Exon 3 is spliced out of the transcript initiated at Exon 1, but Exon 4 is common to both transcripts

The ChIP-chip microarray analysis indicated that the first promoter is inactive in the control experiment, but is activated with E2 treatment at a low level, a result that is verified by qRT-PCR results (B). The second promoter was predicted to be active at a low level with and without E2 treatment, which again was verified (C). Error bars indicate standard errors from the mean for three replicates.<p><b>Copyright information:</b></p><p>Taken from "Genome-wide analysis of alternative promoters of human genes using a custom promoter tiling array"</p><p>http://www.biomedcentral.com/1471-2164/9/349</p><p>BMC Genomics 2008;9():349-349.</p><p>Published online 25 Jul 2008</p><p>PMCID:PMC2527337.</p><p></p

Similar trends are observed in the case of genes with two active promoters where neither is affected by E2 treatment

Here, one of the promoters is likely to be at the 5' end of the gene, while the other promoter can occur anywhere else along the gene length with roughly equal probability (B). A different pattern is observed in genes with two active promoters where one is affected by E2 treatment (either activated or inactivated). In this case we can see that, as before, the upstream active promoter is likely to be located at the 5' end of the gene, but the downstream promoter is strongly biased towards the 3' end of the gene (C).<p><b>Copyright information:</b></p><p>Taken from "Genome-wide analysis of alternative promoters of human genes using a custom promoter tiling array"</p><p>http://www.biomedcentral.com/1471-2164/9/349</p><p>BMC Genomics 2008;9():349-349.</p><p>Published online 25 Jul 2008</p><p>PMCID:PMC2527337.</p><p></p

Of these, the upstream promoter was activated by E2 in 25 genes (A), and was inactivated by E2 in 61 cases (B)

The downstream promoter was activated by E2 treatment in 62 cases (C), and inactivated by E2 in 64 cases (D).<p><b>Copyright information:</b></p><p>Taken from "Genome-wide analysis of alternative promoters of human genes using a custom promoter tiling array"</p><p>http://www.biomedcentral.com/1471-2164/9/349</p><p>BMC Genomics 2008;9():349-349.</p><p>Published online 25 Jul 2008</p><p>PMCID:PMC2527337.</p><p></p

Plots of observed versus expected DNA methylation values for SALL3, TWIST2 and C/EBPα methylation standards

<p><b>Copyright information:</b></p><p>Taken from "Accurate quantification of DNA methylation using combined bisulfite restriction analysis coupled with the Agilent 2100 Bioanalyzer platform"</p><p>Nucleic Acids Research 2006;34(3):e17-e17.</p><p>Published online 7 Feb 2006</p><p>PMCID:PMC1361623.</p><p>© The Author 2006. Published by Oxford University Press. All rights reserved</p> () SALL3, () TWIST2 and () C/EBPα results. Trend lines and values are displayed for each plot. The non-linearity of the observed versus expected methylation values is most likely due to a PCR amplification bias

This promoter was shown to be highly active in both treatments, which was verified by qRT-PCR

Error bars indicate standard errors from the mean for three replicates.<p><b>Copyright information:</b></p><p>Taken from "Genome-wide analysis of alternative promoters of human genes using a custom promoter tiling array"</p><p>http://www.biomedcentral.com/1471-2164/9/349</p><p>BMC Genomics 2008;9():349-349.</p><p>Published online 25 Jul 2008</p><p>PMCID:PMC2527337.</p><p></p

Assessment of DNA methylation in clinical CLL samples and a human lung cancer cell line treated with 5-aza-2′dC

<p><b>Copyright information:</b></p><p>Taken from "Accurate quantification of DNA methylation using combined bisulfite restriction analysis coupled with the Agilent 2100 Bioanalyzer platform"</p><p>Nucleic Acids Research 2006;34(3):e17-e17.</p><p>Published online 7 Feb 2006</p><p>PMCID:PMC1361623.</p><p>© The Author 2006. Published by Oxford University Press. All rights reserved</p> () Methylation levels of TWIST2 in 19 primary CLL samples generated by Bio-COBRA and Southern blot. The correlation coefficient between the two data sets was 0.98. ( and ) Restriction digestions of SALL3 (B) and C/EBPα (E) in A549 cells treated with 5-aza-dC at six different concentrations for 72 h (concentrations are indicated at the top). ( and ) Bio-COBRA quantification of the restriction digestions shown in (B) and (E). As expected, low doses of the demethylating agent showed a pronounced effect in the DNA methylation status of the analyzed loci. ( and ) mRNA expression level of SALL3 (D) and C/EBPα (G). Three separate measurements were performed for each sample. For C/EBPα, the expression level measured in the untreated cell line was normalized to 1. For SALL3, the expression level detected at 0.10 µM was normalized to 1, since the untreated cell line shows no expression under the experimental conditions utilized in this study

Epigenetic dysregulation of the erythropoietic transcription factor <i>KLF1</i> and the β-like globin locus in juvenile myelomonocytic leukemia

<p>Increased levels of fetal hemoglobin (HbF) are a hallmark of more than half of the children diagnosed with juvenile myelomonocytic leukemia (JMML). Elevated HbF levels in JMML are associated with DNA hypermethylation of distinct gene promoter regions in leukemic cells. Since the regulation of globin gene transcription is known to be under epigenetic control, we set out to study the relation of DNA methylation patterns at β-/γ-globin promoters, mRNA and protein expression of globins, and epigenetic modifications of genes encoding the globin-regulatory transcription factors <i>BCL11A</i> and <i>KLF1</i> in nucleated erythropoietic precursor cells of patients with JMML. We describe several altered epigenetic components resulting in disordered globin synthesis in JMML. We identify a cis-regulatory upstream <i>KLF1</i> enhancer sequence as highly sensitive to DNA methylation and frequently hypermethylated in JMML. The data indicate that the dysregulation of β-like globin genes is a genuine attribute of the leukemic cell clone in JMML and involves mechanisms not taking part in the normal fetal-to-adult hemoglobin switch.</p

Diverse histone modifications on histone 3 lysine 9 and their relation to DNA methylation in specifying gene silencing-0

<p><b>Copyright information:</b></p><p>Taken from "Diverse histone modifications on histone 3 lysine 9 and their relation to DNA methylation in specifying gene silencing"</p><p>http://www.biomedcentral.com/1471-2164/8/131</p><p>BMC Genomics 2007;8():131-131.</p><p>Published online 24 May 2007</p><p>PMCID:PMC1888705.</p><p></p>ol, with Cy3. . Scatter plot of histone modification level to density index. Histone modification level is indicated by the fold enrichment of ChIP DNA vs input DNA

Diverse histone modifications on histone 3 lysine 9 and their relation to DNA methylation in specifying gene silencing-6

<p><b>Copyright information:</b></p><p>Taken from "Diverse histone modifications on histone 3 lysine 9 and their relation to DNA methylation in specifying gene silencing"</p><p>http://www.biomedcentral.com/1471-2164/8/131</p><p>BMC Genomics 2007;8():131-131.</p><p>Published online 24 May 2007</p><p>PMCID:PMC1888705.</p><p></p>ination of TSA and AzadC (1 M of AzadC for 1, 3 and 5 days followed by 300 nM of TSA for 24 h). Expression of targets were identified by quantitative RT-PCR. and . and are methylated and associated with hypoacetyl-H3K9. and . and are unmethylated and associated with hyperacetyl-H3K9. Each error bar represents the standard deviation calculated from triplicates

Diverse histone modifications on histone 3 lysine 9 and their relation to DNA methylation in specifying gene silencing-5

<p><b>Copyright information:</b></p><p>Taken from "Diverse histone modifications on histone 3 lysine 9 and their relation to DNA methylation in specifying gene silencing"</p><p>http://www.biomedcentral.com/1471-2164/8/131</p><p>BMC Genomics 2007;8():131-131.</p><p>Published online 24 May 2007</p><p>PMCID:PMC1888705.</p><p></p>12 PCR positions for each gene are indicated as the distances from transcription start site (0). Each error bar represents the standard deviation calculated from triplicates