Anti-mIL-1β-mIgG1
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Cat.code:
mil1b-mab9-02
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ABOUT
Recombinant mouse IL-1 beta antibody
InvivoGen provides a recombinant fully mouse anti-mouse IL-1β monoclonal antibody (mAb) that was previously extracted from hybridoma. It is now expressed and produced in Chinese hamster ovary (CHO) cells, ensuring reliability and lot-to-lot reproducibility. Thereby, common hybridoma-related drawbacks such as the generation of non-relevant mAbs containing aberrant light chains are avoided [1]. The sequence of the Anti-mIL-1β-mIgG1 is 100% murine (constant and variable regions), as the original clone (clone 7E3) was raised in mice using a proprietary method. This feature allows for reduced immunogenicity and risks of fatal hypersensitivity reactions upon repeated mAb injections into mice [2-4].
InvivoGen provides this antibody in two grades:
- In vitro use: Anti-mIL-1β-mIgG1
- In vivo use: Anti-mIL-1β-mIgG1 InvivoFit™
All InvivoFit™ products are handled in a clean room, filter-sterilized, and tested for bacterial contaminants. Additionally, this grade guarantees a low levels of endotoxins (<1 EU/ml). The buffer formulation is specifically adapted for in vivo studies.
Key features:
- Potent and specific neutralizing activity against mIL-1β (see figure)
- Sequence is 100% murine
- Murine IgG1 isotype (constant region)
- Free from non-relevant mAbs found in hybridoma-based productions
- Produced in animal-free facilities and defined media
- Low aggregation <5%
- InvivoFit™ grade is available
Anti-mIL-1β-mIgG1 is designed to efficiently neutralize the biological activity of mIL-1β. Interleukin 1β (IL-1β) is a soluble pro-inflammatory cytokine that plays a critical role in the host’s response to infection and injury [5].
References:
1. Bradbury, A. et al. 2018. When monoclonal antibodies are not monospecific: Hybridomas frequently express additional functional variable regions. mAbs, 10(4), 539–546
2. Mall C. et al., 2016. Repeated PD-1/PD-L1 monoclonal antibody administration induces fatal xenogenic hypersensitivity reactions in a murine model of breast cancer. Onco Immunol. 5(2):e1075114.
3. Murphy, J.T. et al., 2014. Anaphylaxis caused by repetitive doses of a GITR agonist monoclonal antibody in mice. Blood. 123(14):2172-2180.
4. Belmar N.A. et al., 2017. Murinization and H chain isotype matching of Anti-GITR antibody DTA-1 reduces immunogenicity-mediated anaphylaxis in C57BL/6 mice. J Immunol. 198:4502-4512.
5. Dinarello CA., 2011. Interleukin-1 in the pathogenesis and treatment of inflammatory diseases. Blood. 117:3720–3732.
All products are for research use only, and not for human or veterinary use.
InvivoFit™
InvivoFit™ is a high-quality standard specifically adapted for in vivo studies.
InvivoFit™ products are filter-sterilized (0.2 µm) and filled under strict aseptic conditions in a clean room. The level of bacterial contaminants (endotoxins and lipoproteins) in each lot is verified using a LAL assay and a TLR2 and TLR4 reporter assay
SPECIFICATIONS
Specifications
IL-1β
Mouse
Neutralization assays
Sodium phosphate buffer, glycine, saccharose, stabilizing agents
<5%
0,2 µm filtration (InvivoFit™)
Neutralization assay, in vivo studies
Each lot is functionally tested and validated.
CONTENTS
Contents
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Product:Anti-mIL-1β-mIgG1
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Cat code:mil1b-mab9-02
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Quantity:200 µg
Shipping & Storage
- Shipping method: Room temperature
- -20 °C
- Avoid repeated freeze-thaw cycles
Storage:
Caution:
Details
Interleukin-1 beta (IL-1β) is a potent pro-inflammatory cytokine involved in a variety of cellular activities including cell migration, T lymphocyte activation and pro-inflammatory cytokine production [1]. Its inactive precursor, pro-IL-1β, is secreted by immune cells, notably the innate system as well as epithelia cells in response to stimuli such as inflammation, infection or cell damage. In order to get activated, pro-IL-1β is cleaved by caspase-1 upon inflammasome activation [1,2].
Following caspase-1-dependent processing, the mature IL-1β is rapidly secreted through pores of the plasma membrane. There, it interacts with the IL-1 receptor 1 (IL-1R1), which is shared with IL-1α. Upon receptor-ligand binding, a structural change of the receptor occurs allowing the co-receptor IL-1R3 to bind and form a trimeric complex. Subsequently, the intracellular adapter protein MyD88 (myeloid differentiation primary response 88) becomes phosphorylated triggering an intricate sequence of (auto-) phosphorylation, complex formation and ubiquitination events. Finally, activated NK-kB, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) pathways induce the expression of inflammatory cytokines and chemokines, such as IL-6 and IL-8 [3]. Due to its role in mediating acute and chronic inflammation, IL-1β has emerged as a therapeutic target for auto-inflammatory diseases [4].
References:
1. O’Neill L., 2008. The interleukin-1 receptor/Toll-like receptor superfamily: 10 years of progress. Immunol. Rev. 226, 10–18. 4. 2.
2. Dinarello C., 2018. Overview of the IL-1 family in innate inflammation and acquired immunity. Immunol Rev. 281(1): 8–27.
3. Weber A. et al., 2010. Interleukin-1 (IL-1) pathway. Sci Signal. 3(105).
4. Dinarello CA., 2011. Interleukin-1 in the pathogenesis and treatment of inflammatory diseases. Blood. 117:3720–3732.
DOCUMENTS
Documents
Technical Data Sheet
Validation Data Sheet
Safety Data Sheet
Certificate of analysis
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