A5085851557- Cancer Genomics and Diagnostics
- Advanced Breast Cancer Therapies
- Protein Degradation and Inhibitors
- Acute Myeloid Leukemia Research
- Epigenetics and DNA Methylation
- Genomics and Chromatin Dynamics
- RNA modifications and cancer
- Histone Deacetylase Inhibitors Research
- CRISPR and Genetic Engineering
- Plant Virus Research Studies
- PI3K/AKT/mTOR signaling in cancer
- RNA Research and Splicing
- Plant Pathogenic Bacteria Studies
- Chromosomal and Genetic Variations
- Protein Kinase Regulation and GTPase Signaling
- Ion Transport and Channel Regulation
- Fungal and yeast genetics research
- ATP Synthase and ATPases Research
- Cancer-related Molecular Pathways
- Cancer-related gene regulation
- Nitric Oxide and Endothelin Effects
- RNA and protein synthesis mechanisms
- Plant and Fungal Interactions Research
- Biochemical and Molecular Research
- Metalloenzymes and iron-sulfur proteins
Emory University
2020-2025
Cancer Institute (WIA)
2025
Emory and Henry College
2023
National Clonal Germplasm Repository for Citrus
2010-2011
University of Oregon
1993
McMaster University
1984
Abstract Sequencing of human patient tumors has identified recurrent missense mutations in genes encoding core histones. We report that convert histone H3 amino acid 50 from a glutamate to lysine (H3E50K) support an oncogenic phenotype. Expression H3E50K is sufficient transform cells as evidenced by increase cell migration and invasion, proliferation clonogenicity. also increases the invasive phenotype context co-occurring BRAF mutations, which are present characterized H3E50K. H3E50 lies on...
Dynamic protein post-translational methylation is essential for cellular function, highlighted by the role of in transcriptional regulation and its aberrant dysregulation diseases, including cancer. This underscores importance cataloging methylproteome. However, comprehensive analysis methylproteome remains elusive due to limitations current enrichment pipelines. Here, we employ an l-methionine analogue, ProSeMet, that chemoenzymatically converted SAM analogue ProSeAM cells vivo tag proteins...
The high frequency of aberrant PI3K pathway activation in hormone receptor-positive (HR
Breast cancer pathogenesis, treatment, and patient outcomes are shaped by tumor-intrinsic genomic alterations that divide breast tumors into molecular subtypes. These subtypes often dictate viable therapeutic interventions, ultimately, outcomes. However, heterogeneity of response may be a result underlying epigenetic features further stratify In this review we examine non-genetic mechanisms drive functional changes to chromatin in contribute cell tumor fitness, highlight how activity inform...
Mutation of the alpha subunit Escherichia coli F1-ATPase to convert Arg-376 a Cys (alpha R376C) lowers multisite ATPase activity 400-1,000-fold while affecting unisite catalysis only around 6-fold, suggesting that mutation is in region important for transmission conformational changes between catalytic sites (Soga, S., Noumi, T., Takeyama, M., Maeda, and Futai, M. (1989) Arch. Biochem. Biophys. 268, 643-648; this study). To learn more structural features segment Arg-376, mutant enzyme with...
The nucleotide sequence of Dweet mottle virus (DMV) was determined and compared to sequences members the families Alphaflexiviridae Betaflexiviridae. DMV genome has 8,747 nucleotides (nt) excluding 3' poly-(A) tail. genomic RNA contains three putative open reading frames (ORFs) untranslated regions 73 nt at 5' 541 termini. ORF1 potentially encoding a 227.48-kDa polyprotein, which methyltransferase, oxygenase, endopeptidase, helicase, RNA-dependent polymerase (RdRP) domains. ORF2 encodes...
Abstract Somatic missense mutations in histone genes turn these essential proteins into oncohistones, which can drive oncogenesis. Understanding how alter function is challenging mammals as occur a single gene. For example, described oncohistone predominantly the H3.3 gene, despite human genome encoding 15 H3 genes. To understand oncogenic function, we leveraged budding yeast model, contains only 2 genes, to explore functional consequences of oncohistones H3K36M, H3G34W, H3G34L, H3G34R, and...
RNA exosomopathies, a growing family of diseases, are linked to missense mutations in genes encoding structural subunits the evolutionarily conserved, 10-subunit exoribonuclease complex, exosome. This complex consists three-subunit cap, six-subunit, barrel-shaped core, and catalytic base subunit. While number exosome cause pontocerebellar hypoplasia, cap subunit gene EXOSC2 an apparently distinct clinical presentation that has been defined as novel syndrome SHRF ( s hort stature, h earing...
<div><p>The high frequency of aberrant PI3K pathway activation in hormone receptor–positive (HR<sup>+</sup>) breast cancer has led to the development, clinical testing, and approval p110α-selective inhibitor alpelisib. The limited efficacy alpelisib other inhibitors is partially attributed functional antagonism between estrogen receptor (ER) signaling, which mitigated via combined inhibition endocrine therapy. We others have previously demonstrated...
<div><p>The high frequency of aberrant PI3K pathway activation in hormone receptor–positive (HR<sup>+</sup>) breast cancer has led to the development, clinical testing, and approval p110α-selective inhibitor alpelisib. The limited efficacy alpelisib other inhibitors is partially attributed functional antagonism between estrogen receptor (ER) signaling, which mitigated via combined inhibition endocrine therapy. We others have previously demonstrated...
<p>Figure S1 shows combined effects of PI3K and MLL1 inhibition in clonogenic assays</p>
<p>Figure S4 shows combined PI3K and MLL1 inhibition reduces cell viability enhances apoptosis</p>
<p>Figure S2 shows on-target activity of PI3K and MLL1 inhibitors</p>
<p>Figure S3 shows additional transcriptional and genomics analyses that support MLL1 inhibitor-driven hyperactivation of AKT</p>
<p>Figure S5 shows that combined PI3K and MLL inhibition provides therapeutic benefit in vitro vivo</p>
<p>Figure S4 shows combined PI3K and MLL1 inhibition reduces cell viability enhances apoptosis</p>
<p>Figure S2 shows on-target activity of PI3K and MLL1 inhibitors</p>
<p>Figure S3 shows additional transcriptional and genomics analyses that support MLL1 inhibitor-driven hyperactivation of AKT</p>
<p>Figure S5 shows that combined PI3K and MLL inhibition provides therapeutic benefit in vitro vivo</p>
<p>Figure S1 shows combined effects of PI3K and MLL1 inhibition in clonogenic assays</p>