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Elizabeth V. Wattenberg
Researcher at University of Minnesota
Publications - 42
Citations - 2010
Elizabeth V. Wattenberg is an academic researcher from University of Minnesota. The author has contributed to research in topics: Palytoxin & Kinase. The author has an hindex of 21, co-authored 41 publications receiving 1627 citations. Previous affiliations of Elizabeth V. Wattenberg include Massachusetts Institute of Technology & University of North Carolina at Chapel Hill.
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Journal ArticleDOI
Anthropogenic contamination of tap water, beer, and sea salt.
TL;DR: Based on consumer guidelines, the results indicate the average person ingests over 5,800 particles of synthetic debris from these three sources annually, with the largest contribution coming from tap water (88%).
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Sustained activation of the mitogen-activated protein kinase pathway. A mechanism underlying receptor tyrosine kinase specificity for matrix metalloproteinase-9 induction and cell migration.
TL;DR: Evidence of an underlying mechanism to account for observed differences in receptor tyrosine kinase-mediated response is presented and supports the conclusion that duration of MAPK activation is an important determinant for certain growth factor-mediated functions in keratinocytes.
Journal Article
Phosphatidylinositol 3-kinase activity in epidermal growth factor-stimulated matrix metalloproteinase-9 production and cell surface association.
Shawn M. Ellerbroek,Jennifer M. Halbleib,Mario Benavidez,Janel K. Warmka,Elizabeth V. Wattenberg,M. Sharon Stack,Laurie G. Hudson,Laurie G. Hudson +7 more
TL;DR: The data suggest that EGF receptor activation promotes aPI3K-dependent induction of a cell surface pro-MMP-9 binding component that may facilitate gelatinase-mediated cellular invasion and supports an expanded role for elevated PI3K activity in cellular responses associated with ovarian tumor metastasis.
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T3 increases Na-K-ATPase activity via a MAPK/ERK1/2-dependent pathway in rat adult alveolar epithelial cells.
TL;DR: Data indicate that activation of MAPK-ERK1/2 was required for the T3-induced increase in Na-K-ATPase activity in addition to the requirement for the PI3K pathway.
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Mitogen-activated Protein Kinase Phosphatase-3 Is a Tumor Promoter Target in Initiated Cells That Express Oncogenic Ras
TL;DR: It is reported here that palytoxin activates extracellular signal-regulated kinase (ERK) through a novel mechanism that involves inactivation of an ERK phosphatase in keratinocytes derived from initiated mouse skin (308 cells), and that MKP-3 may be a vulnerable target in cells that express oncogenic Ras.