Valerio Bianchi
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View article: PhenoFeatureFinder: a python package for linkingdevelopmental phenotypes to omics features
PhenoFeatureFinder: a python package for linkingdevelopmental phenotypes to omics features Open
International audience
View article: Supplementary Figure S6 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S6 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
RNA Pol II intensities on promoters vary between control and tumor samples and correlate with gene deregulation.
View article: Supplementary Figure S4 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S4 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Analyses and characterization of Myc-dependent and Myc-independent differentially expressed genes.
View article: Supplementary Figure S3 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S3 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
MycVD induces proliferation to a similar extend as MycWT but is impaired in cellular transformation.
View article: Supplementary Figure S2 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S2 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
tet-MycWT and tet-MycVD overexpression induces liver tumorigenesis.
View article: Supplementary Table S1 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Table S1 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
List of gene symbols with gene expression levels, fold change values and adjusted p-values (padj; q-value) derived from RNA-seq analyses.
View article: Supplementary Figure S1 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S1 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
tet-Myc induction in utero leads to fast and highly penetrant tumorigenesis.
View article: Supplementary Table S2 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Table S2 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Gene ontology analyses of Myc-dependent and -independent DEG categories.
View article: Supplementary Table S3 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Table S3 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
MycVD-sensitive genes.
View article: Supplementary Methods and References from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Methods and References from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Description of additional methods and procedures used in the study. Also includes Supplementary References.
View article: Data from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Data from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Tumors driven by activation of the transcription factor MYC generally show oncogene addiction. However, the gene expression programs that depend upon sustained MYC activity remain unknown. In this study, we employed a mouse model of liver …
View article: Supplementary Methods and References from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Methods and References from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Description of additional methods and procedures used in the study. Also includes Supplementary References.
View article: Supplementary Table S2 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Table S2 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Gene ontology analyses of Myc-dependent and -independent DEG categories.
View article: Supplementary Figure S5 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S5 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Genome-wide distribution and binding intensities of Myc in control and tumor samples.
View article: Supplementary Figure S6 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S6 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
RNA Pol II intensities on promoters vary between control and tumor samples and correlate with gene deregulation.
View article: Supplementary Figure S5 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S5 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Genome-wide distribution and binding intensities of Myc in control and tumor samples.
View article: Supplementary Table S1 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Table S1 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
List of gene symbols with gene expression levels, fold change values and adjusted p-values (padj; q-value) derived from RNA-seq analyses.
View article: Supplementary Figure and Table Legends from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure and Table Legends from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Legend for Supplementary Figures S1-S6 and Supplementary Table S1-S3.
View article: Data from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Data from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Tumors driven by activation of the transcription factor MYC generally show oncogene addiction. However, the gene expression programs that depend upon sustained MYC activity remain unknown. In this study, we employed a mouse model of liver …
View article: Supplementary Figure and Table Legends from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure and Table Legends from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Legend for Supplementary Figures S1-S6 and Supplementary Table S1-S3.
View article: Supplementary Table S3 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Table S3 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
MycVD-sensitive genes.
View article: Supplementary Figure S2 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S2 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
tet-MycWT and tet-MycVD overexpression induces liver tumorigenesis.
View article: Supplementary Figure S4 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S4 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
Analyses and characterization of Myc-dependent and Myc-independent differentially expressed genes.
View article: Supplementary Figure S3 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S3 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
MycVD induces proliferation to a similar extend as MycWT but is impaired in cellular transformation.
View article: Supplementary Figure S1 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors
Supplementary Figure S1 from Identification of MYC-Dependent Transcriptional Programs in Oncogene-Addicted Liver Tumors Open
tet-Myc induction in utero leads to fast and highly penetrant tumorigenesis.
View article: Epigenetic Analyses of Human Left Atrial Tissue Identifies Gene Networks Underlying Atrial Fibrillation
Epigenetic Analyses of Human Left Atrial Tissue Identifies Gene Networks Underlying Atrial Fibrillation Open
Background: Atrial fibrillation (AF) often arises from structural abnormalities in the left atria (LA). Annotation of the noncoding genome in human LA is limited, as are effects on gene expression and chromatin architecture. Many AF-associ…
View article: <scp>BAZ</scp> 2A safeguards genome architecture of ground‐state pluripotent stem cells
<span>BAZ</span> 2A safeguards genome architecture of ground‐state pluripotent stem cells Open
Chromosomes have an intrinsic tendency to segregate into compartments, forming long-distance contacts between loci of similar chromatin states. How genome compartmentalization is regulated remains elusive. Here, comparison of mouse ground-…
View article: Epigenetic and Transcriptional Networks Underlying Atrial Fibrillation
Epigenetic and Transcriptional Networks Underlying Atrial Fibrillation Open
Genome-wide association studies have uncovered over a 100 genetic loci associated with atrial fibrillation (AF), the most common arrhythmia. Many of the top AF-associated loci harbor key cardiac transcription factors, including PITX2, TBX5…
View article: Hominin-specific regulatory elements selectively emerged in oligodendrocytes and are disrupted in autism patients
Hominin-specific regulatory elements selectively emerged in oligodendrocytes and are disrupted in autism patients Open
View article: TIP5 safeguards genome architecture of ground-state pluripotent stem cells
TIP5 safeguards genome architecture of ground-state pluripotent stem cells Open
Chromosomes have an intrinsic tendency to segregate into compartments, forming long-distance contacts between loci of similar chromatin states. However, how genome compartmentalization is regulated remains elusive. We analyzed two closely …