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AdipoGen Life Sciences
anti-IL-1α (p18) (mouse), mAb (Teo-1)
Method: IL-1α was analyzed by Western blot in cell extracts of bone marrow-derived dendritic cells (BMDCs) treated by LPS and the several inflammasome activators as indicated in the figure. Cell extracts were separated by SDS-PAGE under reducing conditions, transferred to nitrocellulose and incubated with anti-IL-1α (p18) (mouse), mAb (Teo-1) (1µg /ml). After addition of an anti-mouse secondary antibody coupled to HRP, proteins were visualized by a chemiluminescence detection system.
Product Details | |
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Synonyms | Interleukin-1α IL-1alpha |
Product Type | Monoclonal Antibody |
Properties | |
Clone | Teo-1 |
Isotype | Mouse IgG |
Source/Host | Purified from concentrated hybridoma tissue culture supernatant. |
Immunogen/Antigen | Recombinant mouse mature IL-1α. |
Application |
Western Blot: (1μg/ml) ELISA |
Crossreactivity | Mouse |
Specificity | Recognizes mouse IL-1α p18 cleaved and full-length fragments. |
Purity | ≥95% (SDS-PAGE) |
Purity Detail | Protein G-affinity purified. |
Concentration | 1mg/ml |
Formulation | Liquid. In PBS containing 10% glycerol and 0.02% sodium azide. |
Shipping and Handling | |
Shipping | BLUE ICE |
Short Term Storage | +4°C |
Long Term Storage | -20°C |
Handling Advice |
After opening, prepare aliquots and store at -20°C. Avoid freeze/thaw cycles. |
Use/Stability | Stable for at least 1 year after receipt when stored at -20°C. |
Documents | |
MSDS | Download PDF |
Product Specification Sheet | |
Datasheet | Download PDF |
The most prominent members of the interleukin-1 (IL-1) superfamily are IL-1α and IL-1β. They lack a signal peptide and are secreted by an unconventional, endoplasmic reticulum-Golgi-independent mechanism. IL-1α was reported to be more widely and constitutively expressed and has intracellular functions, but also acts locally in a membrane-bound form by activating IL-1R1. Additionally, passive release of IL-1α upon cell death can trigger a sterile inflammatory response to dying cells. The cleavage of IL-1α is not mediated by caspase-1 and is not required for binding to IL-1R1. Recently it has been observed that all activators of the inflammasome NLRP3/NALP3 induce the simultaneous secretion of IL-1α and IL-1β. Although most activators fully rely on the inflammasome for IL-1α secretion, some induce the processing and secretion of IL-1α in an inflammasome-independent manner.
- Formyl peptide receptor 1 signaling potentiates inflammatory brain injury: Z. Li, et al.; Sci. Transl. Med. 13, 605 (2021)