Dean P. Edwards
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View article: 3C. 3-Ketosteroid receptors in GtoPdb v.2025.3
3C. 3-Ketosteroid receptors in GtoPdb v.2025.3 Open
Steroid hormone receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Nuclear Hormone Receptors [75, 221, 3]) are nuclear hormone receptors of the NR3 class, with endogenous agonists that may be divided into 3-hydroxysteroids …
View article: Structural proteomics defines a sequential priming mechanism for the progesterone receptor
Structural proteomics defines a sequential priming mechanism for the progesterone receptor Open
View article: Acetylation of RORβ by histone acetyltransferase p300 and deacetylation by SIRT1 modulates receptor stability, turnover and transcriptional activity
Acetylation of RORβ by histone acetyltransferase p300 and deacetylation by SIRT1 modulates receptor stability, turnover and transcriptional activity Open
RORβ is an understudied nuclear receptor recently implicated in numerous pathologies. Using immunoprecipitation mass spectrometry, the transcription factor coregulatory protein and histone acetyltransferase p300 ( EP300 ) was identified as…
View article: Structural proteomics defines a sequential priming mechanism for the progesterone receptor
Structural proteomics defines a sequential priming mechanism for the progesterone receptor Open
The progesterone receptor (PR) is a steroid-responsive nuclear receptor with two isoforms: PR-A and PR-B. Disruption of PR-A:PR-B signaling is associated with breast cancer through interactions with oncogenic co-regulatory proteins (CoRs).…
View article: Molecular mechanisms of TWIST1‐regulated transcription in EMT and cancer metastasis
Molecular mechanisms of TWIST1‐regulated transcription in EMT and cancer metastasis Open
View article: International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily—Update 2023
International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily—Update 2023 Open
View article: 3C. 3-Ketosteroid receptors in GtoPdb v.2023.1
3C. 3-Ketosteroid receptors in GtoPdb v.2023.1 Open
Steroid hormone receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Nuclear Hormone Receptors [75, 218, 3]) are nuclear hormone receptors of the NR3 class, with endogenous agonists that may be divided into 3-hydroxysteroids …
View article: Figures S1-7 from Loss of MutL Disrupts CHK2-Dependent Cell-Cycle Control through CDK4/6 to Promote Intrinsic Endocrine Therapy Resistance in Primary Breast Cancer
Figures S1-7 from Loss of MutL Disrupts CHK2-Dependent Cell-Cycle Control through CDK4/6 to Promote Intrinsic Endocrine Therapy Resistance in Primary Breast Cancer Open
Supplementary Figure 1 Mismatch repair dysregulation associates with high mutation load and poor clinical outcome in patients with ER breast cancer. Supplementary Figure 2 MutL complex disruption in ER breast cancer cells induces endocrine…
View article: Data from Loss of MutL Disrupts CHK2-Dependent Cell-Cycle Control through CDK4/6 to Promote Intrinsic Endocrine Therapy Resistance in Primary Breast Cancer
Data from Loss of MutL Disrupts CHK2-Dependent Cell-Cycle Control through CDK4/6 to Promote Intrinsic Endocrine Therapy Resistance in Primary Breast Cancer Open
Significant endocrine therapy–resistant tumor proliferation is present in ≥20% of estrogen receptor–positive (ER+) primary breast cancers and is associated with disease recurrence and death. Here, we uncover a link between intri…
View article: Data from Loss of MutL Disrupts CHK2-Dependent Cell-Cycle Control through CDK4/6 to Promote Intrinsic Endocrine Therapy Resistance in Primary Breast Cancer
Data from Loss of MutL Disrupts CHK2-Dependent Cell-Cycle Control through CDK4/6 to Promote Intrinsic Endocrine Therapy Resistance in Primary Breast Cancer Open
Significant endocrine therapy–resistant tumor proliferation is present in ≥20% of estrogen receptor–positive (ER+) primary breast cancers and is associated with disease recurrence and death. Here, we uncover a link between intri…
View article: Figures S1-7 from Loss of MutL Disrupts CHK2-Dependent Cell-Cycle Control through CDK4/6 to Promote Intrinsic Endocrine Therapy Resistance in Primary Breast Cancer
Figures S1-7 from Loss of MutL Disrupts CHK2-Dependent Cell-Cycle Control through CDK4/6 to Promote Intrinsic Endocrine Therapy Resistance in Primary Breast Cancer Open
Supplementary Figure 1 Mismatch repair dysregulation associates with high mutation load and poor clinical outcome in patients with ER breast cancer. Supplementary Figure 2 MutL complex disruption in ER breast cancer cells induces endocrine…
View article: Data from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
Data from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer Open
The beneficial versus detrimental roles of estrogen plus progesterone (E+P) in breast cancer remains controversial. Here we report a beneficial mechanism of E+P treatment in breast cancer cells driven by transcriptional upregulation of the…
View article: Figure S5 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S5 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
RCAS-KrasG12D can induce tumors from KRT6A+ cells in K6a-tva/MMTV-Wnt1 mouse precancerous lesions.
View article: Figure S8 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S8 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
Additional information on the histopathological characteristics of tumors originated from KRT6A+ and WAP+ cells.
View article: Supplementary Figure S2. from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
Supplementary Figure S2. from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer Open
NEMO is required for E+P induced expression of IL-6 and NFkB signaling in ER+PR+ overexpressing DCIS.com breast cancer cells.
View article: Figure S3 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S3 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
KRT6+ cells in the precancerous stage and cancer stage of MMTV-Wnt1 mammary glands are different from those in the normal mammary glands
View article: Figure S1 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S1 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
MMTV-Wnt1 precancerous glands contain WAP+ cells.
View article: Figure S6 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S6 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
Wnt1 gene expression in KRT6A+ and WAP+ cells in MMTV-Wnt1 precancerous mammary glands.
View article: Figure S2 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S2 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
Mutated Ras is sufficient to transform precancerous cells in the MMTV-Wnt1 mammary glands into cancer
View article: Supplementary Figure S2. from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
Supplementary Figure S2. from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer Open
NEMO is required for E+P induced expression of IL-6 and NFkB signaling in ER+PR+ overexpressing DCIS.com breast cancer cells.
View article: Supplementary Material and Methods from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
Supplementary Material and Methods from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer Open
Description of additional experiments and procedures carried out in this study
View article: Supplementary File 5 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers
Supplementary File 5 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers Open
Response markers (pathways)
View article: Data from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer
Data from NEMO, a Transcriptional Target of Estrogen and Progesterone, Is Linked to Tumor Suppressor PML in Breast Cancer Open
The beneficial versus detrimental roles of estrogen plus progesterone (E+P) in breast cancer remains controversial. Here we report a beneficial mechanism of E+P treatment in breast cancer cells driven by transcriptional upregulation of the…
View article: Figure S6 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S6 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
Wnt1 gene expression in KRT6A+ and WAP+ cells in MMTV-Wnt1 precancerous mammary glands.
View article: Supplementary File 4 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers
Supplementary File 4 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers Open
Response markers
View article: Figure S5 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S5 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
RCAS-KrasG12D can induce tumors from KRT6A+ cells in K6a-tva/MMTV-Wnt1 mouse precancerous lesions.
View article: Extended Methods from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers
Extended Methods from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers Open
Extended Materials and Methods with in depth details about experimental procedures and protocols
View article: Supplementary File 4 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers
Supplementary File 4 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers Open
Response markers
View article: Figure S4 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes
Figure S4 from Mammary Precancerous Stem and Non-Stem Cells Evolve into Cancers of Distinct Subtypes Open
HrasQ61L is not sufficient to induce tumors from KRT6a+ cells in normal mammary glands.
View article: Supplementary File 1 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers
Supplementary File 1 from Mass Spectrometry–Based Proteomics Reveals Potential Roles of NEK9 and MAP2K4 in Resistance to PI3K Inhibition in Triple-Negative Breast Cancers Open
mRNA isoforms