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Articles by L. J Su
Total Records ( 2 ) for L. J Su
  J Zabaleta , L. J Su , H. Y Lin , R. A Sierra , M. C Hall , A. O Sartor , P. E Clark , J. J Hu and A. C. Ochoa
 

Prostate cancer (PCa) is one of the most common cancers in the world. Inflammation has been described as a risk factor for PCa and depends on the production of cytokines in response to tissue damage or the presence of stimuli that induces cellular stress. Interindividual variation in cytokine production is partially controlled by single-nucleotide polymorphisms (SNPs) that have been associated with differential production of cytokines. We have recently showed that SNP–SNP interactions of cytokine genes are associated with PCa risk. However, little is known about the association of cytokine SNPs and PCa aggressiveness. In this study, we evaluated the association of 15 SNPs in five cytokine genes and aggressiveness of PCa in African- and Caucasian-American individuals. Caucasian Americans with the genotypes IL10–1082GG or IL1B+3954TT had 2.31-fold [95% confidence interval (CI) = 1.13–4.72] and 3.11 (95% CI = 1.20–8.06)-fold risk, respectively, of developing aggressive PCa, as compared with individuals without those genotypes. We did not find any associations in the African-American group. Using Multivariate Adaptive Regression Splines modeling for exploratory SNP–SNP interactions, our results showed that more aggressive PCa in Caucasians Americans is associated with the CT genotype at IL8–47 [odds ratios (OR) = 3.50; 95% CI = 1.13–10.88] or combined genotypes of IL1B–511CC and IL10–1082GG (OR = 3.38; 95% CI = 1.70–6.71). Unfortunately, the same analysis could not be performed in the African-Americans due to limited number of individuals. With limited sample size, the results from this study suggest that SNPs in cytokine genes may be associated with PCa aggressiveness. More extensive studies are warranted to validate our findings.

  L. J Su , P. K Auluck , T. F Outeiro , E Yeger Lotem , J. A Kritzer , D. F Tardiff , K. E Strathearn , F Liu , S Cao , S Hamamichi , K. J Hill , K. A Caldwell , G. W Bell , E Fraenkel , A. A Cooper , G. A Caldwell , J. M McCaffery , J. C Rochet and S. Lindquist
  Linhui Julie Su, Pavan K. Auluck, Tiago Fleming Outeiro, Esti Yeger-Lotem, Joshua A. Kritzer, Daniel F. Tardiff, Katherine E. Strathearn, Fang Liu, Songsong Cao, Shusei Hamamichi, Kathryn J. Hill, Kim A. Caldwell, George W. Bell, Ernest Fraenkel, Antony A. Cooper, Guy A. Caldwell, J. Michael McCaffery, Jean-Christophe Rochet, and Susan Lindquist

-Synuclein (-syn) is a small lipid-binding protein involved in vesicle trafficking whose function is poorly characterized. It is of great interest to human biology and medicine because -syn dysfunction is associated with several neurodegenerative disorders, including Parkinson’s disease (PD). We previously created a yeast model of -syn pathobiology, which established vesicle trafficking as a process that is particularly sensitive to -syn expression. We also uncovered a core group of proteins with diverse activities related to -syn toxicity that is conserved from yeast to mammalian neurons. Here, we report that a yeast strain expressing a somewhat higher level of -syn also exhibits strong defects in mitochondrial function. Unlike our previous strain, genetic suppression of endoplasmic reticulum (ER)-to-Golgi trafficking alone does not suppress -syn toxicity in this strain. In an effort to identify individual compounds that could simultaneously rescue these apparently disparate pathological effects of -syn, we screened a library of 115,000 compounds. We identified a class of small molecules that reduced -syn toxicity at micromolar concentrations in this higher toxicity strain. These compounds reduced the formation of -syn foci, re-established ER-to-Golgi trafficking and ameliorated -syn-mediated damage to mitochondria. They also corrected the toxicity of -syn in nematode neurons and in primary rat neuronal midbrain cultures. Remarkably, the compounds also protected neurons against rotenone-induced toxicity, which has been used to model the mitochondrial defects associated with PD in humans. That single compounds are capable of rescuing the diverse toxicities of -syn in yeast and neurons suggests that they are acting on deeply rooted biological processes that connect these toxicities and have been conserved for a billion years of eukaryotic evolution. Thus, it seems possible to develop novel therapeutic strategies to simultaneously target the multiple pathological features of PD.

 
 
 
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