| Author | Title | Year | Journal/Proceedings | Reftype | DOI/URL |
|---|---|---|---|---|---|
| Adrian Alexa *, J. R. & Lengauer, T. | Improved scoring of functional groups from gene expression data by decorrelating GO graph structure | 2006 | Bioinformatics | article | DOIURL |
| Abstract: Motivation: The result of a typical microarray experiment is a long list of genes with corresponding expression measurements. This list is only the starting point for a meaningful biological interpretation. Modern methods identify relevant biological processes or functions from gene expression data by scoring the statistical significance of predefined functional gene groups, e.g. based on Gene Ontology (GO). We develop methods that increase the explanatory power of this approach by integrating knowledge about relationships between the GO terms into the calculation of the statistical significance. Results: We present two novel algorithms that improve GO group scoring using the underlying GO graph topology. The algorithms are evaluated on real and simulated gene expression data. We show that both methods eliminate local dependencies between GO terms and point to relevant areas in the GO graph that remain undetected with state-of-the-art algorithms for scoring functional terms. A simulation study demonstrates that the new methods exhibit a higher level of detecting relevant biological terms than competing methods. Availability: topgo.bioinf.mpi-inf.mpg.de |
|||||
BibTeX:
@article{alexa,
author = {Adrian Alexa *, Jörg Rahnenführer and Thomas Lengauer},
title = {Improved scoring of functional groups from gene expression data by decorrelating GO graph structure},
journal = {Bioinformatics},
year = {2006},
volume = {22},
number = {13},
pages = {1600-1607},
url = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/22/13/1600},
doi = {http://dx.doi.org/10.1093/bioinformatics/btl140}
}
|
|||||
| Ayanna S. Augustus, Jonathan Buchanan, T. P. K. H. H. N. J. S. S. H. J. D. E. D. A. & Goldberg, I. J. | Loss of Lipoprotein Lipase-derived Fatty Acids Leads to Increased Cardiac Glucose Metabolism and Heart Dysfunction | 2006 | the Journal of Biological Chemistry | article | DOIURL |
| Abstract: Long-chain fatty acids (FAs) are the predominant energy substrate utilized by the adult heart. The heart can utilize unesterified FA bound to albumin or FA obtained from lipolysis of lipoprotein-bound triglyceride (TG). We used heart-specific lipoprotein lipase knock-out mice (hLpL0) to test whether these two sources of FA are interchangeable and necessary for optimal heart function. Hearts unable to obtain FA from lipoprotein TG were able to compensate by increasing glucose uptake, glycolysis, and glucose oxidation. HLpL0 hearts had decreased expression of pyruvate dehydrogenase kinase 4 and increased cardiomyocyte expression of glucose transporter 4. Conversely, FA oxidation rates were reduced in isolated perfused hLpL0 hearts. Following abdominal aortic constriction expression levels of genes regulating FA and glucose metabolism were acutely up-regulated in control and hLpL0 mice, yet all hLpL0 mice died within 48 h of abdominal aortic constriction. Older hLpL0 mice developed cardiac dysfunction characterized by decreased fractional shortening and interstitial and perivascular fibrosis. HLpL0 hearts had increased expression of several genes associated with transforming growth factor-beta signaling. Thus, long term reduction of lipoprotein FA uptake is associated with impaired cardiac function despite a compensatory increase in glucose utilization. | |||||
BibTeX:
@article{augustus,
author = {Ayanna S. Augustus, Jonathan Buchanan, Tae-Sik Park, Kumiko Hirata, Hye-lim Noh, Jie Sun||, Shunichi Homma, Jeanine D'armiento||, E. Dale Abel, and Ira J. Goldberg},
title = {Loss of Lipoprotein Lipase-derived Fatty Acids Leads to Increased Cardiac Glucose Metabolism and Heart Dysfunction},
journal = {the Journal of Biological Chemistry},
year = {2006},
volume = {281},
number = {12},
pages = {8716-8723},
url = {http://www.jbc.org/cgi/content/abstract/281/13/8716},
doi = {doi:10.1074/jbc.M509890200}
}
|
|||||
| Benjamini, Y. & Hochbert, Y. | Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing [BibTeX] |
1995 | Journal of the Royal Statistical Society. Series B | article | URL |
BibTeX:
@article{benjamini,
author = {Yoav Benjamini and Yosef Hochbert},
title = {Controlling the False Discovery Rate: A Practical and Powerful Approach to Multiple Testing},
journal = {Journal of the Royal Statistical Society. Series B},
year = {1995},
volume = {57},
number = {1},
pages = {289-300},
url = {http://www.jstor.org/view/00359246/di993246/99p0222p/0}
}
|
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| D. Bruemmer, F. Yin, J. L. J. P. B. T. S. F. B. E. F. A. J. V. H. B. M. F. R. E. L. | Regulation of the Growth Arrest and DNA Damage-Inducible Gene 45 (GADD45) by Peroxisome Proliferator-Activated Receptor $ in Vascular Smooth Muscle Cells [BibTeX] |
2003 | Circ. Res. | article | DOIURL |
BibTeX:
@article{bruemmer,
author = {D. Bruemmer, F. Yin, J. Liu, J. P. Berger, T. Sakai, F. Blaschke,E. Fleck, A. J. Van Herle, B. M. Forman, R. E. Law},
title = {Regulation of the Growth Arrest and DNA Damage-Inducible Gene 45 (GADD45) by Peroxisome Proliferator-Activated Receptor $ in Vascular Smooth Muscle Cells},
journal = {Circ. Res.},
year = {2003},
volume = {93},
pages = {38-47},
url = {http://circres.ahajournals.org/cgi/content/abstract/93/4/e38?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=regulation+of+the+growth+arrest+and+DNA&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT},
doi = {http://dx.doi.org/10.1161/01.RES.0000088344.15288.E6}
}
|
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| F. Liang, F. Wang, S. Z. & Gardner, D. | Peroxisome Proliferator activated Receptor (PPAR$) Agonists Inhibit Hypertrophy of Neonatal Rat Cardiac Myocytes [BibTeX] |
2003 | Endocrinology | article | DOIURL |
BibTeX:
@article{liang,
author = {F. Liang, F. Wang, S. Zhang, and D. Gardner},
title = {Peroxisome Proliferator activated Receptor (PPAR$) Agonists Inhibit Hypertrophy of Neonatal Rat Cardiac Myocytes},
journal = {Endocrinology},
year = {2003},
volume = {144},
number = {9},
pages = {4187-4194},
url = {http://endo.endojournals.org/cgi/reprint/144/9/4187.pdf},
doi = {http://dx.doi.org/10.1210/en.2002-0217}
}
|
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| Falcon, S. & Gentleman, R. | How to Use GOstats Testing Gene Lists for GO Terms Association [BibTeX] |
manual | URL | ||
BibTeX:
@manual{falcon2,
author = {Seth Falcon and Robert Gentleman},
title = {How to Use GOstats Testing Gene Lists for GO Terms Association},
url = {http://bioconductor.org/packages/2.1/bioc/vignettes/GOstats/inst/doc/GOstatsHyperG.pdf}
}
|
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| Falcon, S. & Gentleman, R. | Using Gostats to Test Gene List for GO Term Association | 2007 | Bioinformatics | article | DOIURL |
| Abstract: Motivation: Functional analyses based on the association of Gene Ontology (GO) terms to genes in a selected gene list are useful bioinformatic tools and the GOstats package has been widely used to perform such computations. In this paper we report significant improvements and extensions such as support for conditional testing. Results: We discuss the capabilities of GOstats, a Bioconductor package written in R, that allows users to test GO terms for over or under-representation using either a classical Hypergeometric test or a conditional Hypergeometric that uses the relationships among GO terms to decorrelate the results. Availability: GOstats is available as an R package from the Bioconductor project: http://bioconductor.org. |
|||||
BibTeX:
@article{falcon,
author = {S. Falcon and R. Gentleman},
title = {Using Gostats to Test Gene List for GO Term Association},
journal = {Bioinformatics},
year = {2007},
volume = {23},
pages = {257-258},
url = {http://bioinformatics.oxfordjournals.org/cgi/content/abstract/btl567v1},
doi = {http://dx.doi.org/10.1093/bioinformatics/btl567}
}
|
|||||
| Ferrannini, E. | Rosiglitazone and lipid metabolism [BibTeX] |
2005 | Diabetologia | article | DOIURL |
BibTeX:
@article{ferrannini,
author = {E. Ferrannini},
title = {Rosiglitazone and lipid metabolism},
journal = {Diabetologia},
year = {2005},
volume = {48},
pages = {6-7},
url = {http://www.springerlink.com/content/bf508rd54vfa8hdw/},
doi = {http://dx.doi.org/10.1007/s00125-004-1616-z}
}
|
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| G. D. Tan Contact Information, B. A. Fielding, J. M. C. S. M. H. M. D. K. N. F. M. L. H. V. & Karpe, F. | The effects of rosiglitazone on fatty acid and triglyceride metabolism in type 2 diabetes | 2005 | Diabetologia | article | DOIURL |
| Abstract: Aims/hypothesis We investigated the effects of rosiglitazone on NEFA and triglyceride metabolism in type 2 diabetes. Methods In a double-blind, placebo-controlled, cross-over study of rosiglitazone in diet-treated type 2 diabetic subjects, we measured arteriovenous differences and tissue blood flow in forearm muscle and subcutaneous abdominal adipose tissue, used stable isotope techniques, and analysed gene expression. Responses to a mixed meal containing [1,1,1-13C]tripalmitin were assessed. Results Rosiglitazone induced insulin sensitisation without altering fasting NEFA concentrations (–6.6%, p=0.16). Postprandial NEFA concentrations were lowered by rosiglitazone compared with placebo (–21%, p=0.04). Adipose tissue NEFA release was not decreased in the fasting state by rosiglitazone treatment (+24%, p=0.17) and was associated with an increased fasting hormone-sensitive lipase rate of action (+118%, p=0.01). Postprandial triglyceride concentrations were decreased by rosiglitazone treatment (–26%, p<0.01) despite unchanged fasting concentrations. Rosiglitazone did not change concentrations of triglyceride-rich lipoprotein remnants. Adipose tissue blood flow increased with rosiglitazone (+32%, p=0.03). Postprandial triglyceride [13C]palmitic acid concentrations were unchanged, whilst NEFA [13C]palmitic acid concentrations were decreased (p=0.04). In muscle, hexokinase II mRNA expression was increased by rosiglitazone (+166%, p=0.001) whilst the expression of genes involved in insulin signalling was unchanged. Adipose tissue expression of FABP4, LPL and FAT/CD36 was increased. Conclusions/interpretation Rosiglitazone decreases postprandial NEFA and triglyceride concentrations. This may represent decreased spillover of NEFAs from adipose tissue depots. Decreased delivery of NEFAs to the liver may lead to lowered postprandial triglyceride concentrations. Upregulation of hexokinase II expression in muscle may contribute to insulin sensitisation by rosiglitazone. Keywords Human metabolism - Insulin resistance - Integrative physiology - NEFA - Postprandial metabolism - Systems physiology |
|||||
BibTeX:
@article{tan,
author = {G. D. Tan Contact Information, B. A. Fielding, J. M. Currie, S. M. Humphreys, M. Désage, K. N. Frayn, M. Laville, H. Vidal. and F. Karpe},
title = {The effects of rosiglitazone on fatty acid and triglyceride metabolism in type 2 diabetes},
journal = {Diabetologia},
year = {2005},
volume = {48},
url = {http://www.springerlink.com/content/6h5qfbxnkgrn0e35/},
doi = {http://dx.doi.org/10.1007/s00125-004-1619-9}
}
|
|||||
| Hayashi, Yasuhiro Iida, S. S. Y. N. A. S. A. K. N. K. H. B. Y. H. H. | DNA Microarray Analysis of Type 2 Diabetes-Related Genes Co-regulated Between White Blood Cells and Livers of Diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) Rats | 2007 | Biological & Pharmaceutical Bulletin | article | DOIURL |
| Abstract: In a previous study, we hypothesized that some type 2 diabetes mellitus susceptible genes may be up/downregulated in white blood cells (WBC) of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, reflecting their up/down-regulation in major insulin-target tissues such as the liver before the onset of diabetes. We identified 57 potential candidate genes for predicting diabetes. In this study, we examined this hypothesis further by extending the experimental conditions from before the onset (6 weeks) to after the onset (24 weeks) of diabetes that type 2 diabetes mellitus susceptible genes are co-regulated in WBC, reflecting their expression in the liver. Using rat oligo DNA microarrays, we found that 48 genes are up/down-regulated in OLETF rats compared to control Long-Evans Tokushima Otsuka (LETO) rats in WBC and liver under fasting or insulin administration conditions. Twenty nine and 33 genes were up/down-regulated in both WBC and livers, respectively, under fasting and insulin administration conditions, respectively. Eight out of 29 genes in fasting condition and 12 out of 33 genes in insulin administration conditions have been reported to be type 2 diabetes mellitus susceptible genes and the remainder have not been reported to be related to type 2 diabetes mellitus. These results support our hypothesis that the expression levels of type 2 diabetes mellitus related genes in WBC are reflective of those in the liver after the onset of diabetes. | |||||
BibTeX:
@article{hayashi,
author = {Hayashi, Yasuhiro |
|||||
| Jürgen M. Lehmann, Linda B. Moore, T. A. S. W. O. W. T. M. W. & Kliewer, S. A. | An Antidiabetic Thiazolidinedione Is a High Affinity Ligand for Peroxisome Proliferator-activated Receptor (PPAR) [BibTeX] |
1995 | J. Biol. Chem | article | DOI |
BibTeX:
@article{lehmann,
author = {Jürgen M. Lehmann, Linda B. Moore, Tracey A. Smith-Oliver, William O. Wilkison, Timothy M. Willson, and Steven A. Kliewer},
title = {An Antidiabetic Thiazolidinedione Is a High Affinity Ligand for Peroxisome Proliferator-activated Receptor (PPAR)},
journal = {J. Biol. Chem},
year = {1995},
volume = {270},
pages = {12953 - 12956},
doi = {doi:10.1074/jbc.270.22.12953}
}
|
|||||
| K. L. Levert, G. L. W. & Stephens, J. M. | A Biotin Analog Inhibits Acetyl-CoA Carboxylase Activity and Adipogenesis [BibTeX] |
2002 | The Journal of Biological Chemistry | article | DOIURL |
BibTeX:
@article{levert,
author = {K. L. Levert, G. L. Waldrop, and J. M Stephens},
title = {A Biotin Analog Inhibits Acetyl-CoA Carboxylase Activity and Adipogenesis},
journal = {The Journal of Biological Chemistry},
year = {2002},
volume = {277},
number = {19},
pages = {16347-16350},
url = {http://www.jbc.org/cgi/content/abstract/277/19/16347?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&andorexacttitle=and&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT},
doi = {http://dx.doi.org/10.1074/jbc.C200113200}
}
|
|||||
| Kirsty Salmon, She-pin Hung, K. M. P. B. G. W. H. & Gunsalus, R. P. | Global Gene Expression Profiling in Escherichia coli K12 | 2003 | the Journal of Biological Chemistry | article | DOIURL |
| Abstract: The work presented here is a first step toward a long term goal of systems biology, the complete elucidation of the gene regulatory networks of a living organism. To this end, we have employed DNA microarray technology to identify genes involved in the regulatory networks that facilitate the transition of Escherichia coli cells from an aerobic to an anaerobic growth state. We also report the identification of a subset of these genes that are regulated by a global regulatory protein for anaerobic metabolism, FNR. Analysis of these data demonstrated that the expression of over one-third of the genes expressed during growth under aerobic conditions are altered when E. coli cells transition to an anaerobic growth state, and that the expression of 712 (49%) of these genes are either directly or indirectly modulated by FNR. The results presented here also suggest interactions between the FNR and the leucine-responsive regulatory protein (Lrp) regulatory networks. Because computational methods to analyze and interpret high dimensional DNA microarray data are still at an early stage, and because basic issues of data analysis are still being sorted out, much of the emphasis of this work is directed toward the development of methods to identify differentially expressed genes with a high level of confidence. In particular, we describe an approach for identifying gene expression patterns (clusters) obtained from multiple perturbation experiments based on a subset of genes that exhibit high probability for differential expression values. | |||||
BibTeX:
@article{salmon,
author = {Kirsty Salmon, She-pin Hung, Kathy Mekjian, Pierre Baldi, G. Wesley Hatfield, and Robert P. Gunsalus},
title = {Global Gene Expression Profiling in Escherichia coli K12},
journal = {the Journal of Biological Chemistry},
year = {2003},
volume = {278},
number = {32},
pages = {29837-29855},
url = {http://www.jbc.org/cgi/content/abstract/278/32/29837},
doi = {doi:10.1074/jbc.M213060200}
}
|
|||||
| Lorraine L. Lipscombe, MD, M. T. G. M. L. E. L. B. M. J. E. H. M. M. D. N. J. B. M. P. D. A. A. M. P. | Thiazolidinediones and Cardiovascular Outcomes in Older Patients With Diabetes [BibTeX] |
2007 | JAMA | article | URL |
BibTeX:
@article{,
author = {Lorraine L. Lipscombe, MD, MSc; Tara Gomes, MHSc; Linda E. Lévesque, BScPhm, MSc; Janet E. Hux, MD, MSc; David N. Juurlink, BPhm, MD, PhD; David A. Alter, MD, PhD},
title = {Thiazolidinediones and Cardiovascular Outcomes in Older Patients With Diabetes},
journal = {JAMA},
year = {2007},
volume = {298},
number = {22},
pages = {2634-2643},
url = {http://jama.ama-assn.org/cgi/content/abstract/298/22/2634}
}
|
|||||
| M. Cahova, H. Vavrinkova, L. K. | Glucose-fatty Acid Interaction in Skeletal Muscle and Adipose Tissue in Insulin Resistance [BibTeX] |
2007 | Physiol. Res | article | URL |
BibTeX:
@article{cahova,
author = {M. Cahova, H. Vavrinkova, L. Kazdova},
title = {Glucose-fatty Acid Interaction in Skeletal Muscle and Adipose Tissue in Insulin Resistance},
journal = {Physiol. Res},
year = {2007},
volume = {56},
pages = {1-15},
url = {www.biomed.cas.cz/physiolres/pdf/56/56_1.pdf}
}
|
|||||
| Masayuki Asakawa, Hiroyuki Takano, T. N. H. U. H. H. N. K. T. S. Y. M. T. K. & Komuro, I. | Peroxisome Proliferator--Activated Receptor gamma Plays a Critical Role in Inhibition of Cardiac Hypertrophy In Vitro and In Vivo | 2002 | Circulation | article | DOIURL |
| Abstract: Background—Peroxisome proliferator-activated receptors (PPARs) are transcription factors of the nuclear receptor superfamily. It has been reported that the thiazolidinediones, which are antidiabetic agents and high-affinity ligands for PPARgamma, regulate growth of vascular cells. In the present study, we examined the role of PPARgamma in angiotensin II (Ang II)--induced hypertrophy of neonatal rat cardiac myocytes and in pressure overload--induced cardiac hypertrophy of mice. Methods and Results—Treatment of cultured cardiac myocytes with PPARgamma ligands such as troglitazone, pioglitazone, and rosiglitazone inhibited Ang II--induced upregulation of skeletal alpha-actin and atrial natriuretic peptide genes and an increase in cell surface area. Treatment of mice with a PPARgamma ligand, pioglitazone, inhibited pressure overload--induced increases in the heart weight--to--body weight ratio, wall thickness, and myocyte diameter in wild-type mice and an increase in the heart weight--to--body weight ratio in heterozygous PPARgamma-deficient mice. In contrast, pressure overload--induced increases in the heart weight--to--body weight ratio and wall thickness were more prominent in heterozygous PPARgamma-deficient mice than in wild-type mice. Conclusions—These results suggest that the PPARgamma-dependent pathway is critically involved in the inhibition of cardiac hypertrophy. |
|||||
BibTeX:
@article{asakawa,
author = {Masayuki Asakawa, Hiroyuki Takano, Toshio Nagai, Hiroki Uozumi, Hiroshi Hasegawa, Naoto Kubota, Toshihiro Saito, Yoshiaki Masuda, Takashi Kadowaki, and Issei Komuro},
title = {Peroxisome Proliferator--Activated Receptor gamma Plays a Critical Role in Inhibition of Cardiac Hypertrophy In Vitro and In Vivo},
journal = {Circulation},
year = {2002},
volume = {105},
pages = {1240-1246},
url = {http://circ.ahajournals.org/cgi/content/short/hc1002.105225v1},
doi = {http://dx.doi.org/10.1161.hc1002.105225}
}
|
|||||
| McGarry, J. D. | Dysregulation of Fatty Acid Metabolism in the Etiology of Type 2 Diabetes [BibTeX] |
2002 | Diabetes | article | URL |
BibTeX:
@article{,
author = {J. Denis McGarry},
title = {Dysregulation of Fatty Acid Metabolism in the Etiology of Type 2 Diabetes},
journal = {Diabetes},
year = {2002},
volume = {51},
url = {http://diabetes.diabetesjournals.org/cgi/reprint/51/1/7.pdf}
}
|
|||||
| Pan Du, W. A. K. & Lin, S. | Using lumi, a package procession Illumina Microarray [BibTeX] |
2007 | manual | URL | |
BibTeX:
@manual{du,
author = {Pan Du, Warren A. Kibbe, and Simmon Lin},
title = {Using lumi, a package procession Illumina Microarray},
year = {2007},
url = {www.bioconductor.org/packages/2.0/bioc/vignettes/lumi/inst/doc/lumi.pdf}
}
|
|||||
| Sabina Chiaretti, Xiaochun Li, R. G. A. V. M. V. F. M. J. R. & Foa, R. | Gene expression profile of adult T-cell acute lymphocytic leukemia identifies distinct subsets of patients with different response to therapy and survival | 2004 | Blood | article | DOIURL |
| Abstract: Gene expression profiles were examined in 33 adult patients with T-cell acute lymphocytic leukemia (T-ALL). Nonspecific filtering criteria identified 313 genes differentially expressed in the leukemic cells. Hierarchical clustering of samples identified 2 groups that reflected the degree of T-cell differentiation but was not associated with clinical outcome. Comparison between refractory patients and those who responded to induction chemotherapy identified a single gene, interleukin 8 (IL-8), that was highly expressed in refractory T-ALL cells and a set of 30 genes that was highly expressed in leukemic cells from patients who achieved complete remission. We next identified 19 genes that were differentially expressed in T-ALL cells from patients who either had a relapse or remained in continuous complete remission. A model based on the expression of 3 of these genes was predictive of duration of remission. The 3-gene model was validated on a further set of T-ALL samples from 18 additional patients treated on the same clinical protocol. This study demonstrates that gene expression profiling can identify a limited number of genes that are predictive of response to induction therapy and remission duration in adult patients with T-ALL. | |||||
BibTeX:
@article{chiaretti,
author = {Sabina Chiaretti, Xiaochun Li, Robert Gentleman, Antonella Vitale, Marco Vignetti, Franco Mandelli, Jerome Ritz, and Robin Foa},
title = {Gene expression profile of adult T-cell acute lymphocytic leukemia identifies distinct subsets of patients with different response to therapy and survival},
journal = {Blood},
year = {2004},
volume = {103},
number = {7},
pages = {2771-2778},
url = {http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=14684422},
doi = {http://dx.doi.org/10.1182/blood-2003-09-3243}
}
|
|||||
| Smyth, G. K. | Limma: Linear Models for Microarray Data [BibTeX] |
2005 | manual | URL | |
BibTeX:
@manual{smyth2,
author = {Gordon K. Smyth},
title = {Limma: Linear Models for Microarray Data},
year = {2005},
url = {www.statsci.org/smyth/pubs/limma-biocbook-reprint.pdf}
}
|
|||||
| Smyth, G. K. | Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments [BibTeX] |
2004 | Statistical Applications in Genetics and Molecular Biology | article | URL |
BibTeX:
@article{smyth,
author = {Gordon K. Smyth},
title = {Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments},
journal = {Statistical Applications in Genetics and Molecular Biology},
year = {2004},
volume = {3},
number = {1},
url = {www.statsci.org/smyth/pubs/ebayes.pdf}
}
|
|||||
| Walczaka, R. & Tontonoza, P. | PPARadigms and PPARadoxes: expanding roles for PPAR$ in the control of lipid metabolism | 2002 | Journal of Lipid Research | article | URL |
| Abstract: The nuclear receptor PPARgamma is a central regulator of adipose tissue development and an important modulator of gene expression in a number of specialized cell types including adipocytes, epithelial cells, and macrophages. PPARgamma signaling pathways impact both cellular and systemic lipid metabolism and have links to obesity, diabetes, and cardiovascular disease. The ability to activate this receptor with small molecule ligands has made PPARgamma an attractive target for intervention in human metabolic disease. As our understanding of PPARgamma biology has expanded, so has the therapeutic potential of PPARgamma ligands. Recent studies have provided insight into the paradoxical relationship between PPARgamma and metabolic disease and established new paradigms for the control of lipid metabolism. This review focuses on recent advances in PPARgamma biology in the areas of adipocyte differentiation, insulin resistance, and atherosclerosis. — Walczak, R., and P. Tontonoz. PPARadigms and PPARadoxes: expanding roles for PPARgamma in the control of lipid metabolism. J. Lipid. Res. 2002. 43: 177–186. |
|||||
BibTeX:
@article{walczak,
author = {R. Walczaka and P. Tontonoza},
title = {PPARadigms and PPARadoxes: expanding roles for PPAR$ in the control of lipid metabolism},
journal = {Journal of Lipid Research},
year = {2002},
volume = {43},
url = {http://www.jlr.org/cgi/content/abstract/43/2/177}
}
|
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| X. Yu, S. C. Burgess, H. G. K. K. W. R. H. N. D. J. G. A. S. C. R. M. J. P. B. & Li, C. | Inhibition of Cardiac Lipoprotein Utilization By Transgenic Overexpression of Angptl4 in the Heart [BibTeX] |
2005 | PNAS | article | URL |
BibTeX:
@article{yu,
author = {X. Yu, S. C. Burgess, H. Ge, K. K. Wong, R. H. Nassem, D. J. Garry, A.D. Sherry, C. R. Malloy, J. P. Berger, and C. Li},
title = {Inhibition of Cardiac Lipoprotein Utilization By Transgenic Overexpression of Angptl4 in the Heart},
journal = {PNAS},
year = {2005},
volume = {102},
number = {5},
pages = {1767-1772},
url = {http://www.pnas.org/cgi/doi/10.1073/pnas.0409564102}
}
|
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Created by JabRef on 09/02/2008.