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Dietmar Kültz

Researcher at University of California, Davis

Publications -  117
Citations -  8257

Dietmar Kültz is an academic researcher from University of California, Davis. The author has contributed to research in topics: Oreochromis mossambicus & Osmotic shock. The author has an hindex of 41, co-authored 112 publications receiving 7513 citations. Previous affiliations of Dietmar Kültz include University of California, Berkeley & Mount Desert Island Biological Laboratory.

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Molecular and evolutionary basis of the cellular stress response

TL;DR: Functional analysis of the minimal stress proteome yields information about key aspects of the cellular stress response, including physiological mechanisms of sensing membrane lipid, protein, and DNA damage; redox sensing and regulation; cell cycle control; macromolecular stabilization/repair; and control of energy metabolism.
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The ecoresponsive genome of Daphnia pulex

John K. Colbourne, +85 more
- 04 Feb 2011 - 
TL;DR: The Daphnia genome reveals a multitude of genes and shows adaptation through gene family expansions, and the coexpansion of gene families interacting within metabolic pathways suggests that the maintenance of duplicated genes is not random.
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Regulation of gene expression by hypertonicity.

TL;DR: This review considers how solutes help relieve the stress of hypertonicity and the nature of transporters and enzymes responsible for their variable accumulation and the molecular basis for osmotic regulation of these genes.
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In vitro biologic activities of the antimicrobials triclocarban, its analogs, and triclosan in bioassay screens: receptor-based bioassay screens.

TL;DR: Carbanilides, including TCC, enhanced hormone-dependent induction of ER- and AR-dependent gene expression but had little agonist activity, suggesting a new mechanism of action of endocrine-disrupting compounds.
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Evolution of the cellular stress proteome: from monophyletic origin to ubiquitous function.

TL;DR: The need for a holistic view emphasizing the key aspects of the stress response is addressed by the following hypothesis: a phylogenetically conserved set of genes and pathways that mediate global macromolecular stabilization and repair to promote cellular and organismal integrity under suboptimal conditions.