A5059120798- Cell death mechanisms and regulation
- Autophagy in Disease and Therapy
- Cancer, Hypoxia, and Metabolism
- CAR-T cell therapy research
- Immune Cell Function and Interaction
- Adenosine and Purinergic Signaling
- Virus-based gene therapy research
- Cancer-related Molecular Pathways
- T-cell and B-cell Immunology
- Eicosanoids and Hypertension Pharmacology
- Metabolism, Diabetes, and Cancer
- Phagocytosis and Immune Regulation
- Mitochondrial Function and Pathology
- Histone Deacetylase Inhibitors Research
- Cancer Research and Treatments
- Sphingolipid Metabolism and Signaling
- Cardiac Ischemia and Reperfusion
- Photosynthetic Processes and Mechanisms
- Lipid Membrane Structure and Behavior
- Pharmacogenetics and Drug Metabolism
- RNA Interference and Gene Delivery
- Ubiquitin and proteasome pathways
- PI3K/AKT/mTOR signaling in cancer
- Hematopoietic Stem Cell Transplantation
- Endoplasmic Reticulum Stress and Disease
University of Minnesota
2010-2023
University of Minnesota Medical Center
2008-2022
Masonic Cancer Center
2003-2021
University of Minnesota System
2002-2015
Minneapolis Institute of Arts
2015
Twin Cities Orthopedics
2007
University of Chicago
1997-2001
Howard Hughes Medical Institute
1997-2001
Duke University
1987-1994
Duke University Hospital
1990-1994
AbstractThe Bcl-2 related protein Bad is a promoter of apoptosis and has been shown to dimerize with the anti-apoptotic proteins Bcl-XL. Overexpression in murine FL5.12 cells demonstrated that not only could abrogate protective capacity coexpressed Bcl-XL but accelerate apoptotic response death signal when it was expressed absence exogenous Using deletion analysis, we have identified minimal domain can A 26-amino-acid peptide within this domain, which showed significant homology...
Glucose uptake and utilization are growth factor-stimulated processes that frequently upregulated in cancer cells correlate with enhanced cell survival. The mechanism of metabolic protection from apoptosis, however, has been unclear. Here we identify a novel signaling pathway initiated by glucose catabolism inhibited apoptotic death factor-deprived cells. We show increased metabolism protected against the proapoptotic Bcl-2 family protein Bim attenuated degradation antiapoptotic Mcl-1....
Suppressive regulatory T cell (Treg) differentiation is controlled by diverse immunometabolic signaling pathways and intracellular metabolites. Here we show that cell-permeable α-ketoglutarate (αKG) alters the DNA methylation profile of naive CD4 cells activated under Treg polarizing conditions, markedly attenuating FoxP3+ increasing inflammatory cytokines. Adoptive transfer these into tumor-bearing mice results in enhanced tumor infiltration, decreased FoxP3 expression, delayed growth....
Abstract Granulysin is an antimicrobial and tumoricidal molecule expressed in granules of CTL NK cells. In this study, we show that granulysin damages cell membranes based upon negative charge, disrupts the transmembrane potential (Δψ) mitochondria, causes release cytochrome c. Granulysin-induced apoptosis blocked cells overexpressing Bcl-2. Despite c, procaspase 9 not processed. Nevertheless, activation caspase 3 observed granulysin-treated cells, suggesting activates a novel pathway CTL-...
Recent studies have implicated multipotential mesenchymal stem cells (MSCs) as an aid to breast cancer cell proliferation and metastasis, partly a result of the MSCs secretome. As tumor gets beyond 2 mm in diameter, stromal could undergo starvation due lack sufficient nutrients solid microenvironment. In this study, we investigated survival mechanisms used by stressed cancers. We serum-deprived (SD-MSCs) MCF-7 model system with hypothesis that nutrient-deprived core utilize for supporting...
Endostatin is a well-characterized endogenous inhibitor of angiogenesis that affects cell proliferation and migration by inhibiting integrin Wnt-mediated signalling pathways. Here, we show endothelial cells treated with native P125A-endostatin activate autophagy. Because autophagy can either be protective or induce programmed death, experiments were carried out to understand the pathways leading in cells. treatment increased levels Beclin 1, crucial molecule vesicle nucleation The also...
AbstractAngiogenesis, the process by which new blood vessels are formed is critical for embryonic development and physiological functioning of normal tissues. Angiogenesis also plays a role in pathology many diseases including cancer, wherein supply demand determines rate cancer growth. A number therapeutic strategies being developed to inhibit pathological angiogenesis. Kringle domains plasminogen such as kringle 5 (K5) proteolytic fragment collagen type XVIII (endostatin)...
Cellular and viral oncogenes have been linked to the transformation of established cell lines in vitro, induction tumors vivo, partial or immortalization primary cells. Based on ability cooperate with mutated ras cells, adenovirus E1a cellular p53 genes assigned an immortalizing activity. It is demonstrated this paper that type 5 gene simian virus 40 promoter-linked cDNA are able transform previously immortalized cells a tumorigenic phenotype without significant change morphology. also shown...
Early-passage rat kidney cells were immortalized or rescued from senescence with three different oncogenes: viral promoter-driven c-myc, H-ras (Val-12), and adenovirus type 5 E1a. The normal c-myc (Gly-12) unable to immortalize under similar conditions. Quantitation of RNA in the ras-immortalized lines demonstrated that oncogene was expressed at a level equivalent gene established human cell lines. Cell by oncogenes found have distinct growth responses individual factors short-term assay....
Regulatory T cells (Tregs) are critical for maintaining immune homeostasis. However, current Treg immunotherapies do not optimally treat inflammatory diseases in patients. Understanding the cellular processes that control function may allow augmentation of therapeutic efficacy. In contrast to activated conventional cells, which protein kinase C-θ (PKC-θ) localizes contact point between and antigen-presenting human mouse Tregs, PKC-θ opposite end cell distal pole complex (DPC). Here, using a...