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Associate Professor of Anatomy and Cell Biology
Office: 1-570 Bowen Science BuildingIowa City, IA 52242
Lab: 1-500 Bowen Science BuildingIowa City, IA 52242
Email: email@example.comWeb: Publications via PubMed
BS, Biotechnology, University of DelawarePhD, Cell Biology, University of California
Post Doctorate, Howard Hughes Medical Institute, University of Michigan Medical Center
Department of Anatomy and Cell Biology Graduate ProgramInterdisciplinary Graduate Program in Molecular and Cellular BiologyMedical Scientist Training Program
Our laboratory seeks to understand a fundamental but very poorly understood question in biology: When a cell encounters stress (i.e., anything that perturbs normal cellular function), how does it decide whether to adapt to the stress or die? We use diverse experimental approaches to address this question, encompassing systems biology, molecular and cell biology, and vertebrate genetics and physiology. By tackling this question, we hope to better understand diseases of stress, including neurodegeneration, cancer, metabolic syndrome, and others, and even normal cellular development and function.
There are many ways in which stress can be manifested to a cell, including pathogenic infection, chemical insult, genetic mutation, nutrient deprivation, and the course of normal cellular function. The endoplasmic reticulum (ER) is the site of synthesis and folding of secretory and cell-surface proteins. The cellular response to ER stress (also known as the Unfolded Protein Response, or UPR) serves as a model for understanding not only the mechanisms by which stress is sensed, but also the ways in which the consequences of alterations of homeostasis in one location (i.e., the ER) impact diverse areas of cell function, including gene expression, metabolism, cancer, cell signaling, and apoptosis.
Center for Gene Therapy of Cystic Fibrosis and other Genetic DiseasesFraternal Order of Eagles Diabetes Research CenterHolden Comprehensive Cancer Center
The stress-regulated transcription factor CHOP promotes hepatic inflammatory gene expression, fibrosis, and oncogenesis.
2013 December. 9:e1003937.
Regulation of the transcriptome by ER stress: non-canonical mechanisms and physiological consequences.
Frontiers in Genetics.
2013 November. 4:256.
Endoplasmic reticulum stress impairs IL-4/IL-13 signaling through C/EBPβ-mediated transcriptional suppression.
Journal of Cell Science.
2013 September. 126:4026-4036.
Temporal clustering of gene expression links the transcription factor HNF4α to ER stress-induced fatty liver.
Frontiers in Genetics.
2013 September. 4:188.
C/EBP homologous protein (CHOP) contributes to suppression of metabolic genes during endoplasmic reticulum stress in the liver..
The Journal of biological chemistry.
2013 February. 288(6):4405-15.
Synthetic embryonic lethality upon deletion of the ER cochaperone p58IPK and the ER stress sensor ATF6α.
Biochemical and Biophysical Research Communications.
2013. Tyra H,
Inhibition of fatty acid oxidation enhances oxidative protein folding and protects hepatocytes from endoplasmic reticulum stress..
Molecular biology of the cell.
2012 March. 23(5):811-9.
The unfolded protein response mediates adaptation to exercise in skeletal muscle through a PGC-1α/ATF6α complex.
2011 February 2. 13(2):160-169.
Regulation of basal cellular physiology by the homeostatic unfolded protein response..
The Journal of cell biology.
2010 May. 189(5):783-94.
A gluconeogenic tryst in the nucleus, with ER stress as the third wheel..
Date Last Modified: 11/11/2015 -
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