A5044659510- Acute Myeloid Leukemia Research
- Protein Degradation and Inhibitors
- Genomics and Chromatin Dynamics
- Hemoglobinopathies and Related Disorders
- Epigenetics and DNA Methylation
- Prenatal Screening and Diagnostics
- Ubiquitin and proteasome pathways
- Chronic Myeloid Leukemia Treatments
- RNA modifications and cancer
- Cancer-related Molecular Pathways
- CRISPR and Genetic Engineering
- Histone Deacetylase Inhibitors Research
- Cancer Genomics and Diagnostics
- Folate and B Vitamins Research
- Single-cell and spatial transcriptomics
- Blood groups and transfusion
- FOXO transcription factor regulation
- Parvovirus B19 Infection Studies
- Cancer-related molecular mechanisms research
- Developmental Biology and Gene Regulation
- RNA Research and Splicing
Van Andel Institute
2019-2023
Michigan State University
2018-2020
Mutations in the adult β-globin gene can lead to a variety of hemoglobinopathies, including sickle cell disease and β-thalassemia. An increase fetal hemoglobin expression throughout adulthood, condition named hereditary persistence (HPFH), has been found ameliorate hemoglobinopathies. Deletional HPFH occurs through excision significant portion 3′ end locus, CTCF binding site termed 3′HS1. Here, we show that deletion this alone induces both CD34+ hematopoietic stem progenitor cells HUDEP-2...
Abstract We present Single-cell TOtal RNA Miniaturized sequencing (STORM-seq), a full-length single-cell ribo-reduced protocol, optimized to profile thousands of cells per run. Using off-the-shelf reagents and random hexamer priming, STORM-seq recovers comprehensive profiles from single with library complexity approaching that bulk RNA-seq. Importantly, does not require specialized equipment can be performed using standard lab equipment. identifies additional coding non-coding transcripts...
Retinoblastoma proteins are eukaryotic transcriptional corepressors that play central roles in cell cycle control, among other functions. Although most metazoan genomes encode a single retinoblastoma protein, gene duplications have occurred at least twice: the vertebrate lineage, leading to Rb, p107, and p130, Drosophila, an ancestral Rbf1 derived Rbf2 gene. Structurally, resembles p107 mutation of is lethal. more divergent does not lead lethality. However, retention >60 My Drosophila points...
Abstract Proper gene regulation is crucial for cellular differentiation, and dysregulation of key genes can lead to diseased states such as cancer. The HOX transcription factors play a role during hematopoiesis, aberrant expression certain HOXA found in acute myeloid leukemias (AMLs). While studies have shown that these are targeted by variety mutant proteins including NPM1, MLL fusions, NUP98 little known about how long-range 3D chromatin interactions regulate the normal hematopoiesis...
Abstract Retinoblastoma proteins are eukaryotic transcriptional co-repressors that play central roles in cell cycle control, among other functions. Although most metazoan genomes encode a single retinoblastoma protein, gene duplications have occurred at least twice: the vertebrate lineage, leading to three genes encoding Rb, p107, and p130, while separately Drosophila lineage an ancestral Rbf1 derived Rbf2 gene. Structurally, resembles p107 p130 closely, mutation of is lethal, more...
<div>Abstract<p>Nucleophosmin (NPM1) is a ubiquitously expressed nucleolar protein with wide range of biological functions. In 30% acute myeloid leukemia (AML), the terminal exon <i>NPM1</i> often found mutated, resulting in addition nuclear export signal and shift to cytoplasm (NPM1c). AMLs carrying this mutation have aberrant expression <i>HOXA/B</i> genes, whose overexpression leads leukemogenic transformation. Here, for first time, we comprehensively...
<div>Abstract<p>Nucleophosmin (NPM1) is a ubiquitously expressed nucleolar protein with wide range of biological functions. In 30% acute myeloid leukemia (AML), the terminal exon <i>NPM1</i> often found mutated, resulting in addition nuclear export signal and shift to cytoplasm (NPM1c). AMLs carrying this mutation have aberrant expression <i>HOXA/B</i> genes, whose overexpression leads leukemogenic transformation. Here, for first time, we comprehensively...
<p>Supplementary Figure S1 is associated with Figure1 and it shows the NPM1-WT binds to rDNA arrays NPM1c non-repetitive genomic regions. Supplementary S2 NPM1c’s chromatin binding association gene expression. S3 Figure2 regulates transcription of its target genes BRU-seq. S4 characterization condensate biochemical assay imaging assay. S5 figure 3. The landacpe dymanics during dTag-13 treatment wash-off. S6 4. It supplemental data HOXB8-NPM1c-knock-in model. S7 5. XPO1's in various...
<p>Supplementary Figure S1 is associated with Figure1 and it shows the NPM1-WT binds to rDNA arrays NPM1c non-repetitive genomic regions. Supplementary S2 NPM1c’s chromatin binding association gene expression. S3 Figure2 regulates transcription of its target genes BRU-seq. S4 characterization condensate biochemical assay imaging assay. S5 figure 3. The landacpe dymanics during dTag-13 treatment wash-off. S6 4. It supplemental data HOXB8-NPM1c-knock-in model. S7 5. XPO1's in various...
Abstract Nucleophosmin (NPM1) is a ubiquitously expressed nucleolar protein with wide range of functions including ribosome biogenesis, mRNA processing, and maintenance genomic stability. In acute myeloid leukemia (AML), the terminal exon NPM1 often mutated (~30% adult AMLs), resulting in change localization signal into nuclear export shift to cytoplasm (NPM1c). AMLs carrying this mutation have aberrant expression HOXA genes, whose overexpression leads leukemogenic transformation. Recently,...