商品编号


CHI-HR-20001A-C050



品牌


Adipogen



公司


Adipogen



公司分类


Proteins



Size

50 ?g

商品信息


More Information



Product Details



Synonyms

Interleukin-1α; IL-1F1; IL-1A



Product Type

Protein



Properties



Source/Host

E. coli



Sequence

Human IL-1α (aa 113-271) is fused at the C-terminus to a His-tag.



Crossreactivity

Human



Purity

≥98% (SDS-PAGE)



Endotoxin Content

<0.1eu mu;g="" protein="" (lal="" test;="" lonza).="">0.1eu>



Reconstitution

Reconstituted in sterile H
2
O not less than 100μg/ml, which can then be further diluted in other aqueous solutions.



Formulation

Lyophilized from a concentrated sterile solution containing 50mM Tris-HCl buffer (pH 8.0) and 100mM NaCl.



Other Product Data

NCBI reference NP_000566.3: IL-1α (human)



Declaration

Manufactured by Chimerigen.



Shipping and Handling



Shipping

BLUE ICE



Short Term Storage

+4°C



Long Term Storage

-20°C



Handling Advice

Avoid freeze/thaw cycles.



Use/St
ABI
lity

Stable for at least 1 year after receipt when stored at -20°C.
Working aliquots are stable for up to 3 months when stored at -20°C.



Documents



MSD
S

No



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.