antibodies, or plant studies; the stem cell/KRAS literature is the principal context in which clone R1-2 is cited.

Dosing regimens for monoclonal antibody clone R1-2 in mice can vary substantially depending on the specific mouse model, the experimental design, and the study goals. However, current search results do not provide direct dosing guidance or comparative data for clone R1-2. Instead, they illustrate general principles for in vivo antibody dosing regimens that can inform its use.

Essential context and supporting details:

  • The dosing of antibodies in mouse models is typically influenced by factors such as:

    • The type of mouse model (e.g., syngeneic tumor, transgenic disease, infection).
    • The intended biological effect: depletion, blockade, induction, or neutralization.
    • Route of administration (most commonly intraperitoneal injection).
    • Frequency (often every 3-4 days or 2-3 times per week for checkpoint blockade antibodies).
    • Dose (for antibodies targeting similar cell-surface markers, a range of 100–500 μg per mouse is typical).
  • While clone R1-2 itself isn’t specifically listed in the provided antibody dosing guide, related antibodies (targeting MHC molecules and used for depletion/blockade) generally follow these dosing paradigms. For example:

    • Anti-PD-1 (RMP1-14): 200–500 μg/mouse, every 3–4 days, intraperitoneal.
    • Anti-CTLA-4 (9H10): 100–200 μg/mouse, every ~3 days, intraperitoneal.
    • These regimens often vary according to disease model, mouse strain, and therapeutic objectives.
  • Experimental setup and model-specific variables:

    • Disease models may require higher or lower doses based on disease severity, immune cell numbers, or target expression.
    • Genetic background can affect antibody pharmacokinetics and pharmacodynamics, leading to further adjustments.
    • Immunogenicity studies emphasize choosing appropriate schedules to balance efficacy and immune response evaluation.

Additional relevant information:

  • When applying clone R1-2 in a new mouse model, researchers usually start with:

    • Pilot titration experiments.
    • Consideration of literature precedent for similar monoclonal antibodies.
    • Adjustment based on observed biological activity and tolerance.
  • The absence of reported dosing specifics for clone R1-2 in the search results suggests a need to consult product data sheets or published studies for precise recommendations.

  • When adapting regimens:

    • Monitor laboratory endpoints (e.g., target cell depletion, cytokine response).
    • Document and optimize for each new strain/model due to inter-model variability.

In summary, although direct comparative data on clone R1-2 dosing across mouse models is not available in the provided search results, regimens for similar monoclonal antibodies suggest starting with 100–500 μg per mouse, administered intraperitoneally every 3–4 days, and then tailoring the regimen based on model-specific requirements and observed responses.

References & Citations

1. Holzmann B, Weissman IL. EMBO J. 8(6):1735-1741. 1989.
2. Holzmann B, McIntyre BW, Weissman IL. Cell. 56(1):37-46. 1989.
3. Jin H, Aiyer A, Su J, et al. J Clin Invest. 116(3):652-662. 2006.
4. DeNucci CC, Pagán AJ, Mitchell JS, et al. J Immunol. 184(5):2458-2467. 2010.
5. Uchida Y, Kawai K, Ibusuki A, et al. J Immunol. 186(12):6945-6954. 2011.
6. Hadeiba H, Lahl K, Edalati A, et al. Immunity. 36(3):438-450. 2012.
7. Shokeen M, Zheleznyak A, Wilson JM, et al. J Nucl Med. 53(5):779-786. 2012.
8. Renkema KR, Li G, Wu A, et al. J Immunol. 192(1):151-159. 2014.
9. Hermida MD, Doria PG, Taguchi AM, et al. BMC Infect Dis. 14:450. 2014.
10. Mamedov MR, Scholzen A, Nair RV, et al. Immunity. 48(2):350-363.e7. 2018.
11. Rolot M, Dougall AM, Chetty A, et al. Nat Commun. 9(1):4516. 2018.
12. Martin MD, Sompallae R, Winborn CS, et al. Cell Rep. 31(2):107508. 2020.
13. Müller K, Gibbins MP, Roberts M, et al. EMBO Mol Med. 13(4):e13390. 2021.
14. Barrett SP, Riordon A, Toh BH, et al. J Leukoc Biol. 67(2):169-173. 2000.
15. Lin J, Qin L, Chavin KD, et al. Pathobiology. 63(3):119-132. 1995.
16. Chisholm PL, Williams CA, Lobb RR. Eur J Immunol. 23(3):682-688. 1993.
FA
Flow Cytometry
IHC
Immunoprecipitation Protocol

Certificate of Analysis

Formats Available

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