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 ◽  
...  
Talanta ◽  
2006 ◽  
Vol 70 (3) ◽  
pp. 485-488 ◽  
Author(s):  
Bao-yan Wu ◽  
Yan-yan Wang ◽  
Jing Li ◽  
Zhao Song ◽  
Jia-dong Huang ◽  
...  

FEBS Letters ◽  
1993 ◽  
Vol 334 (2) ◽  
pp. 229-232 ◽  
Author(s):  
Ladislav Burýs̆ek ◽  
Petr Tvrdí ◽  
Josef Hous̆tĕk

2018 ◽  
Vol 33 (4) ◽  
pp. 401-406 ◽  
Author(s):  
Qizhao Ma ◽  
Zhigang Mao ◽  
Jipei Du ◽  
Shiping Liao ◽  
Yanjiang Zheng ◽  
...  

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.


2007 ◽  
Vol 76 (3) ◽  
pp. 942-951 ◽  
Author(s):  
Wen Cheng ◽  
Pooja Shivshankar ◽  
Youmin Zhong ◽  
Ding Chen ◽  
Zhongyu Li ◽  
...  

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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