H
Heidrun Witan
Researcher at University of Mainz
Publications - 4
Citations - 408
Heidrun Witan is an academic researcher from University of Mainz. The author has contributed to research in topics: Protein aggregation & Wild type. The author has an hindex of 4, co-authored 4 publications receiving 364 citations.
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Journal ArticleDOI
Differential Promotion of Glutamate Transporter Expression and Function by Glucocorticoids in Astrocytes from Various Brain Regions
Jürgen Zschocke,Nadhim Bayatti,Albrecht M. Clement,Heidrun Witan,Maciej Figiel,Jürgen Engele,Christian Behl +6 more
TL;DR: A potential role for glucocorticoids in regulating GLT-1 gene expression during central nervous system development or pathophysiogical processes including stress is highlighted.
Journal ArticleDOI
One enzyme, two functions: PON2 prevents mitochondrial superoxide formation and apoptosis independent from its lactonase activity
Sebastian Altenhöfer,Ines Witte,John F. Teiber,Petra Wilgenbus,Andrea Pautz,Huige Li,Andreas Daiber,Heidrun Witan,Albrecht M. Clement,Ulrich Förstermann,Sven Horke +10 more
TL;DR: This study provides detailed mechanistic insight into the functions of PON2, which is important for its role in innate immunity, atherosclerosis, and cancer.
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Heterodimer formation of wild-type and amyotrophic lateral sclerosis-causing mutant Cu/Zn-superoxide dismutase induces toxicity independent of protein aggregation
Heidrun Witan,Andreas Kern,Ingrid Koziollek-Drechsler,Rebecca C. Wade,Christian Behl,Albrecht M. Clement +5 more
TL;DR: It is concluded that toxicity of mutant SOD1 is at least partially mediated through heterodimer formation with S OD1(hWT) in vivo and does not correlate with the aggregation potential of individual mutants.
Journal ArticleDOI
Wild-type Cu/Zn superoxide dismutase (SOD1) does not facilitate, but impedes the formation of protein aggregates of amyotrophic lateral sclerosis causing mutant SOD1.
Heidrun Witan,Philipp Gorlovoy,Ali M. Kaya,Ingrid Koziollek-Drechsler,Harald Neumann,Christian Behl,Albrecht M. Clement +6 more
TL;DR: It is proposed that S OD1(WT) contributes to disease by heterodimerization with mutant SOD1 forms by increasing the presence of heterodimers upon SOD 1(hWT) co-expression.