A5003104699- Cancer-related gene regulation
- Kruppel-like factors research
- Cancer-related Molecular Pathways
- Bacteriophages and microbial interactions
- RNA and protein synthesis mechanisms
- Genetic Syndromes and Imprinting
- Ubiquitin and proteasome pathways
- Bacterial Genetics and Biotechnology
- Antimicrobial Resistance in Staphylococcus
- Epigenetics and DNA Methylation
- Cancer, Hypoxia, and Metabolism
- Genomics and Phylogenetic Studies
- Child Nutrition and Feeding Issues
- CRISPR and Genetic Engineering
- Bioenergy crop production and management
- Advanced Electron Microscopy Techniques and Applications
- Molecular Biology Techniques and Applications
- Muscle metabolism and nutrition
- DNA Repair Mechanisms
- Microbial Metabolism and Applications
- Integrated Circuits and Semiconductor Failure Analysis
- Metabolism and Genetic Disorders
- Galectins and Cancer Biology
- Pancreatic and Hepatic Oncology Research
- Fibroblast Growth Factor Research
Virginia Commonwealth University
2012-2024
Virginia Cancer Institute
2019
VCU Massey Comprehensive Cancer Center
2019
University of Massachusetts Chan Medical School
2019
Staphylococcal pathogenicity islands (SaPIs) carry superantigen and resistance genes are extremely widespread in Staphylococcus aureus other Gram-positive bacteria. SaPIs represent a major source of intrageneric horizontal gene transfer stealth conduit for intergeneric transfer; they phage satellites that exploit the life cycle their temperate helper phages with elegant precision to enable rapid replication promiscuous spread. also interfere reproduction, blocking plaque formation, sharply...
Abstract C-terminal binding protein 2 (CtBP2) is elevated in epithelial ovarian cancer, especially the aggressive and highly lethal subtype, high-grade serous cancer (HGSOC). However, whether HGSOC tumor progression dependent on CtBP2 or its paralog CtBP1, not well understood. Here we report that CtBP1/2 repress cell apoptosis through silencing of death receptors (DRs) 4/5. CtBP1 knockdown upregulated DR4/5 expression, triggered autonomous via caspase 8 activation, but cell-type context....
Many mutant p53 proteins exhibit an abnormally long half-life and overall increased abundance compared with wild-type in tumors, contributing to p53's gain-of-function oncogenic properties. Here, a novel mechanism is revealed for the maintenance of cancer that dependent on DNA damage checkpoint activation. High-level expression lung cells was associated preferential monoubiquitination versus polyubiquitination, suggesting role ubiquitin/proteasome system regulation cells. Interestingly,...
The control of p53 protein stability is critical to its tumor suppressor functions. CREB binding (CBP) transcriptional co-activator co-operates with MDM2 maintain normally low physiological levels in cells via exclusively cytoplasmic E4 polyubiquitination activity. Using mass spectrometry identify nuclear and CBP-interacting proteins that regulate compartmentalized CBP activity, we identified deleted breast cancer 1 (DBC1) as a stoichiometric negatively regulates CBP-dependent...
C-terminal binding proteins (CtBP1/2) are oncogenic transcriptional coregulators and dehydrogenases often overexpressed in multiple solid tumors, including breast, colon, ovarian cancer, associated with poor survival. CtBPs act by repressing expression of genes responsible for apoptosis (e.g., PUMA, BIK) metastasis-associated epithelial–mesenchymal transition CDH1), activating that promote migratory invasive properties cancer cells TIAM1) enhanced drug resistance MDR1). CtBP's functions also...
Acid maltase deficiency in adults is associated with progressive muscle weakness and may effect respiratory muscles resulting failure. The biochemical clinical manifestations of acid arise from a marked the lysosomal enzyme alpha‐glucosidase (acid maltase), which normally degrades glycogen to free glucose. In past few years, high‐protein diets have provided an alternative energy source for these patients resulted improved strength. Recently, we treated ventilator‐dependent maltase‐deficient...
C-terminal binding protein 2 (CtBP2) drives intestinal polyposis in the Apcmin mouse model of human Familial Adenomatous Polyposis. As CtBP2 is targetable by an inhibitor its dehydrogenase domain, understanding CtBP2's role adenoma formation necessary to optimize CtBP-targeted therapies Apc mutated neoplasia. Tumor initiating cell (TIC) populations were substantially decreased ApcminCtbp2+/- epithelia. Moreover, normally nuclear Ctbp2 was mislocalized cytoplasm crypt stem cells Ctbp2+/-...
Abstract There is a critical need to identify new therapeutic vulnerabilities in pancreatic ductal adenocarcinoma (PDAC). Transcriptional co-regulators C-terminal binding proteins (CtBP) 1 and 2 are highly overexpressed human PDAC, CRISPR-based homozygous deletion of Ctbp2 mouse PDAC cell line (CKP) dramatically decreased tumor growth, reduced metastasis, prolonged survival orthotopic allografts. Transcriptomic profiling tumors derived from CKP vs. -deleted cells (CKP/KO) revealed...
Extended abstract of a paper presented at Microscopy and Microanalysis 2011 in Nashville, Tennessee, USA, August 7–August 11, 2011.
Abstract Introduction: Cancer cell dormancy and the cancer stem (CSC) phenotype are interlinked play a crucial role in disease relapse. The pp38/pERK signaling ratio positively regulates cellular dormancy. We observed that heparin hexasaccharide (HS06) inhibited colon CSC self-renewal through isoform specific induction of pp38α/β, increasing ratio, downregulation C-terminal binding protein-2 (CtBP2) levels which is known to critical growth. Hence, we hypothesized HS06 inhibits CSCs prevents...
Abstract C-terminal binding proteins (CtBP) 1 and 2 are transcriptional coregulators that upregulated in several cancers, including a majority of studied breast, colorectal, ovarian tumor samples. CtBPs drive many cellular oncogenic properties, migration, invasion, proliferation, survival, part through repression suppressor genes, such as E-cadherin, PTEN, BRCA1, p16. encode an intrinsic dehydrogenase activity regulated by both intracellular NADH concentration the putative substrate...
<p>Supplementary figures (1-12) Supplemental Fig. 1. Normalized levels of monoubiquitinated mutant p53 are shown for indicated cell lines analyzed in 1a. 2. Longer single exposure blot 2a is displayed to demonstrate the relative abundance native species. Fig 3. (a) WI38 cells were transfected with p53-273H and MDM2 40- 48 hours later, plates treated 2 μM Dox presence or absence mM caffeine. Caffeine-treated samples pre-treated caffeine 20 min prior addition Dox. 4. from...
<p>Supplementary figure legends</p>
<div>Abstract<p>Many mutant p53 proteins exhibit an abnormally long half-life and overall increased abundance compared with wild-type in tumors, contributing to p53's gain-of-function oncogenic properties. Here, a novel mechanism is revealed for the maintenance of cancer that dependent on DNA damage checkpoint activation. High-level expression lung cells was associated preferential monoubiquitination versus polyubiquitination, suggesting role ubiquitin/proteasome system...
<p>Supplementary figures (1-12) Supplemental Fig. 1. Normalized levels of monoubiquitinated mutant p53 are shown for indicated cell lines analyzed in 1a. 2. Longer single exposure blot 2a is displayed to demonstrate the relative abundance native species. Fig 3. (a) WI38 cells were transfected with p53-273H and MDM2 40- 48 hours later, plates treated 2 μM Dox presence or absence mM caffeine. Caffeine-treated samples pre-treated caffeine 20 min prior addition Dox. 4. from...
<p>Supplementary figure legends</p>