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    <title>Nature Precedings - Subject feed for Genetics &amp; Genomics</title>
    <link>http://precedings.nature.com/subjects/genetics/</link>
    <description>Recently posted documents in Genetics &amp; Genomics</description>
    <dc:publisher>Nature Publishing Group</dc:publisher>
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      <title>9aaTAD Prediction result (2006)</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3984.1</link>
      <description>Recently reported, 9aaTAD transcription factors p53, VP16, MLL/ALL, E2A, HSF1, NF-IL6, NFAT1 and NF-kB interact directly with the general coactivator CBP/p300 aside from already referred TAF9. All four domains of CBP/p300 &amp;#8211; KIX, TAZ1, TAZ2 and IBiD provide multiple interactions with 9aaTADs, e.g. p53. Annotation of predicted 9aa TAD using Pattern search ScanProsite on ExPASy and relevant experimental data are listed. </description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3984.1</guid>
      <pubDate>Fri, 20 Nov 2009 13:04:12 UTC</pubDate>
      <dc:title>9aaTAD Prediction result (2006)</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3984.1</dc:identifier>
      <dc:date>2009-11-20</dc:date>
      <dc:creator>Martin Piskacek</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-20T13:04:12Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
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      <title>The genetics of colored sequence synesthesia: Evidence of linkage to chromosome 16q and genetic heterogeneity for the condition</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3987.1</link>
      <description>Synesthesia is a perceptual condition in which normal sensory stimulation can trigger anomalous sensory experiences. For example, synesthetes may experience colors in response to sounds, tastes in response to words, or smells in response to touch. We here focus on colored sequence synesthesia, in which color experiences are triggered by learned ordinal sequences such as letters, numbers, weekdays and months. Although synesthesia has been noted in the scientific literature for over a century, it is understood only at the level of the phenomenology, and not at the molecular and neural levels. We have performed a linkage analysis to identify the first genetic loci responsible for the increased neural crosstalk underlying colored sequence synesthesia. Our analysis has identified a 23 MB region on chromosome 16 as a putative locus for the trait. Our data provide the first step in understanding neural crosstalk from its molecular basis to its behavioral consequences, opening a new inroad into the understanding of the multisensory brain. </description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3987.1</guid>
      <pubDate>Fri, 20 Nov 2009 07:08:42 UTC</pubDate>
      <dc:title>The genetics of colored sequence synesthesia: Evidence of linkage to chromosome 16q and genetic heterogeneity for the condition</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3987.1</dc:identifier>
      <dc:date>2009-11-20</dc:date>
      <dc:creator>Stephanie S. Nelson</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-20T07:08:42Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
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    <item>
      <title>Reacquainting two cultures. Preventing a de-elsification of European nutrigenomics?</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3981.1</link>
      <description>Sir Charles Snow, being a writer and a scientist, felt that he &amp;#8220;was moving among two groups &amp;#8211; comparable in intelligence, identical in race, not grossly different in social origin, earning about the same incomes, who had ceased to communicate at all&amp;#8221;(Snow, 1993 [1959], p.2). He called these two groups, the two cultures, referring to those in the natural sciences and those in the humanities. Many argue that this division is an awful thing. This poster discusses strategies to reacquaint the two cultures in the case of genomics. </description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3981.1</guid>
      <pubDate>Tue, 17 Nov 2009 11:28:40 UTC</pubDate>
      <dc:title>Reacquainting two cultures. Preventing a de-elsification of European nutrigenomics?</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3981.1</dc:identifier>
      <dc:date>2009-11-17</dc:date>
      <dc:creator>Bart Penders</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-17T11:28:40Z</prism:publicationDate>
      <prism:category>Poster</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
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      <title>Rsp5 promotes Gene Activation mediated by 9aaTAD Transcription Factors Oaf1 and Gal4 </title>
      <link>http://precedings.nature.com/documents/3968/version/1</link>
      <description>Nine-amino-acid transactivation domain, 9aaTAD, defines a large superfamily of yeast and mammals transcription factors. The transactivation of the 9aaTAD has been addressed to multiple general co-activators TAF9, MED15, CBP and p300. We demonstrate for the 9aaTAD transcription factors Oaf1 and Gal4 functional and physical interaction with E3-Ubiquitin Ligase Rsp5. The Rsp5-associations with RNA polymerase II and TFIID were reported previously.</description>
      <guid>http://precedings.nature.com/documents/3968/version/1</guid>
      <pubDate>Mon, 16 Nov 2009 23:52:09 UTC</pubDate>
      <dc:title>Rsp5 promotes Gene Activation mediated by 9aaTAD Transcription Factors Oaf1 and Gal4 </dc:title>
      <dc:identifier>hdl:10101/npre.2009.3968.1</dc:identifier>
      <dc:date>2009-11-16</dc:date>
      <dc:creator>Joachim Lipp</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-16T23:52:09Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Molecular Cell Biology</prism:section>
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      <title>The cultural epigenetics of psychopathology: The missing heritability of complex diseases found?</title>
      <link>http://precedings.nature.com/documents/3894/version/2</link>
      <description>We extend a cognitive paradigm for gene expression to the epigenetic epidemiology of mental disorders, recognizing the fundamental role that culture plays in human biology as another heritage mechanism parallel to, and interacting with, the more familiar genetic and epigenetic systems. In the mathematical model, culture acts as another tunable epigenetic catalyst that both directs developmental trajectories and becomes convoluted with individual ontology via a mutually interacting crosstalk mediated by a social interaction that is itself culturally driven. We call for the incorporation of embedding culture as an essential component of the epigenetic regulation of human mental development and its dysfunctions, bringing what is perhaps the central reality of human biology into the center of biological psychiatry. The cultural and epigenetic systems of heritage may well provide the &amp;#8216;missing&amp;#8217; heritability of complex diseases now under so much intense discussion.</description>
      <guid>http://precedings.nature.com/documents/3894/version/2</guid>
      <pubDate>Wed, 11 Nov 2009 18:29:58 UTC</pubDate>
      <dc:title>The cultural epigenetics of psychopathology: The missing heritability of complex diseases found?</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3894.2</dc:identifier>
      <dc:date>2009-11-11</dc:date>
      <dc:creator>Rodrick Wallace</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-11T18:29:58Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Developmental Biology</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Neuroscience</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3894/version/2/files/npre20093894-2.pdf.thumb.png"/>
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    <item>
      <title>Are endocannabinoid type 1 receptor gene (CNR1) polymorphisms associated with obesity and metabolic syndrome in postmenopausal Polish women?</title>
      <link>http://precedings.nature.com/documents/3946/version/1</link>
      <description>Objective: The aim of this study was to determine whether genetic variation at the cannabinoid receptor-1 (CNR1) locus could have an effect on adiposity, fat distribution and obesity-related metabolic disorders in Polish postmenopausal women.Design and Subjects: The A3813G, G1422A and A4895G single nucleotide polymorphisms of CNR1 were genotyped in 348 randomly selected postmenopausal women aged 50-60 years recruited from the Wroclaw city population. Measurements: CNR1 genotypes, anthropometric measures (BMI, WC, body fat distribution by DEXA) and metabolic parameters (glucose, lipid profile, insulin FIRI) were determined.Results: The 3813G allele was not significantly associated with higher body mass, BMI, WC, total fat, or fat percentage, but was associated with higher android fat deposit (2971.78 &amp;#177; 1655.08 &amp;#177; 2472.64 &amp;#177; 1300.53, p = 0.007) and percentage of android fat (37.59 &amp;#177; 8.45 vs. 35.66 &amp;#177; 7.63, p = 0.062). The 1422A allele was associated with higher total fat (31587.72 &amp;#177; 9161.28 g vs. 26078.26 &amp;#177; 7552.14 g, p = 0.019), fat percentage (40.51 &amp;#177; 5.66% vs. 37.51 &amp;#177; 4.99%, p = 0.052), and percentage of android fat (40.86 &amp;#177; 9.73% vs. 36.09 &amp;#177; 7.70%, p = 0.047). No associations were observed for the A4895G variant.Conclusions: There is an association of variants of CNR1 with obesity-related phenotypes in Polish postmenopausal women. As CB1 is a drug target for obesity, pharmacogenetic receptor gene analysis of obesity treatment by endocannabinoid blockade may be of interest to identify the best responders.</description>
      <guid>http://precedings.nature.com/documents/3946/version/1</guid>
      <pubDate>Fri, 06 Nov 2009 10:47:40 UTC</pubDate>
      <dc:title>Are endocannabinoid type 1 receptor gene (CNR1) polymorphisms associated with obesity and metabolic syndrome in postmenopausal Polish women?</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3946.1</dc:identifier>
      <dc:date>2009-11-06</dc:date>
      <dc:creator>Katarzyna Dunajska</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-06T10:47:40Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
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    <item>
      <title>9aaTADs mimic DNA to interact with a pseudo-DNA Binding Domain KIX of Med15 (Molecular Chameleons)</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3939.1</link>
      <description>The KIX-domain of Gal11/MED15 was shown to interact with short transactivation domain of Pdr1 and Oaf1 (12 and 9 amino acids respectively) annotated to 9aaTAD family. Reported NMR data revealed a surprising sequence similarity of KIX domain and basic-leucine zipper (bZIP). </description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3939.1</guid>
      <pubDate>Thu, 05 Nov 2009 10:19:51 UTC</pubDate>
      <dc:title>9aaTADs mimic DNA to interact with a pseudo-DNA Binding Domain KIX of Med15 (Molecular Chameleons)</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3939.1</dc:identifier>
      <dc:date>2009-11-05</dc:date>
      <dc:creator>martin piskacek</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-05T10:19:51Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <media:thumbnail url="http://precedings.nature.com/documents/3939/version/1/files/npre20093939-1.pdf.thumb.png"/>
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    <item>
      <title>Common Transactivation Motif 9aaTAD recruits multiple general co-activators TAF9, MED15, CBP and p300</title>
      <link>http://dx.doi.org/10.1038/npre.2009.3488.2</link>
      <description>More than 2000 transcription factors are involved in the human gene regulation to provide cellular function and development. Transactivation domain, TAD, mediates the interaction of transcription factors with general transcriptional co-activators such as TAF9, MED15, CBP and p300. Recently reported NMR-data for interactions of these co-activators with transcription factors reveal tightly binding of KIX and TAZ domains to common 9aaTAD motif. Nine-amino-acid Trans-Activation Domain, 9aaTAD, defines a transactivation domain common to a large super-family of eukaryotic transcription factors represented in yeast by Gal4, Oaf1, Pdr1, Rtg3, Pho4, Gln3, Gcn4 and in mammals by p53, E2A, NFAT, NFkB, HSF1, NF-IL6, MLL, EBNA2, VP16. The 9aaTAD family was derived from the transcription factor Oaf1 and its close orthologs Gal4, Pdr1, Leu3, Tea1 and Cha4.</description>
      <guid>http://dx.doi.org/10.1038/npre.2009.3488.2</guid>
      <pubDate>Thu, 05 Nov 2009 00:57:07 UTC</pubDate>
      <dc:title>Common Transactivation Motif 9aaTAD recruits multiple general co-activators TAF9, MED15, CBP and p300</dc:title>
      <dc:identifier>doi:10.1038/npre.2009.3488.2</dc:identifier>
      <dc:date>2009-11-05</dc:date>
      <dc:creator>Martin Piskacek</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-05T00:57:07Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
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      <creativeCommons:license>http://creativecommons.org/licenses/by/3.0/</creativeCommons:license>
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      <title>MicroDNAs and Transcriptional Regulation</title>
      <link>http://precedings.nature.com/documents/3931/version/1</link>
      <description>Synthetic &amp;quot;microDNAs (MIDs)&amp;quot;is a new class of ~ 20-25 nucleotide-long DNAs capable of repressing the activity of the target gene at the level of transcription by mechanisms that have not been clarified yet. However they are designed to target non-coding regions of the cancer causing genes, thus interfering with transcription. The inhibition might be possible through the direct binding of MIDs to cis-regulatory sites and/or to some Transcription Factors (TF) that normally activate transcription. Synthetic MIDs in some ways are similar to the newly discovered microRNAs a mechanism by which cell regulates its genetic activities at post-transcriptional level. Synthetic MIDs can provide a powerful tool to prevent massive production of mRNA by undesired gene activities. Therefore drugs are not required to interact with overwhelming number of mRNA and microRNA copies that may present unwanted side effects. In vitro studies suggest that the inhibition of the target gene starts after the first round of DNA replication, usually 24 hours after treatment depending on cell doubling time. Cell growth suppression maximizes at day 6 or 7 and the inhibition effect is sustained for weeks. We have shown that blocking of both bcl-2 and k-ras transcription by their specific microDNA Inhibitors induced apoptosis in HL60 leukemia cells and B-cell lymphomas.</description>
      <guid>http://precedings.nature.com/documents/3931/version/1</guid>
      <pubDate>Wed, 04 Nov 2009 10:28:46 UTC</pubDate>
      <dc:title>MicroDNAs and Transcriptional Regulation</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3931.1</dc:identifier>
      <dc:date>2009-11-04</dc:date>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-04T10:28:46Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Cancer</prism:section>
      <prism:section>Genetics &amp; Genomics</prism:section>
      <prism:section>Molecular Cell Biology</prism:section>
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    <item>
      <title>No evidence for a recent genetic bottleneck in the endangered Sheko cattle breed (African Bos taurus) revealed by microsatellite analysis</title>
      <link>http://precedings.nature.com/documents/3925/version/1</link>
      <description>Sheko is African taurine cattle, valued for its milk yield, adaptation to humid tsetse infested environment and trypanotolerance. We used 30 microsatellite markers in analyzing 30 DNA samples. We found high genetic diversity and no genetic bottlenecks in endangered Sheko cattle. Sheko cattle have not undergone recent genetic bottlenecks, in spite of drastic reduction in its overall demographic population size. The results were supported by three statistical methods: (i) detection of heterozygosity excess (ii) a mode-shift indicator of allele distribution pattern (iii) the ratio of the number of alleles to the range of allele size, M-ratio test. This breed reflects historical and cultural identity of local communities and represents a unique component of the global domestic animal biodiversity that deserve priority for conservation.</description>
      <guid>http://precedings.nature.com/documents/3925/version/1</guid>
      <pubDate>Tue, 03 Nov 2009 15:15:15 UTC</pubDate>
      <dc:title>No evidence for a recent genetic bottleneck in the endangered Sheko cattle breed (African Bos taurus) revealed by microsatellite analysis</dc:title>
      <dc:identifier>hdl:10101/npre.2009.3925.1</dc:identifier>
      <dc:date>2009-11-03</dc:date>
      <dc:creator>Markos Tibbo</dc:creator>
      <prism:publicationName>Nature Precedings</prism:publicationName>
      <prism:publicationDate>2009-11-03T15:15:15Z</prism:publicationDate>
      <prism:category>Manuscript</prism:category>
      <prism:section>Genetics &amp; Genomics</prism:section>
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