IL-1alpha Antibody [Bamboo-1] | 36-161

IL-1alpha Antibody [Bamboo-1] | 36-161 | Gentaur UK, US & Europe Distribution

Host: Mouse

Reactivity: Mouse

Homology: N/A

Immunogen: Recombinant mouse mature IL-1alpha.

Research Area: Apoptosis, Immunology, Innate Immunity

Tested Application: E, WB

Application: ChIP: (1:100) . Immunohistochemistry: (1:50) . Immunoprecipitation: (1:100) . Western Blot: (1:500) . Optimal conditions must be determined individually for each application.

Specificiy: Recognizes mouse IL-1alpha.

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: N/A

Validation: N/A

Isoform: N/A

Purification: >95% (SDS-PAGE)

Clonality: Monoclonal

Clone: Bamboo-1

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Liquid. In PBS containing 10% glycerol and 0.02% sodium azide.

Concentration: 1 mg/ml

Storage Condition: Stable for at least 1 year after receipt when stored at -20˚C.

Alternate Name: Interleukin-1alpha

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: 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.