A5083970118- Peptidase Inhibition and Analysis
- Neuropeptides and Animal Physiology
- Immune Cell Function and Interaction
- Adipose Tissue and Metabolism
- Digestive system and related health
- Birth, Development, and Health
- PARP inhibition in cancer therapy
- Cell Adhesion Molecules Research
- T-cell and B-cell Immunology
- Immunotherapy and Immune Responses
- Helicobacter pylori-related gastroenterology studies
- Wound Healing and Treatments
- Genomics, phytochemicals, and oxidative stress
- Cellular Mechanics and Interactions
- Antimicrobial Peptides and Activities
- IL-33, ST2, and ILC Pathways
- Gestational Diabetes Research and Management
- Diet and metabolism studies
- Cancer Immunotherapy and Biomarkers
- Chemokine receptors and signaling
- Ovarian cancer diagnosis and treatment
- Protease and Inhibitor Mechanisms
- Epigenetics and DNA Methylation
- Wnt/β-catenin signaling in development and cancer
- Asthma and respiratory diseases
University of North Dakota
2015-2024
Trudeau Institute
2014-2021
Grand Forks Human Nutrition Research Center
2012-2016
United States Department of Agriculture
2015
Agricultural Research Service
2011-2015
University of Minnesota
2015
North Dakota State University
2008-2011
Dakota State University
2010
Lyme disease, which is caused by infection with Borrelia burgdorferi and related species, can lead to inflammatory pathologies affecting the joints, heart, nervous systems including central system (CNS). Inbred laboratory mice have been used define kinetics of B . host immune responses in joints however similar studies are lacking CNS these animals. A tractable animal model for investigating host- interactions key understanding mechanisms pathogenesis. Therefore, we characterized...
Significance Invariant natural killer T (iNKT) cells can facilitate B-cell responses by enhancing helper signals from protein-specific or independently induce a developmental program; however, key differences in humoral memory after iNKT-cell help remain unclear. We determined that, unlike T-cell help, cognate expands large number of IL-10–producing B10 regulatory cells. These findings have broad implications for the types B that may be generated when synthetic iNKT glycolipid ligands are...
GI mucosal healing requires epithelial sheet migration. The non-receptor tyrosine kinase focal adhesion (FAK) stimulates motility. A virtual screen identified the small drug-like FAK mimic ZINC40099027, which activates FAK. We assessed whether ZINC40099027 promotes FAK-Tyr-397 phosphorylation and wound in Caco-2 monolayers two mouse intestinal injury models. Murine bowel ulcers were generated by topical serosal acetic acid or subcutaneous indomethacin C57BL/6J mice. One day later, we began...
Human enterocytic differentiation is altered during development, fasting, adaptation, and bariatric surgery, but its intracellular control remains unclear. We hypothesized that Schlafen 12 (SLFN12) regulates enterocyte differentiation.
Abstract Focal adhesion kinase (FAK) regulates gastrointestinal epithelial restitution and healing. ZINC40099027 (Zn27) activates cellular FAK promotes intestinal wound closure in vitro mice. However, whether Zn27 directly or indirectly remains unknown. We evaluated potential modulation of the key phosphatases, PTP‐PEST, PTP1B, SHP2, that inactivate FAK, performed assays with purified to assess direct Zn27‐FAK interaction. In human Caco‐2 cells, Zn27‐stimulated FAK‐Tyr‐397 phosphorylation...
Schlafen 12 (SLFN12) expression correlates with survival in triple negative breast cancer (TNBC). SLFN12 slows TNBC proliferation and induces differentiation, but whether affects the tumoral response to chemotherapy or radiation is unknown.We over-expressed MDA-MB-231 cells using two different lentiviral vectors. We assessed viable cell numbers via crystal violet assay after treatment carboplatin, paclitaxel, olaparib, zoledronic acid, camptothecin, cesium irradiation. CHK1 CHK2...
Self-renewal and differentiation are essential for intestinal epithelium absorptive functioning adaptation to pathological states such as short gut syndrome, ulcers, inflammatory bowel disease. The rodent Slfn3 its human analog Slfn12 critical in regulating epithelial differentiation. We sought characterize function knockout (KO) mice. Male female pair-fed Slfn3KO mice gained less weight with decreased food efficiency than wild type (WT) mice, more pronounced effects females. RNA sequencing...
Schlafen12 (SLFN12) promotes human intestinal and prostatic epithelial differentiation. We sought to determine whether SLFN12 reduces triple-negative breast cancer (TNBC) aggressiveness.We validated bioinformatics analyses of publicly available databases by staining TNBC. After virally overexpressing or siRNA-reducing in TNBC cell lines, we measured proliferation CCK-8 assay, invasion into basement-membrane-coated pores, mRNA q-RT-PCR protein Western blotting. Flow cytometry assessed stem...
Schlafen 12 (SLFN12) is an intermediate human that induces differentiation in enterocytes, prostate, and breast cancer. We hypothesized SLFN12 influences lung cancer biology. investigated survival differences high versus low SLFN12-expressing tumors two databases. then adenovirally overexpressed (AdSLFN12) HCC827, H23, H1975 cells to model adenocarcinoma (LUAD), H2170 HTB-182 representing squamous cell carcinoma (LUSC). analyzed proliferation using a colorimetric assay, mRNA expression by...
Abstract CD4+ T cells enable the critical B cell humoral immune protection afforded by most effective vaccines. We and others have recently identified an alternative source of help for in mice, invariant NK (iNKT) cells. iNKT are innate glycolipid-specific restricted to nonpolymorphic Ag-presenting molecule CD1d. As such, respond glycolipids equally well all people, making them appealing adjuvant universal tested potential glycolipid agonist, α-galactosylceramide (αGC), serve as a known...
Triple-negative breast cancer (TNBC) has a poor prognosis and no targeted therapy for treatment. The Schlafen gene family, particularly SLFN12, critically mediates TNBC biology. Higher expression of SLFN12 correlates with decreased viability increased chemosensitivity patient survival, yet treatment is known to upregulate in TNBC. We hypothesized that Interferon-α (IFN-α2) upregulates TNBC, subsequently reducing cell viability. utilized short hairpin adenovirus knockout (AdvShSLFN12)...