Allison Mayle
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View article: Table S2 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
Table S2 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Sequence of oligos and plasmids used as well as FACS antibody details
View article: Table S2 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
Table S2 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Sequence of oligos and plasmids used as well as FACS antibody details
View article: Data from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
Data from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Mutations in the TP53 tumor suppressor gene are common in many cancer types, including the acute myeloid leukemia (AML) subtype known as complex karyotype AML (CK-AML). Here, we identify a gain-of-function (GOF) Trp53 mutatio…
View article: Data from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
Data from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Mutations in the TP53 tumor suppressor gene are common in many cancer types, including the acute myeloid leukemia (AML) subtype known as complex karyotype AML (CK-AML). Here, we identify a gain-of-function (GOF) Trp53 mutatio…
View article: Supplementary Figures S1-S8 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
Supplementary Figures S1-S8 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Supplementary Figures S1-S8, with legends
View article: Table S1 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
Table S1 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Supplementary Table 1
View article: Supplementary Figures S1-S8 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
Supplementary Figures S1-S8 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Supplementary Figures S1-S8, with legends
View article: Table S1 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
Table S1 from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Supplementary Table 1
View article: The microbes found in the honey of New York City beehives
The microbes found in the honey of New York City beehives Open
Bees are incredibly important to the Earth’s ecosystem and provide humans with a variety of fruits and vegetables; however, due to Colony Collapse Disorder, hives are dying at an alarming rate. Colony Collapse Disorder is caused by a numbe…
View article: Vitamin B6 Addiction in Acute Myeloid Leukemia
Vitamin B6 Addiction in Acute Myeloid Leukemia Open
View article: Preclinical murine platform to evaluate therapeutic countermeasures against radiation-induced gastrointestinal syndrome
Preclinical murine platform to evaluate therapeutic countermeasures against radiation-induced gastrointestinal syndrome Open
Significance Currently, there are no therapies available to mitigate intestinal damage after radiation injury. Efforts to study and design new therapies are hampered by a lack of models that can be readily adopted to study therapeutic targ…
View article: A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1
A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Open
Mutations in the TP53 tumor suppressor gene are common in many cancer types, including the acute myeloid leukemia (AML) subtype known as complex karyotype AML (CK-AML). Here, we identify a gain-of-function (GOF) Trp53 mutation that acceler…
View article: p53 Represses the Mevalonate Pathway to Mediate Tumor Suppression
p53 Represses the Mevalonate Pathway to Mediate Tumor Suppression Open
View article: Highly Efficient Genome Editing of Murine and Human Hematopoietic Progenitor Cells by CRISPR/Cas9
Highly Efficient Genome Editing of Murine and Human Hematopoietic Progenitor Cells by CRISPR/Cas9 Open
Our understanding of the mechanisms that regulate hematopoietic stem/progenitor cells (HSPCs) has been advanced by the ability to genetically manipulate mice; however, germline modification is time consuming and expensive. Here, we describ…
View article: DNMT3A Loss Drives Enhancer Hypomethylation in FLT3-ITD-Associated Leukemias
DNMT3A Loss Drives Enhancer Hypomethylation in FLT3-ITD-Associated Leukemias Open
View article: DNMT3A Loss Drives Enhancer Hypomethylation in FLT3-ITD-Associated Leukemias
DNMT3A Loss Drives Enhancer Hypomethylation in FLT3-ITD-Associated Leukemias Open