Supplementary audio files for ‘Chromas from chromatin: Sonification of the epigenome’

Supplementary audio S1.1: Audio track extracted from region chr17:7531293-7631293<br>Supplementary audio S2.1: Audio track extracted from region chr4:9734445-9834445<br>Supplementary audio S3.1: Audio track extracted from region chr8:145689938-145789938<br>Supplementary audio S4.1: Audio track extracted from region chr2:25460307-25560307<br>Supplementary audio S5.1: Audio track extracted from region chrX:44802134-44902134<br>Supplementary audio S6.1: Audio track extracted from region chr15:44957020-45057020<br>Supplementary audio S7.1: Audio track extracted from region chr13:30986479-31086479<br>Supplementary audio S8.1: Audio track extracted from region chr10:89625864-89725864<br>Supplementary audio S9.1: Audio track extracted from region chr16:10944948-11044948<br>Supplementary audio S10.1: Audio track extracted from region chr8:128700997-128800997<br>Supplementary audio S1.2: Randomized audio track extracted from region chr17:7531293-7631293<br>Supplementary audio S2.2: Randomized audio track extracted from region chr4:9734445-9834445<br>Supplementary audio S3.2: Randomized audio track extracted from region chr8:145689938-145789938<br>Supplementary audio S4.2: Randomized audio track extracted from region chr2:25460307-25560307<br>Supplementary audio S5.2: Randomized audio track extracted from region chrX:44802134-44902134<br>Supplementary audio S6.2: Randomized audio track extracted from region chr15:44957020-45057020<br>Supplementary audio S7.2: Randomized audio track extracted from region chr13:30986479-31086479<br>Supplementary audio S8.2: Randomized audio track extracted from region chr10:89625864-89725864<br>Supplementary audio S9.2: Randomized audio track extracted from region chr16:10944948-11044948<br>Supplementary audio S10.2: Randomized audio track extracted from region chr8:128700997-12880099

Genes showing significant 3′ UTR shortening in poor-prognosis patients of both breast and lung cancer.

<p>Genes showing significant 3′ UTR shortening in poor-prognosis patients of both breast and lung cancer.</p

Affymetrix probes and APA sites in the 3′ UTR of six genes studied in Ref. [<b>10</b>].

<p>The probes shown in red are used, possibly together with probes located in the coding region, to build the 5′ probeset. The probes shown in green are used to build the 3′ probeset. For DICER1 and FGF2 it is not possible to study the APA site since all probes lie beyond it.</p

Schematic representation of two possible mechanisms leading to higher ERI in poor-prognosis tumors.

<p>(A) Differential synthesis: the shorter isoform is synthesized in a higher proportion in the poor-prognosis tumors, leading to less degradation by microRNAs. (B) Differential degradation: the isoforms are produced in the same proportion in the two cases, but a microRNA expressed exclusively in the poor-prognosis tumors selectively degrades the long isoform. In both cases we expect a higher ERI (relative prevalence of short form) in the poor-prognosis group. However in case (A) the overall expression of the two isoforms is expected to be higher in the poor-prognosis case, while the opposite is expected in case (B).</p

Predictive power of the prognostic score based on ERI in two dataset not used to derive the signature.

<p>(A) the Miller breast cancer dataset <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031129#pone.0031129-Miller1" target="_blank">[20]</a> and (B) the Shedden lung cancer dataset <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0031129#pone.0031129-Shedden1" target="_blank">[32]</a>. Patients are divided into groups using the median score as a cutoff.</p

Fraction of gene expression variance explained by models based on chromatin HMM data for each cell line, chromatin HMM data for K562 cells, and TBA alone.

<p>Fraction of gene expression variance explained by models based on chromatin HMM data for each cell line, chromatin HMM data for K562 cells, and TBA alone.</p

Boletín de Segovia: Número 1 - 1851 enero 1

Copia digital. Madrid : Ministerio de Cultura. Subdirección General de Coordinación Bibliotecaria, 200

Additional file 1 of Roar: detecting alternative polyadenylation with standard mRNA sequencing libraries

Lists of samples (GSE and GSM identifiers) with microarray data for human brain and testes. (TXT 5 kb

Histological pattern of cathepsin D expression in human cancers.

<div><p>Representative images of cathepsin D expression in human cancer samples.</p> <p>(A) prostate (B) breast cancer showing cathepsin D expression (brown) by tumor and stromal cells; (C) large-cell lung carcinoma and (D) lung adenocarcinoma showing cathepsin D expression by tumor cells and to a lesser extent by stromal cells; (E, F), cathepsin D is almost exclusively expressed by stromal cells in small-cell lung carcinomas (E) and large-cell neuroendocrine carcinomas (F), whereas tumor cells are almost devoid of cathepin D expression.</p> <p>Nuclei were counterstained with haematoxylin.</p> <p>Magnification 200×.</p></div

Stromal cathepsin D expression promotes PNEC cell migration and proliferation.

<div><p>(A) Quantification of PNEC cell migration in 3D matrigel co-culture with cathepsin D-deficient (CTSD^−/−) or wild-type (CTSD^+/+) fibroblasts after 30h of co-culture; (B) PNEC cell proliferation and (C, D) elongation are increased in the presence of conditioned medium (CM) derived from CTSD^+/+ fibroblasts (C), compared to CM derived from CTSD^−/− fibroblasts (D).</p> <p>Experiments were performed three times, each time in quintuplicate.</p> <p>Representative results are shown.</p> <p>*p<0.05, ***p<0.001, Student t test.</p></div