anti-IL-1alpha (p18) (mouse), mAb (Teo-1)

AdipoGen Life Sciences

anti-IL-1alpha (p18) (mouse), mAb (Teo-1)

10

Recognizes mouse IL-1alpha p18 cleaved and full-length fragments.

Western Blot, ELISA

Research Use Only

Monoclonal

Teo-1

1 mg/ml

>95%

Liquid

Il1a

interleukin 1 alpha

Il; IL-1 alpha; Il-1a; interleukin-1 alpha

Mouse

IgG

Interleukin-1 alpha

Monoclonal Antibody. Recognizes mouse IL-1alpha p18 cleaved and full-length fragments. Isotype: Mouse IgG. Clone: Teo-1. Applications: ELISA, WB. Liquid. In PBS containing 10% glycerol and 0.02% sodium azide. The most prominent members of the interleukin-1 (IL-1) superfamily are IL-1alpha and IL-1beta. They lack a signal peptide and are secreted by an unconventional, endoplasmic reticulum-Golgi-independent mechanism. IL-1alpha 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-1alpha upon cell death can trigger a sterile inflammatory response to dying cells. The cleavage of IL-1alpha 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-1alpha and IL-1beta. Although most activators fully rely on the inflammasome for IL-1alpha secretion, some induce the processing and secretion of IL-1alpha in an inflammasome-independent manner. - The most prominent members of the interleukin-1 (IL-1) superfamily are IL-1alpha and IL-1beta. They lack a signal peptide and are secreted by an unconventional, endoplasmic reticulum-Golgi-independent mechanism. IL-1alpha 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-1alpha upon cell death can trigger a sterile inflammatory response to dying cells. The cleavage of IL-1alpha 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-1alpha and IL-1beta. Although most activators fully rely on the inflammasome for IL-1alpha secretion, some induce the processing and secretion of IL-1alpha in an inflammasome-independent manner.

Mouse

-20°C,2°C to 8°C

12352203