Product: IL18 Antibody
Catalog: DF6252
Description: Rabbit polyclonal antibody to IL18
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Mol.Wt.: 22kDa; 22kD(Calculated).
Uniprot: Q14116
RRID: AB_2838218

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Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Clonality:
Polyclonal
Specificity:
IL18 Antibody detects endogenous levels of total IL18.
RRID:
AB_2838218
Cite Format: Affinity Biosciences Cat# DF6252, RRID:AB_2838218.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

Iboctadekin; IFN gamma inducing factor; IFN-gamma-inducing factor; IGIF; IL 1 gamma; IL 18; IL 1g; IL-1 gamma; IL-18; IL1 gamma; IL18; IL18 protein; IL18_HUMAN; IL1F4; IL1g; IL1gamma; ILIF4; Interferon gamma inducing factor; Interferon gamma-inducing factor; Interleukin 1 gamma; Interleukin 18 (interferon-gamma-inducing factor); Interleukin 18; Interleukin-1 gamma; Interleukin-18; Interleukin18; MGC12320;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Description:
The protein encoded by this gene is a proinflammatory cytokine that augments natural killer cell activity in spleen cells, and stimulates interferon gamma production in T-helper type I cells. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Aug 2011]
Sequence:
MAAEPVEDNCINFVAMKFIDNTLYFIAEDDENLESDYFGKLESKLSVIRNLNDQVLFIDQGNRPLFEDMTDSDCRDNAPRTIFIISMYKDSQPRGMAVTISVKCEKISTLSCENKIISFKEMNPPDNIKDTKSDIIFFQRSVPGHDNKMQFESSSYEGYFLACEKERDLFKLILKKEDELGDRSIMFTVQNED

PTMs - Q14116 As Substrate

Site PTM Type Enzyme
Y37 Phosphorylation
Y88 Phosphorylation
K106 Ubiquitination
K115 Acetylation
K115 Ubiquitination
K120 Acetylation
K120 Ubiquitination
K132 Ubiquitination
S133 Phosphorylation
K171 Ubiquitination

Research Backgrounds

Function:

A proinflammatory cytokine primarily involved in polarized T-helper 1 (Th1) cell and natural killer (NK) cell immune responses (Probable). Upon binding to IL18R1 and IL18RAP, forms a signaling ternary complex which activates NF-kappa-B, triggering synthesis of inflammatory mediators. Synergizes with IL12/interleukin-12 to induce IFNG synthesis from T-helper 1 (Th1) cells and natural killer (NK) cells (Probable).

PTMs:

The pro-IL-18 precursor is processed by CASP1 or CASP4 to yield the active form.

Subcellular Location:

Secreted.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Subunit Structure:

Forms a ternary complex with ligand-binding receptor subunit IL18R1 and signaling receptor subunit IL18RAP at the plasma membrane. Mature IL18 first binds to IL18R1 forming a low affinity binary complex, which then interacts with IL18RAP to form a high affinity ternary complex that signals inside the cell.

Family&Domains:

Belongs to the IL-1 family.

Research Fields

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway.   (View pathway)

References

1). Overexpression of NAG-1/GDF15 prevents hepatic steatosis through inhibiting oxidative stress-mediated dsDNA release and AIM2 inflammasome activation. Redox Biology (PubMed: 35504134) [IF=11.4]

2). Identification of circulating T-cell immunoglobulin and mucin domain 4 as a potential biomarker for coronary heart disease. MedComm (PubMed: 37426678) [IF=9.9]

Application: WB    Species: Mouse    Sample: RAW264.7 cells

FIGURE 3 Ox‐LDL increased ADAM17 and sTIMD4 while decreased mTIMD4 level in macrophages. RAW264.7 cells were treated with ox‐LDL at the indicated concentrations for 24 h (A, D–G) or with 80 μg/mL ox‐LDL for the indicated times (B) or LPS at 1 μg/mL for 24 h (C). After treatment, total cellular proteins, RNA, and treatment mediums were collected. (A–C) Expression of ADAM17, mTIMD4, IL‐6, IL‐10, pro‐IL‐1β, IL‐1β, caspase‐1, and IL‐18 in cells and sTIMD4 in medium was detected by Western blotting (n = 3). (D and E) Expression of TIMD4, ADAM17, TNF‐α, and IL‐6 mRNA was determined by qRT‐PCR (n = 3–4). HSP90 was used as a loading control. *p < 0.05; **p < 0.01; ns, not significant.

3). Betulinic Acid Inhibits ROS-Mediated Pyroptosis in Spinal Cord Injury by Augmenting Autophagy via the AMPK-mTOR-TFEB Signaling Pathway. International Journal of Biological Sciences (PubMed: 33867836) [IF=9.2]

Application: WB    Species: Mice    Sample: spinal cords

Figure 2 BA attenuates pyroptosis after SCI. (A) Immunofluorescence staining for Caspase-1 and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (B) The quantitative mean optical density of the Caspase-1 in motor neurons of spinal cord lesion. (C) Immunofluorescence staining for GSDMD and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (D) The quantitative mean optical density of the GSDMD in motor neurons of spinal cord lesion. (E)Western blotting for ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels in the Sham, SCI, and BA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (F) The optical density values of the ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels were quantified and analyzed in each group. The values are expressed as the means ± SEM, n=5 per group. **p< 0.01, vs. Sham group. #p< 0.05 and ##p< 0.01, vs. SCI group.

Application: WB    Species: Mice    Sample: spinal cords

Figure 2 BA attenuates pyroptosis after SCI. (A) Immunofluorescence staining for Caspase-1 and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (B) The quantitative mean optical density of the Caspase-1 in motor neurons of spinal cord lesion. (C) Immunofluorescence staining for GSDMD and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (D) The quantitative mean optical density of the GSDMD in motor neurons of spinal cord lesion. (E)Western blotting for ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels in the Sham, SCI, and BA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (F) The optical density values of the ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels were quantified and analyzed in each group. The values are expressed as the means ± SEM, n=5 per group. **p< 0.01, vs. Sham group. #p< 0.05 and ##p< 0.01, vs. SCI group.

4). Combination of resolvin E1 and lipoxin A4 promotes the resolution of pulpitis by inhibiting NF-κB activation through upregulating sirtuin 7 in dental pulp fibroblasts. CELL PROLIFERATION (PubMed: 35411569) [IF=8.5]

Application: WB    Species: rat    Sample: Dental pulp fibroblasts

FIGURE 1 |Effects of combined administration of RvE1 and LXA4 on pro-inflammatory factor expression.(C) NLRP3, (D) caspase-1, (E) IL-1β and (F) IL-18 mRNA levels on LPS-induced DPFs detected by qPCR and (G) their protein levels tested by western blotting (normalized to that of β-tubulin).

5). Biliverdin modulates the Nrf2/A20/eEF1A2 axis to alleviate cerebral ischemia-reperfusion injury by inhibiting pyroptosis. Biomedicine & Pharmacotherapy (PubMed: 37399716) [IF=7.5]

Application: WB    Species: Mouse    Sample:

Fig. 2. Biliverdin can alleviate CIRI by inhibiting pyroptosis in mice. A. NLRP3, ASC, GSDMD-N, and β-actin western blot images; B. Cleaved-Caspase-1, IL-1β, IL-18, and β-actin western blot images; C. Expression of NLRP3; D. ASC expression; E. GSDMD-N expression; F. Cleaved-Caspase-1 expression; G. IL-1β expression; H. IL-18 expression. According to Sham group,

6). The gut microbiota attenuate neuroinflammation in manganese exposure by inhibiting cerebral NLRP3 inflammasome. BIOMEDICINE & PHARMACOTHERAPY (PubMed: 32768944) [IF=7.5]

Application: WB    Species: Rat    Sample: brain tissue

Fig. 4. Effect of Mn exposure and FMT on the brain-associated profile of NLRP3 inflammasome and inflammatory factors. (a–e) The activation level of NLRP3 inflammasome and inflammatory factors in the brain of rats. After FMT from healthy rats, the expression of IL-1β, IL-18, NLRP3, and TLR4 in brain was significantly downregulated, which were significantly different from that in Mn-treated group. *P < 0.05, **P < 0.01, ***P < 0.001.

7). Cyclic helix B peptide promotes random‐pattern skin flap survival via TFE3‐mediated enhancement of autophagy and reduction of ROS levels. British Journal of Pharmacology (PubMed: 34622942) [IF=7.3]

Application: WB    Species: Mouse    Sample: skin tissues

FIGURE 3 CHBP inhibits pyroptosis in random-pattern skin flaps. (a–d) Skin tissue sections were stained with anti-GSDMD-N (green) or anti-caspase 1 (CASP1; red) immunofluorescence antibodies (DAPI staining of the nuclei). Scale bar: 10 μm. The number of positive cells is shown on the right of representative images (n = 6 mice per group). (e,f) CHBP treatment reduced the expression of NLRP3, ASC, caspase 1 (CASP1), GSDMD-N, IL-1β and IL-18 in the context of ischaemia–reperfusion injury. Densitometric quantification is shown on the right (n = 6 mice per group). (g–j) CHBP treatment attenuated the activation of GSDMD, IL-1β, IL-18 and caspase 1 in the skin tissues detected by ELISA kits (n = 6 mice per group). Data shown are means ± SEM. *P 

8). Myoglobin promotes macrophage polarization to M1 type and pyroptosis via the RIG-I/Caspase1/GSDMD signaling pathway in CS-AKI. Cell Death Discovery (PubMed: 35228524) [IF=7.0]

9). Advanced glycation end products promote melanogenesis via activating NLRP3 inflammasome in human dermal fibroblasts. Journal of Investigative Dermatology (PubMed: 35421403) [IF=6.5]

10). Quercetin improves cognitive disorder in aging mice by inhibiting NLRP3 inflammasome activation. Food & Function (PubMed: 33338087) [IF=6.1]

Application: WB    Species: Mice    Sample: hippocampus

Fig. 5 The intervention of quercetin can increase SIRT1 expression and prevent the increase of NLRP3 inflammasomes. The results of immunoblotting are shown in A and B. C–H represent the protein quantification results of SIRT1, NLRP3, ASC, IL-18, cleaved-caspase-1, and IL-1β, respectively. Aging + QL: quercetin (35 mg kg−1 d−1 ); and aging + QH: quercetin (70 mg kg−1 d−1 ). Data are presented as mean ± SEM (n = 10 per group). #P < 0.05, ##P < 0.01 vs. control group; *P < 0.05, **P < 0.01, ***P < 0.001 vs. aging group.

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