Real time kinetic analysis of the interaction between interleukin-1α and soluble interleukin-1 receptor I using a resonant mirror biosensor

2006 ◽  
Vol 557 (1-2) ◽  
pp. 106-110 ◽  
Author(s):  
Bao-Yan Wu ◽  
Jing Li ◽  
Jia-Dong Huang ◽  
Yan-Yan Wang ◽  
Hui-Jun Yin ◽  
...  
Keyword(s):  
Kinetic Analysis ◽  
Real Time ◽  
Interleukin 1 ◽  
Interleukin 1Α ◽  
Resonant Mirror Biosensor

An optical biosensor for kinetic analysis of soluble Interleukin-1 receptor I binding to immobilized Interleukin-1α

Talanta ◽  
2006 ◽  
Vol 70 (3) ◽  
pp. 485-488 ◽  
Author(s):  
Bao-yan Wu ◽  
Yan-yan Wang ◽  
Jing Li ◽  
Zhao Song ◽  
Jia-dong Huang ◽  
...  
Keyword(s):  
Kinetic Analysis ◽  
Interleukin 1 ◽  
Optical Biosensor ◽  
Interleukin 1Α

scholarly journals Expression of interleukin-1α and interleukin-1 receptor type I genes in murine brown adipose tissue

FEBS Letters ◽  
1993 ◽  
Vol 334 (2) ◽  
pp. 229-232 ◽  
Author(s):  
Ladislav Burýs̆ek ◽  
Petr Tvrdí ◽  
Josef Hous̆tĕk
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Interleukin 1 ◽  
Receptor Type ◽  
Type I ◽  
Brown Adipose ◽  
Interleukin 1Α

scholarly journals Association between an insertion/deletion polymorphism in the interleukin-1α gene and the risk of colorectal cancer in a Chinese population

2018 ◽  
Vol 33 (4) ◽  
pp. 401-406 ◽  
Author(s):  
Qizhao Ma ◽  
Zhigang Mao ◽  
Jipei Du ◽  
Shiping Liao ◽  
Yanjiang Zheng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Chinese Population ◽  
Target Gene ◽  
Interleukin 1 ◽  
Venous Blood ◽  
Deletion Polymorphism ◽  
Chain Reaction ◽  
Interleukin 1Α ◽  
Polymerase Chain ◽  
Insertion Allele

Background: Previous studies have reported that polymorphisms in the interleukin-1 gene may be involved in tumorigenesis and tumor progression. Aim: The purpose of the present study was to evaluate whether an insertion/deletion polymorphism, rs3783553, located in the miR-122 target gene interleukin-1α, was associated with the risk of colorectal cancer. Methods: Genomic DNA was extracted from peripheral venous blood of 382 patients with colorectal cancer and 433 controls, and the polymorphism was genotyped using a polymerase chain reaction assay. Results: Significantly decreased colorectal cancer risk was observed to be associated with the interleukin-1α rs3783553 insertion/insertion genotype ( P=0.0001; OR=0.41; 95% CI 0.26, 0.65) and the insertion allele ( P<0.001; OR=0.68; 95% CI 0.55, 0.83). Stratification analysis based on clinical and pathological features also revealed that the “TTCA” insertion allele of rs3783553 contributes to slow the progression of colorectal cancer. Conclusion: These results suggest that the rs3783553 polymorphism could be a useful genetic marker to predict the size/extent of colorectal cancer.

scholarly journals Intracellular Interleukin-1α Mediates Interleukin-8 Production Induced by Chlamydia trachomatis Infection via a Mechanism Independent of Type I Interleukin-1 Receptor

2007 ◽  
Vol 76 (3) ◽  
pp. 942-951 ◽  
Author(s):  
Wen Cheng ◽  
Pooja Shivshankar ◽  
Youmin Zhong ◽  
Ding Chen ◽  
Zhongyu Li ◽  
...  
Keyword(s):  
Chlamydia Trachomatis ◽  
Early Stage ◽  
Interleukin 1 ◽  
Type I ◽  
Infection Cycle ◽  
Chlamydia Trachomatis Infection ◽  
Cytokines And Chemokines ◽  
Intracellular Mechanism ◽  
Interleukin 1Α ◽  
Interfering Rna

ABSTRACT Chlamydia trachomatis infection induces a wide array of inflammatory cytokines and chemokines, which may contribute to chlamydia-induced pathologies. However, the precise mechanisms by which Chlamydia induces cytokines remain unclear. Here we demonstrate that the proinflammatory cytokine interleukin-1α (IL-1α) plays an essential role in chlamydial induction of the chemokine IL-8. Cells deficient in IL-1α expression or IL-1α-competent cells treated with IL-1α-specific small interfering RNA failed to produce IL-8 in response to chlamydial infection. However, neutralization of extracellular IL-1α or blockade of or deficiency in type I IL-1 receptor (IL-1RI) signaling did not affect chlamydial induction of IL-8 in cells capable of producing IL-1α. These results suggest that IL-1α can mediate the chlamydial induction of IL-8 via an intracellular mechanism independent of IL-1RI, especially during the early stage of the infection cycle. This conclusion is further supported by the observations that expression of a transgene-encoded full-length IL-1α fusion protein in the nuclei enhanced IL-8 production and that nuclear localization of chlamydia-induced precursor IL-1α correlated with chlamydial induction of IL-8. Thus, we have identified a novel mechanism for chlamydial induction of the chemokine IL-8.

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