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Primary Phone: (520) 6269126
Life Sciences North 545
College of Medicine
University of Arizona
1501 N. Campbell Ave
Tucson AZ 85724
Primary Phone: (520) 6269126
Ph.D., Cell Biology, Clarkson University, 1991
- College Of Medicine
Molecular Mechanisms of Oxidative Injury and Adaptation
Protein Translation under Oxidative Stress
Environmental Health Research & Expertise:
Dr. Chen has served as the Director of NIEHS Training Program from 2002-2014. Dr. Chen’s research focuses on 1) mechanisms of protein translation under oxidative stress, 2) cytoprotective effect of corticosteroids, and 3) proteomic methods for biomarkers of oxidative injury. Her research programs have been founded through Burroughs Wellcome Foundation, Society of Toxicology Colgate Palmolive Award for Alternative Research, Arizona Biomedical Research Commission, and R01 or R21 grants from the National Institute of Environmental Health Sciences, National Institute of Heart, Lung and Blood, and National Institute of General Medical Sciences,.
- Myocardial ischemic reperfusion induces de novo Nrf2 protein translation.
- Glucocorticoid induced leucine zipper inhibits apoptosis of cardiomyocytes by doxorubicin.
- Modern Medicine and the Garden of Eden.
- Far upstream element binding protein 1: a commander of transcription, translation and beyond.
- So, you want to live to 120? The genie in the bottle.
- Histone deacetylase 6 associates with ribosomes and regulates de novo protein translation during arsenite stress.
- Has the genomic revolution failed?
- La autoantigen mediates oxidant induced de novo Nrf2 protein translation.
- p21(WAF1/Cip1/Sdi1) knockout mice respond to doxorubicin with reduced cardiotoxicity.
- Dexamethasone induces transcriptional activation of Bcl-xL gene and inhibits cardiac injury by myocardial ischemia.
- Methylation of FEN1 suppresses nearby phosphorylation and facilitates PCNA binding.
- Cystatin C increases in cardiac injury: a role in extracellular matrix protein modulation.
- Partial proteasome inhibition in human fibroblasts triggers accelerated M1 senescence or M2 crisis depending on p53 and Rb status.
- Genomic and proteomic profiling of oxidative stress response in human diploid fibroblasts.
- Corticosteroids induce COX-2 expression in cardiomyocytes: role of glucocorticoid receptor and C/EBP-beta.
- P38 MAPK mediates COX-2 gene expression by corticosterone in cardiomyocytes.
- Corticosteroids induce cyclooxygenase 1 expression in cardiomyocytes: role of glucocorticoid receptor and Sp3 transcription factor.
- Inhibitors of GSK-3 prevent corticosterone from inducing COX-1 expression in cardiomyocytes.
- LY294002 inhibits glucocorticoid-induced COX-2 gene expression in cardiomyocytes through a phosphatidylinositol 3 kinase-independent mechanism.
- Arsenic alters vascular smooth muscle cell focal adhesion complexes leading to activation of FAK-src mediated pathways.
- FP prostanoid receptor-mediated induction of the expression of early growth response factor-1 by activation of a Ras/Raf/mitogen-activated protein kinase signaling cascade.
- Translational control of nrf2 protein in activation of antioxidant response by oxidants.
- Involvement of oxidants and AP-1 in angiotensin II-activated NFAT3 transcription factor.
- Induction of antioxidant and detoxification response by oxidants in cardiomyocytes: evidence from gene expression profiling and activation of Nrf2 transcription factor.
- Proteomic identification of insulin-like growth factor-binding protein-6 induced by sublethal H2O2 stress from human diploid fibroblasts.
- Corticosteroids inhibit cell death induced by doxorubicin in cardiomyocytes: induction of antiapoptosis, antioxidant, and detoxification genes.
- Epidermal growth factor receptor-dependent and -independent pathways in hydrogen peroxide-induced mitogen-activated protein kinase activation in cardiomyocytes and heart fibroblasts.
- c-Fos phosphorylation induced by H2O2 prevents proteasomal degradation of c-Fos in cardiomyocytes. Previous years
- Expression of glucocorticoid-induced leucine zipper (GILZ) in cardiomyocytes.
- p66(Shc): at the crossroad of oxidative stress and the genetics of aging.
- Down regulation of p53 with HPV E6 delays and modifies cell death in oxidant response of human diploid fibroblasts: an apoptosis-like cell death associated with mitosis.
- Dodecafluoropentane Emulsion Elicits Cardiac Protection Against Myocardial Infarction Through an ATP-Sensitive K(+) Channel Dependent Mechanism.
- Distinct roles of p42/p44(ERK) and p38 MAPK in oxidant-induced AP-1 activation and cardiomyocyte hypertrophy.
- Apoptosis and heart failure: mechanisms and therapeutic implications.
- Signals of oxidant-induced cardiomyocyte hypertrophy: key activation of p70 S6 kinase-1 and phosphoinositide 3-kinase.
- NAD(P)H: quinone oxidoreductase 1 is induced by progesterone in cardiomyocytes.
- Inhibition of apoptosis by progesterone in cardiomyocytes.
- Novel mechanisms of sublethal oxidant toxicity: induction of premature senescence in human fibroblasts confers tumor promoter activity.
- Linking oxidative stress and genetics of aging with p66Shc signaling and forkhead transcription factors.