Emily Heikamp
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View article: Supplementary Figure S8 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Figure S8 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Figure S8 shows that KAT6A/7 and Menin inhibition have combinatorial effects in vivo.
View article: Supplementary Figure S1 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Figure S1 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Figure S1 shows that some NUP98 fusions drive cell transformation and leukemogenesis.
View article: Supplementary Figure S7 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Figure S7 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Figure S7 shows that KAT6A/7 and Menin inhibition alter gene expression and remodel chromatin in NUP98-rearranged cells.
View article: Data from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Data from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
NUP98 fusion oncoproteins (FO) are a hallmark of childhood acute myeloid leukemia. NUP98 FOs drive leukemogenesis through phase-separated condensate formation and maintenance of an active chromatin landscape at stem cell–associated genes i…
View article: Supplementary Figure S4 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Figure S4 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Figure S4 shows that MYST family histone acetyltransferase complex members are molecular dependencies in NUP98-rearranged cells.
View article: Supplementary Tables S1-S17 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Tables S1-S17 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Table S1. Exonic mutations/indels in Nup98::Kdm5a;Vav-Cre tumors developing after bone marrow transplant Supplementary Table S2. Exonic mutations/indels in spontaneous Nup98::Kdm5a;Vav-Cre tumors Supplementary Table S3. Enric…
View article: Supplementary Figure S3 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Figure S3 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Figure S3 shows that NUP98 fusion oncoproteins interact with MYST family histone acetyltransferase complex members.
View article: Supplementary Figure S5 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Figure S5 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Figure S5 shows that NUP98-rearranged cells respond to KAT6A/7 inhibition in vitro and in vivo.
View article: Supplementary Figure S2 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Figure S2 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Figure S2 shows that Nup98::Kdm5a;Vav-Cre mice spontaneously develop myeloid disease.
View article: Supplementary Figure S6 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Figure S6 from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Figure S6 shows that KAT6A/7 and Menin inhibition have synergistic effects in NUP98-rearranged cells.
View article: Supplementary Methods and Results from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia
Supplementary Methods and Results from KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
Supplementary Methods, Supplementary Results
View article: KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i> -Rearranged Acute Myeloid Leukemia
KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in <i>NUP98</i> -Rearranged Acute Myeloid Leukemia Open
NUP98 fusion oncoproteins (FO) are a hallmark of childhood acute myeloid leukemia. NUP98 FOs drive leukemogenesis through phase-separated condensate formation and maintenance of an active chromatin landscape at stem cell–associated genes i…
View article: MOZ and HBO1 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in<i>NUP98</i>-Rearranged Acute Myeloid Leukemia
MOZ and HBO1 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in<i>NUP98</i>-Rearranged Acute Myeloid Leukemia Open
NUP98 fusion oncoproteins (FOs) are a hallmark of childhood acute myeloid leukemia (AML) and drive leukemogenesis through liquid-liquid phase separation-mediated nuclear condensate formation. However, the composition and consequences of NU…
View article: Revumenib Revises the Treatment Landscape for <i>KMT2A</i> -r Leukemia
Revumenib Revises the Treatment Landscape for <i>KMT2A</i> -r Leukemia Open
View article: Transient Menin Inhibition Is Sufficient to Induce Irreversible Polycomb-Mediated Silencing and Potent Anti-Proliferative Effects in MLL-Rearranged AML
Transient Menin Inhibition Is Sufficient to Induce Irreversible Polycomb-Mediated Silencing and Potent Anti-Proliferative Effects in MLL-Rearranged AML Open
MLL-Fusion oncoproteins (MLL-FP) are potent oncogenes that drive an aggressive form of acute myeloid leukaemia (AML). MLL-FP activity can be disrupted by blocking its chromatin occupancy with MLL-Menin inhibitors, or by blocking its bioche…
View article: NUP98 fusion proteins and KMT2A-MENIN antagonize PRC1.1 to drive gene expression in AML
NUP98 fusion proteins and KMT2A-MENIN antagonize PRC1.1 to drive gene expression in AML Open
Control of stem cell-associated genes by Trithorax group (TrxG) and Polycomb group (PcG) proteins is frequently misregulated in cancer. In leukemia, oncogenic fusion proteins hijack the TrxG homolog KMT2A and disrupt PcG activity to mainta…
View article: Data from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth <i>In vivo</i>
Data from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth <i>In vivo</i> Open
The vascular endothelial growth factor (VEGF) plays a key role in tumor angiogenesis. However, clinical trials targeting the VEGF pathway are often ineffective, suggesting that other factors/pathways are also important in tumor angiogenesi…
View article: Data from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth <i>In vivo</i>
Data from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth <i>In vivo</i> Open
The vascular endothelial growth factor (VEGF) plays a key role in tumor angiogenesis. However, clinical trials targeting the VEGF pathway are often ineffective, suggesting that other factors/pathways are also important in tumor angiogenesi…
View article: Supplementary Methods and Materials from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth <i>In vivo</i>
Supplementary Methods and Materials from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth <i>In vivo</i> Open
Supplementary Methods and Materials from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth In vivo
View article: Supplementary Methods and Materials from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth <i>In vivo</i>
Supplementary Methods and Materials from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth <i>In vivo</i> Open
Supplementary Methods and Materials from Delta-like 4 Notch Ligand Regulates Tumor Angiogenesis, Improves Tumor Vascular Function, and Promotes Tumor Growth In vivo
View article: Cutting Edge: mTORC2 Regulates CD8+ Effector and Memory T Cell Differentiation through Serum and Glucocorticoid Kinase 1
Cutting Edge: mTORC2 Regulates CD8+ Effector and Memory T Cell Differentiation through Serum and Glucocorticoid Kinase 1 Open
The mechanistic target of rapamycin is an essential regulator of T cell metabolism and differentiation. In this study, we demonstrate that serum- and glucocorticoid-regulated kinase 1 (SGK1), a downstream node of mechanistic target of rapa…
View article: The menin-MLL1 interaction is a molecular dependency in <i>NUP98</i>-rearranged AML
The menin-MLL1 interaction is a molecular dependency in <i>NUP98</i>-rearranged AML Open
Translocations involving the NUP98 gene produce NUP98-fusion proteins and are associated with a poor prognosis in acute myeloid leukemia (AML). MLL1 is a molecular dependency in NUP98-fusion leukemia, and therefore we investigated the effi…
View article: Large DNA Methylation Nadirs Anchor Chromatin Loops Maintaining Hematopoietic Stem Cell Identity
Large DNA Methylation Nadirs Anchor Chromatin Loops Maintaining Hematopoietic Stem Cell Identity Open
View article: 50 Years Ago in T J P
50 Years Ago in T J P Open
View article: Masthead
Masthead Open
View article: A Cell type-specific Class of Chromatin Loops Anchored at Large DNA Methylation Nadirs
A Cell type-specific Class of Chromatin Loops Anchored at Large DNA Methylation Nadirs Open
Higher order chromatin structure and DNA methylation are implicated in multiple developmental processes, but their relationship to cell state is unknown. Here, we found that large (~10kb) DNA methylation nadirs can form long loops connecti…
View article: Masthead
Masthead Open
View article: Masthead
Masthead Open
View article: Masthead
Masthead Open
View article: Masthead
Masthead Open