IL12B Protein (AA 23-335, Homodimer)

Catalog No. ABIN2666652

Recombinant IL12B protein expressed in Insect Cells.

Quick Overview for IL12B Protein (AA 23-335, Homodimer) (ABIN2666652)

Target: IL12B (Interleukin 12 beta (IL12B))

Protein Type: Recombinant

Biological Activity: Active

Origin: Mouse

Source: Insect Cells

Application: Western Blotting (WB)

Purity: > 98 % , as determined by Coomassie stained SDS-PAGE.

Product Details

Protein Characteristics: Homodimer, AA 23-335

Sterility: 0.22 μm filtered

Endotoxin Level:

Less than 0.01 ng per μg cytokine as determined by the LAL method.

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Comment:

Biological activity: ED50 = 1- 4 ng/ml corresponding to a specific activity of 1.0 - 0.25 x 106 units/mg, as determined by the dose dependent inhibition of IL-12-dependent IFNγ production in splenocytes.

Restrictions: For Research Use only

Handling

Format: Liquid

Reconstitution: For maximum results, quick spin vial prior to opening. The protein can be aliquoted and stored from -20 °C to -70 °C. Stock solutions can also be prepared at 50-100 μg/mL in sterile buffer (PBS, HPBS, DPBS, or EBSS) containing carrier protein such as 0.2-1 % BSA or HSA and stored in working aliquots at -20 °C to -70 °C.

Buffer: 0.22 μm filtered protein solution is in 20 mM Tris-HCl, pH 8.0, 0.1 M NaCl

Handling Advice: Avoid repeated freeze/thaw cycles.

Storage: -20 °C

Storage Comment: Unopened vial can be stored between 2°C and 8°C for one month, at -20°C for six months, or at -70°C for one year.

Target Details

Target: IL12B (Interleukin 12 beta (IL12B))

Alternative Name: IL-12 p40

Background: IL-12 and IL-23 share the p40 subunit, which heterodimerizes respectively with IL-12 p35 or IL-23 p19 subunits to form IL-12 or IL-23. IL-12 p40 exists as a monomer and as a homodimer (IL-12 p80). IL-12 induction is relevant in asthmatic airway inflammation. IL-12 expression can be induced by mouse parainfluenza type I (Sendai) virus and its source is airway epithelial cells. In that experimental model, IL-12 induction is followed by excessive expression of IL-12 p40 that could be further enhanced in IL-12 p35-deficient mice. Overexpression of IL-12 p80 causes macrophage accumulation and contributes to airway inflammation and consequent morbidity during viral bronchitis. Amplified epithelial IL-12 p40 expression and augmented concentrations of BAL fluid IL-12 p40 (but not IL-12 p70) has been detected in asthmatic subjects. It has been demonstrated that p80, but not IL-12 or p40, induces macrophage chemotaxis that is independent of IL-12 and mediated through the cytoplasmic tail of IL-12b1. Additional studies with transgenic mice suggest that overexpression of IL-12 p80 prior to a viral infection increases the number of resident airway macrophages, and this primes the host for a protective response against a lethal respiratory viral infection. In addition, it has been suggested that p80 functions as a competitive antagonist of IL-12 p70. Mouse Con A-activated splenocytes display identical binding affinities for p80 and IL-12, and in these cells p80 competitively inhibited IL-12 binding and IL-12-dependent proliferation. Furthermore, p80 is able to inhibit IL-12-dependent IFNγ production in freshly isolated splenocytes.

Molecular Weight: The 313 amino acid recombinant protein has a predicted molecular mass of 35.8 kDa. The DTT-reduced protein migrates at approximately 40 kDa and the non-reduced protein migrates at approximately 75 kDa by SDS-PAGE. The N-terminal amino acid is Met.

Pathways: JAK-STAT Signaling, Cellular Response to Molecule of Bacterial Origin, Regulation of Leukocyte Mediated Immunity, Positive Regulation of Immune Effector Process, Activated T Cell Proliferation