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    <title>Nature Precedings - Tag feed for gene expression</title>
    <link>http://precedings.nature.com/tags/gene%20expression</link>
    <description>Recently posted documents tagged with 'gene expression'</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
    <dc:language>en</dc:language>
    <prism:publicationName>Nature Precedings</prism:publicationName>
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      <title>Nature Precedings</title>
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      <link>http://precedings.nature.com</link>
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    <item>
      <title>Limusaurus and bird digit identity</title>
      <link>http://precedings.nature.com/documents/3828/version/1</link>
      <description>Limusaurus is a remarkable herbivorous ceratosaur unique among theropods in having digits II, III and IV, with only a small metacarpal vestige of digit I. This raises interesting questions regarding the controversial identity of avian wing digits. The early tetanuran ancestors of birds had tridactyl hands with digital morphologies corresponding to digits I, II &amp;#38; III of other dinosaurs. In bird embryos, however, the pattern of cartilage formation indicates that their digits develop from positions that become digits II, III, &amp;#38; IV in other amniotes. Limusaurus has been argued to provide evidence that the digits of tetanurans, currently considered to be I, II and III, may actually be digits II, III, &amp;#38; IV, thus explaining the embryological position of bird wing digits. However, morphology and gene expression of the anterior bird wing digit specifically resemble digit I, not II, of other amniotes. We argue that digit I loss in Limusaurus is derived and thus irrelevant to understanding the development of the bird wing.  </description>
      <guid>http://precedings.nature.com/documents/3828/version/1</guid>
      <pubDate>Tue, 06 Oct 2009 12:15:57 UTC</pubDate>
      <dc:title>Limusaurus and bird digit identity</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3828.1</dc:identifier>
      <dc:date>2009-10-06</dc:date>
      <dc:creator>Alexander O. Vargas</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-10-06T12:15:57Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Molecular Cell Biology</prism:section>
      <prism:section>Evolutionary Biology</prism:section>
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    <item>
      <title>Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit</title>
      <link>http://precedings.nature.com/documents/3460/version/1</link>
      <description>A male Drosophila model of locomotor deficit induced by chronic pentylenetetrazole (PTZ), a proconvulsant used to model epileptogenesis in rodents, has recently been described. Antiepileptic drugs (AEDs) ameliorate development of this behavioral abnormality. Time-series of microarray profiling of heads of male flies treated with PTZ has shown epileptogenesis-like transcriptomic perturbation in the fly model. Gender differences are known to exist in neurological and psychiatric conditions including epileptogenesis. We describe here the effects of chronic PTZ in Drosophila females, and compare the results with the male model. As in males, chronic PTZ was found found to cause a decreased climbing speed in females. In males, overrepresentation of Wnt, MAPK, TGF-beta, JAK-STAT, Cell communication, and Dorso-Ventral axis formation pathways in downregulated genes was previously described. Of these, female genes showed enrichment only for Dorso-Ventral axis formation. Most significant, ribosomal pathway was uniquely overrepresented in genes downregulated in females. Gender differences thus exist in the Drosophila model. Gender neutral, Dorso-Ventral axis formation may be considered as the candidate causal pathway in chronic pentylenetetrazole induced behavioral deficit. Prior evidence of developmental mechanisms in epileptogenesis underscores the usefulness of fly model. Gender specific pathways may provide a lead for understanding brain dimorphism in neuropsychiatric disorders.</description>
      <guid>http://precedings.nature.com/documents/3460/version/1</guid>
      <pubDate>Mon, 27 Jul 2009 20:02:00 UTC</pubDate>
      <dc:title>Gender differences in a Drosophila transcriptomic model of chronic pentylenetetrazole induced behavioral deficit</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3460.1</dc:identifier>
      <dc:date>2009-07-27</dc:date>
      <dc:creator>Abhay Sharma</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-27T20:02:00Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Pharmacology</prism:section>
      <prism:section>Bioinformatics</prism:section>
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    <item>
      <title>A Drosophila systems model of withdrawal from chronic pentylenetetrazole relevant in post-epileptogenesis  </title>
      <link>http://precedings.nature.com/documents/3447/version/1</link>
      <description>Rodent kindling induced by pentylenetetrazole (PTZ) is an established model of epileptogenesis and antiepileptic drug (AED) testing. Recently, a Drosophila systems model has been described in which chronic PTZ causes a decreased climbing speed in adult males on 7th day. Some AEDs ameliorate development of this locomotor deficit. Time-series of microarray expression profiles of heads of flies treated with PTZ has been found to resemble transcriptomic alterations associated with epileptogenesis. In the fly model, withdrawal from seven day long PTZ treatment causes an increased climbing speed on 7th consequent day. Here, we present a systems model of the post-PTZ withdrawal regime. Unlike AED-untreated individuals, flies treated with any of the five AEDs after PTZ discontinuation exhibited normal climbing speed on 7th day, i.e., 14th day from the beginning of PTZ treatment. Time-series of microarray expression profiles of fly heads comparing control PTZ- and AED-untreated, and AED-untreated post PTZ withdrawal groups showed differentially expressed genes throughout. These genes enriched gene ontology (GO) molecular functions including transcription regulator and GTPase regulator activities. Interestingly, expression profiles of fly heads comparing control PTZ- and AED-untreated, and AED-treated post PTZ withdrawal groups showed neutralization of transcription regulator and GTPase regulator activities by the AEDs. Further transcriptomic analysis based on overinteraction in protein interactome and enrichment of miRNA targets implicated axon guidance and neuronal remodeling related perturbations in the fly model. Differential expression of genes belonging to transcription regulator and GTPase regulator activities have previously been reported in post-epileptogenesis in established rodent models. Also, axon guidance and neuronal remodeling related alterations have been implicated in epilepsy. The Drosophila model thus provides a unique opportunity to dissect long-term plasticity relevant in epileptogenesis at cellular and molecular levels. Besides, the model also offers an excellent system to efficiently screen agents with potential therapeutic activity.</description>
      <guid>http://precedings.nature.com/documents/3447/version/1</guid>
      <pubDate>Tue, 21 Jul 2009 16:40:03 UTC</pubDate>
      <dc:title>A Drosophila systems model of withdrawal from chronic pentylenetetrazole relevant in post-epileptogenesis  </dc:title>
      <dc:identifier>hdl:10101/npre.2009.3447.1</dc:identifier>
      <dc:date>2009-07-21</dc:date>
      <dc:creator>Abhay Sharma</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-21T16:40:03Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Pharmacology</prism:section>
      <prism:section>Bioinformatics</prism:section>
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    <item>
      <title>A novel Drosophila transcriptomic and behavioral model detects potassium chloride with therapeutic potential</title>
      <link>http://precedings.nature.com/documents/3429/version/1</link>
      <description>In a newly described Drosophila model, two of the five antiepileptic drugs (AEDs) tested, sodium valproate (NaVP) and levetiracetam (LEV), not ethosuximide (ETH), gabapentin (GBP) and vigabatrin (VGB), ameliorate development of chronic pentylenetetrazole (PTZ) induced locomotor alteration. To further characterize the model, we analyze here the microarray expression profile of heads of flies treated with depolarizing compound potassium chloride (KCl). Surprisingly, microarray clustering showed unexpected similarity among KCl, LEV and NaVP. Further, like the two effective AEDs in the fly model, KCl regulated genes overrepresented ribosomal pathway. Interestingly, KCl also ameliorated development of locomotor deficit in the chronic PTZ model. Both transcriptomic and behavioral analyses thus showed LEV- and NaVP- like neuroprotective effect of KCl. This is consistent with neuroprotective effect of KCl observed previously in mammalian system. The Drosophila model thus provides a unique opportunity to understand long term mechanisms of neuroactive compounds.</description>
      <guid>http://precedings.nature.com/documents/3429/version/1</guid>
      <pubDate>Fri, 17 Jul 2009 14:41:20 UTC</pubDate>
      <dc:title>A novel Drosophila transcriptomic and behavioral model detects potassium chloride with therapeutic potential</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3429.1</dc:identifier>
      <dc:date>2009-07-17</dc:date>
      <dc:creator>Abhay Sharma</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-17T14:41:20Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Pharmacology</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3429/version/1/files/npre20093429-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Transcriptomic analysis implicates ribosomal and energy metabolic pathways in antiepileptic drug action in a Drosophila model</title>
      <link>http://precedings.nature.com/documents/3396/version/1</link>
      <description>Mechanisms of long term action of antiepileptic drugs (AEDs), used in treating epilepsy and many other neurological and psychiatric disorders, are poorly understood. Recently, a novel Drosophila transcriptomic model of locomotor plasticity induced by chronic pentylenetetrazole (PTZ), a chemoconvulsant commonly used to model epileptogenesis and test AEDs in rodents, has been described. In this model, two of the five AEDs tested, sodium valproate (NaVP) and levetiracetam (LEV), not ethosuximide (ETH), gabapentin (GBP) and vigabatrin (VGB), ameliorate development of chronic PTZ induced locomotor alteration. Here, we describe transcriptomic effect of the AEDs in the fly model. Singular treatment with ETH, GBP and VGB in general caused downregulation of genes. In contrast, similar treatment with NaVP and LEV caused upregulation. The GBP and NaVP gene sets showed enrichment of the ribosomal and energy metabolic pathways. The network partners of ETH, VGB and LEV regulated genes in the available interactome map were also found to overrepresent the ribosomal pathway. Unlike PTZ alone, PTZ and LEV combination treatment was found to cause differential regulation of genes that too enriched the ribosomal and energy metabolic pathways. Cumulatively, we provide transcriptomic evidence that suggests involvement of ribosomal and energy metabolic mechanisms in AED action. The Drosophila model provides an excellent opportunity to further understand mechanisms of AED action in molecular details.</description>
      <guid>http://precedings.nature.com/documents/3396/version/1</guid>
      <pubDate>Tue, 07 Jul 2009 16:27:35 UTC</pubDate>
      <dc:title>Transcriptomic analysis implicates ribosomal and energy metabolic pathways in antiepileptic drug action in a Drosophila model</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3396.1</dc:identifier>
      <dc:date>2009-07-07</dc:date>
      <dc:creator>Abhay Sharma</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-07-07T16:27:35Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Pharmacology</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3396/version/1/files/npre20093396-1.pdf.thumb.png"/>
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    </item>
    <item>
      <title>Systems level analysis of transgenerational spermatogenic inheritance predicts biomarkers and underlying pathways</title>
      <link>http://precedings.nature.com/documents/3312/version/1</link>
      <description>Transgenerational spermatogenic inheritance of adult male acquired CNS gene expression characteristics has recently been discovered using a Drosophila systems model. In this novel mode of inheritance, transcriptomic alteration induced by the neuroactive drug pentylenetetrazole (PTZ) has been found to leak to future generations. Here, the available microarray gene expression data pertaining to CNS and/or testis of exposed F0 and the resulting F1 and F2 generations has been pooled and analyzed in an unbiased manner at four levels, namely, biological processes and pathways, protein interactome networks, miRNA-targets, and microarray expression profile similarities. Enrichment for processes related to translation, energy metabolism, cell proliferation, cell differentiation, secretion, central nervous system development, germ cell development, gamete generation, wing development, nutrition etc. was observed. Also, ribosome, oxidative phosphorylation and, to a lesser extent, wingless signaling pathway showed overrepresentation. In the proteomic interactome map, the cell cycle gene Ras85D exhibited overinteraction. In miRNA-target network, the fly transgenerational genes showed overrepresentation of mir-315 targets. Transcriptomic matching revealed overlap of transgenerational set with genes related to epigenetic drug treatment, stem cells, Myc targets and miRNA targets. Many of the findings were consistent with the existing epigenetic evidence in complex mammalian traits. Converging evidence suggests that ribosomal RNA and proteins may serve as candidate biomarkers of transgenerational environmental effect. A compelling systems biology frame-work integrative of transgenerational epigenetic inheritance is suggested. Nutrient, circulating peptide hormone, Myc, Wnt, and stem cell signaling pathways constitute the frame-work. The analysis has implications in explaining missing heritability in complex traits including common human disorders. The fly model offers an excellent opportunity to understand somatic and germline communication, and epigenetic memory formation and its retention across generations in molecular details.</description>
      <guid>http://precedings.nature.com/documents/3312/version/1</guid>
      <pubDate>Fri, 05 Jun 2009 20:16:28 UTC</pubDate>
      <dc:title>Systems level analysis of transgenerational spermatogenic inheritance predicts biomarkers and underlying pathways</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3312.1</dc:identifier>
      <dc:date>2009-06-05</dc:date>
      <dc:creator>Abhay Sharma</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-06-05T20:16:28Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3312/version/1/files/npre20093312-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>GUDMAP &amp;#8211; An Online GenitoUrinary Resource</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3297.1</link>
      <description>The GenitoUrinary Development Molecular Anatomy Project (GUDMAP) is a consortium of laboratories working to provide the scientific and medical community with gene expression data and tools to facilitate research (see www.gudmap.org). The data provided by GUDMAP includes large in situ hybridization screens (wholemount and section) and expression microarray analysis of components of the developing mouse urogenital system (including laser-captured material and FACS-isolated cells from transgenic reporter mice). In addition, a high-resolution anatomy ontology has been developed by members of the GUDMAP consortium to describe the subcompartments of the developing murine genitourinary tract. The GUDMAP Database Development Team and Editorial Office &amp;#8211; both based in Edinburgh &amp;#8211; function to ensure submission, curation, storage and presentation of the data submitted by the GUDMAP consortium. Our collective aim is twofold: 1) to simplify the process of submission so that data is publically available as soon as it is produced; and 2) to organize this information in a database and ensure that the online interface is continuously available and easy to use. Thus far, we have developed a range of tools that help both the submitter and the end user. These include: an online annotation tool that simplifies in situ data submission through an ontology-based graphical user interface; a database interface that allows users to browse and query expression data, and to filter data by organ system; a heat-map display of microarray data and analyses. Furthermore, the Edinburgh team has developed a GUDMAP Disease Database that queries associations between genes, genitourinary diseases, and renal/urinary and reproductive phenotypes. In collaboration with GUDMAP consortium members at the CCHMC (Cincinnati Children&amp;#8217;s Hospital Medical Center), the Disease Database is being extended to include mammalian phenotypes mapped to OMIM entries. By virtue of its impressive dataset and its ease of use we hope that the GUDMAP Website will continue to serve as a powerful resource for biologists, clinicians and bioinformaticians with an interest in the urogenital system.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3297.1</guid>
      <pubDate>Sat, 30 May 2009 14:17:58 UTC</pubDate>
      <dc:title>GUDMAP &amp;#8211; An Online GenitoUrinary Resource</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3297.1</dc:identifier>
      <dc:date>2009-05-30</dc:date>
      <dc:creator>Simon Harding</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-05-30T14:17:58Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3297/version/1/files/npre20093297-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>A novel superior factor widely controlling the rice grain quality</title>
      <link>http://precedings.nature.com/documents/3283/version/1</link>
      <description>Synthesis of storage starch and protein accumulation is the main action of endosperm organogenesis in term of the economic importance of rice. This event is strongly disturbed by abiotic stresses such as high temperature; thus, the upcoming global warming will cause a crisis with a great impact on food production1,2. The enzymes for the protein storage and starch synthesis pathway should work in concert to carry out the organogenesis of rice endosperm3-5, but the regulatory mechanism is largely unknown. Here we show that a novel regulatory factor, named OsCEO1, acts as the conductor of endosperm organogenesis during the rice grain filling stage. The physiological properties of floury-endosperm-2 (flo2) mutants showed many similarities to symptoms of grains developed under high-temperature conditions, suggesting important roles of the responsible gene in sensitivity to high-temperature stress. Our map-based cloning identified the responsible gene for the flo2 mutant, OsCEO1, which has no homology to any genes of known function. The OsCEO1 belongs to a novel conserved gene family and encodes a protein composed of 1,720 amino acid residues containing a TPR (tetratricopeptide repeat) motif, which is considered to mediate a protein-protein interaction. The yeast two-hybrid analysis raised an unknown protein showing homology to a late embryogenesis abundant protein and a putative basic helix-loop-helix protein as candidates for the direct interactor for OsCEO1, whereas no enzyme genes for the synthesis of storage substances were detected. The flo2 mutant exhibited reduced expression of several genes for putative regulatory proteins as well as many enzymes involved in storage starch and proteins. These results suggest that OsCEO1 is a superior conductor of the novel regulatory cascade of endosperm organogenesis and may have important roles in the response to high-temperature stress.</description>
      <guid>http://precedings.nature.com/documents/3283/version/1</guid>
      <pubDate>Tue, 26 May 2009 20:56:50 UTC</pubDate>
      <dc:title>A novel superior factor widely controlling the rice grain quality</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3283.1</dc:identifier>
      <dc:date>2009-05-26</dc:date>
      <dc:creator>Hiroaki Shimada</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-05-26T20:56:50Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Plant Biology</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3283/version/1/files/npre20093283-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Literature Triage and Indexing in the Mouse Genome Informatics (MGI) Group</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3246.1</link>
      <description>The Mouse Genome Informatics (MGI; http://www.informatics.jax.org) group is comprised of several collaborating projects including the Mouse Genome Database (MGD) Project, the Gene Expression Database (GXD) Project, the Mouse Tumor Biology (MTB) Database Project, and the Gene Ontology (GO) Project. Literature identification and collection is performed cooperatively amongst the groups.In recent years many institutional libraries have transitioned from a focus largely on print holdings to one of electronic access to journals. This change has necessitated adaptation on the part of the MGI curatorial group. Whereas the majority of journals covered by the group used to be surveyed in paper form, those journals are now surveyed electronically. Approximately 160 journals have been identified as those most relevant to the various database groups. Each curator in the group has the responsibility of scanning several journals for articles relevant to any of the database projects. Articles chosen via this process are marked as to their potential significance for various projects. Each article is catalogued in a Master Bibliography section of the MGI database system and annotated to the database sections for which it has been identified as relevant. A secondary triage process allows curators from each group to scan the chosen articles and mark ones desired for their project if such annotation has been missed on the initial scan.Once articles have been identified for each database project a variety of processes are implemented to further categorize and index data from those articles. For example, the Alleles and Phenotype section of the MGD database indexes each article marked for MGD and in this indexing process they identify each mouse gene and allele examined in the article. The GXD database indexing process has a different focus. In this case articles are indexed with regard to the stage of development used in the study as well as the assay technique used. In each case the indexing gives an overview of the data held in the article and assists in the more extensive curation performed in the following step of the curation process. Indexing also provides each group with valuable information used to prioritize and streamline the overall curation process.The MGI projects are supported by NHGRI grants HG000330, HG00273, and HG003622, NICHD grant HD033745, and NCI grant CA089713.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3246.1</guid>
      <pubDate>Thu, 14 May 2009 21:29:18 UTC</pubDate>
      <dc:title>Literature Triage and Indexing in the Mouse Genome Informatics (MGI) Group</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3246.1</dc:identifier>
      <dc:date>2009-05-14</dc:date>
      <dc:creator>Debra M. Krupke</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-05-14T21:29:18Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Cancer</prism:section>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Immunology</prism:section>
      <prism:section>Molecular Cell Biology</prism:section>
      <prism:section>Neuroscience</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3246/version/1/files/npre20093246-1.pdf.thumb.png"/>
      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
    </item>
    <item>
      <title>Signi&#64257;cance tests for comparing digital gene  expression pro&#64257;les</title>
      <link>http://precedings.nature.com/documents/2002/version/3</link>
      <description>Most of the statistical tests currently used to detect differentially expressed genes are based on asymptotic results, and perform poorly for low expression tags. Another problem is the common use of a single canonical cutoff for the significance level (p-value) of all the tags, without taking into consideration the type II error and the highly variable character of the sample size of the tags.This work reports the development of two significance tests for the comparison of digital expression profiles, based on frequentist and Bayesian points of view, respectively. Both tests are exact, and do not use any asymptotic considerations, thus producing more correct results for low frequency tags than the chi-square test. The frequentist test uses a tag-customized critical level which minimizes a linear combination of type I and type II errors.  A comparison of the Bayesian and the frequentist tests revealed that they are linked by a Beta distribution function. These tests can be used alone or in conjunction, and represent an improvement over the currently available methods for comparing digital profiles.</description>
      <guid>http://precedings.nature.com/documents/2002/version/3</guid>
      <pubDate>Fri, 29 Aug 2008 21:08:06 UTC</pubDate>
      <dc:title>Signi&#64257;cance tests for comparing digital gene  expression pro&#64257;les</dc:title>
      <dc:identifier>hdl:10101/npre.2008.2002.3</dc:identifier>
      <dc:date>2009-09-03</dc:date>
      <dc:creator>Leonardo Varuzza</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2008-08-29T21:08:06Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Bioinformatics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/2002/version/3/files/npre20082002-3.pdf.thumb.png"/>
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