Ryan Raisner
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Supplementary Fig. 4 from PAX8 Interacts with the SWI/SNF Complex at Enhancers to Drive Proliferation in Ovarian Cancer Open
PAX8 dependent cell lines are sensitive to SWI/SNF ATPase inhibition
Supplementary Figure legends from PAX8 Interacts with the SWI/SNF Complex at Enhancers to Drive Proliferation in Ovarian Cancer Open
Supplementary Figure legends
Supplementary Data 1 from PAX8 Interacts with the SWI/SNF Complex at Enhancers to Drive Proliferation in Ovarian Cancer Open
All identified proteins in Bio-ID Mass spec experiments.
Supplementary Fig. 3 from PAX8 Interacts with the SWI/SNF Complex at Enhancers to Drive Proliferation in Ovarian Cancer Open
PAX8 can recruit the SWI/SNF complex to chromatin
Data from PAX8 Interacts with the SWI/SNF Complex at Enhancers to Drive Proliferation in Ovarian Cancer Open
Activation of lineage-specific gene expression programs is mediated by the recruitment of lineage-specific transcription factors and their coactivators to chromatin. The lineage factor PAX8 drives essential gene expression in ovarian cance…
Supplementary Fig. 2 from PAX8 Interacts with the SWI/SNF Complex at Enhancers to Drive Proliferation in Ovarian Cancer Open
Western blot analyses supporting nanoBRET assays.
Supplementary Fig. 1 from PAX8 Interacts with the SWI/SNF Complex at Enhancers to Drive Proliferation in Ovarian Cancer Open
Proximity labeling of the PAX8 interactome
Supplementary Data 2 from PAX8 Interacts with the SWI/SNF Complex at Enhancers to Drive Proliferation in Ovarian Cancer Open
RNA-seq gene expression data after 48h after PAX8 siRNA knockdown in the indicated cell lines
AzidoTMT Enables Direct Enrichment and Highly Multiplexed Quantitation of Proteome-Wide Functional Residues Open
Recent advances in targeted covalent inhibitors have aroused significant interest for their potential in drug development for difficult therapeutic targets. Proteome-wide profiling of functional residues is an integral step of covalent dru…
Table S2 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
RNA seq analysis of androgen stimulated LNCaP cells treated with GNE-049.
Figure S2 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
qPCR analysis of Myc expression after GNE-049 treatment, effects of GNE-049 combination treatment.
Figure S2 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
qPCR analysis of Myc expression after GNE-049 treatment, effects of GNE-049 combination treatment.
Supplementary Figure legends from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Supplementary Figure legends
Figure S3 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Western blot and ChIP seq analysis of GNE-049 impact on histone acetylation
Data from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Resistance invariably develops to antiandrogen therapies used to treat newly diagnosed prostate cancers, but effective treatments for castration-resistant disease remain elusive. Here, we report that the transcriptional coactivator CBP/p30…
Figure S4 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Western blot analysis of AR mutant and over expressing LNCaP cells
Supplementary Figure legends from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Supplementary Figure legends
Table S1 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Bromodomain selectivity data for GNE-049 using BROMOscan® panel
Note S1 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
GNE-049 chemical synthesis
Figure S3 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Western blot and ChIP seq analysis of GNE-049 impact on histone acetylation
Data from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Resistance invariably develops to antiandrogen therapies used to treat newly diagnosed prostate cancers, but effective treatments for castration-resistant disease remain elusive. Here, we report that the transcriptional coactivator CBP/p30…
Figure S4 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Western blot analysis of AR mutant and over expressing LNCaP cells
Figure S1 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Western blots confirming siRNA knockdowns, GNE-049 compound properties.
Note S1 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
GNE-049 chemical synthesis
Figure S1 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Western blots confirming siRNA knockdowns, GNE-049 compound properties.
Table S1 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Bromodomain selectivity data for GNE-049 using BROMOscan® panel
Table S2 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
RNA seq analysis of androgen stimulated LNCaP cells treated with GNE-049.
Super-enhancer acquisition drives oncogene expression in triple negative breast cancer Open
Triple Negative Breast Cancer (TNBC) is a heterogeneous disease lacking known molecular drivers and effective targeted therapies. Cytotoxic chemotherapy remains the mainstay of treatment for TNBCs, which have significantly poorer survival …
Enhancer Activity Requires CBP/P300 Bromodomain-Dependent Histone H3K27 Acetylation Open
Acetylation of histone H3 at lysine 27 is a well-defined marker of enhancer activity. However, the functional impact of this modification at enhancers is poorly understood. Here, we use a chemical genetics approach to acutely block the fun…
Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer Open
Resistance invariably develops to antiandrogen therapies used to treat newly diagnosed prostate cancers, but effective treatments for castration-resistant disease remain elusive. Here, we report that the transcriptional coactivator CBP/p30…