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IL1A ELISA Kit

Human IL1A ELISA Kit, Colorimetric assay for quantification of Human IL1A.
Catalog No. ABIN455548
$892.32
Plus shipping costs $50.00
96 tests
Shipping to: United States
Delivery in 15 to 19 Business Days

Quick Overview for IL1A ELISA Kit (ABIN455548)

Target

See all IL1A ELISA Kits
IL1A (Interleukin 1 alpha (IL1A))

Reactivity

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Human

Detection Method

Colorimetric

Method Type

Sandwich ELISA

Detection Range

15.6-1000 pg/mL

Application

ELISA

Sample Type

Cell Culture Supernatant, Serum, Plasma
  • Minimum Detection Limit

    15.6 pg/mL

    Purpose

    This immunoassay kit allows for the specific measurement of human IL-1α concentrations in cell culture supernatant, serum and plasma.

    Analytical Method

    Quantitative

    Specificity

    This assay recognizes recombinant and natural human IL-1α.

    Cross-Reactivity (Details)

    No significant cross-reactivity or interference was observed.

    Characteristics

    Homo sapiens,Human,Interleukin-1 alpha,IL-1 alpha,Hematopoietin-1,IL1A,IL1F1
  • Sample Volume

    100 μL

    Plate

    Pre-coated

    Protocol

    2 This assay employs the quantitative sandwich enzyme immunoassay technique. A monoclonal antibody specific for IL-1α has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and any IL-1α present is bound by the immobilized antibody. An enzyme-linked monoclonal antibody specific for IL-1α is added to the wells. Following a wash to remove any unbound antibody-enzyme reagent, a substrate solution is added to the wells and color develops in proportion to the amount of IL-1α bound in the initial step. The color development is stopped and the intensity of the color is measured.

    Restrictions

    For Research Use only
  • Storage

    4 °C/-20 °C

    Storage Comment

    The Standard, Detection Reagent A, Detection Reagent B and the 96-well strip plate should be stored at -20 °C upon being received. The other reagents can be stored at 4 °C.
  • Target See all IL1A ELISA Kits

    IL1A (Interleukin 1 alpha (IL1A))

    Alternative Name

    IL1A

    Background

    IL-1α is a member of interleukin 1 family. IL-1α and IL-1β recognize the same IL-1 receptor and share a number of similar biological functions. IL-1α is predominantly a cell-associated molecule whereas IL-1β is a secreted molecule. IL-1α is synthesized primarily as a 31 kDa precursor that lacks a signal peptide. Cleavage of the precursor is via the cysteine protease calpain, resulting in a 17.5 kDa mature IL-1 molecule. Being active in the processed form, the IL-1 precursor is also biologically active via specific cell binding. A portion of the precursor is transported to the cell surface and associated with the cell membrane. Precursor IL-1α can be released and cleaved by extracellular proteases when the cells die, and can also be cleaved by activation of the calcium-dependent, membrane-associated calpains. Nearly all microbes and microbial products induce the production of IL-1α. Furthermore, IL-1α can be produced in monocytes and other cells in the 31 kDa precursor state. IL-1α can act on macrophages or monocytes by inducing its own synthesis as well as the production of TNF and IL-6. IL-1α induces the production of IL-2, IL-2 receptors, GM-CSF and IL-4 from activated T cells, stimulates B cell proliferation and maturation, and increases immunoglobulin synthesis. IL-1α affects NK cell activation and LAK production associated with other cytokines, and induces prostaglandin synthesis in endothelial cells and smooth muscle cells, collagenase production in synovial cells, and cartilage and calcium resorption in bones. Studies have shown a connection between IL-1α and the pathogenesis of endometriotic lesions. The increased expression of both matrix-degrading MMP-1 and its major stimulatory cytokine IL-1α in endometriotic lesions and the selective co-expression in the stroma of endometriotic foci clearly suggests the involvement of the IL-1α molecule in the pathogenic mechanisms leading to local invasion and tissue destruction. Reports also indicate that the translation of the neurotransmitter gene only occurs after receiving IL-1α stimulation. This effect was supressed by co-stimulation with IL-1 receptor antagonist. High levels of IL-1α are associated with sepsis, rheumatoid arthritis, inflammatory bowel disease, acute and chronic myelogenous leukemia, insulin-dependent diabetes mellitus, and atherosclerosis.

    Pathways

    NF-kappaB Signaling, Autophagy, Cancer Immune Checkpoints
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