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Felizia K. Voss

Researcher at Leibniz Institute for Neurobiology

Publications -  7
Citations -  825

Felizia K. Voss is an academic researcher from Leibniz Institute for Neurobiology. The author has contributed to research in topics: Medicine & Cardiac function curve. The author has an hindex of 4, co-authored 5 publications receiving 643 citations. Previous affiliations of Felizia K. Voss include Free University of Berlin.

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Identification of LRRC8 Heteromers as an Essential Component of the Volume-Regulated Anion Channel VRAC

TL;DR: This work shows thatVRAC defines a class of anion channels, suggests that VRAC is identical to the volume-sensitive organic osmolyte/anion channel VSOAC, and explains the heterogeneity of native VRAC currents.
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VRAC: molecular identification as LRRC8 heteromers with differential functions

TL;DR: The remarkable journey which led to the molecular identification of VRAC is discussed, evidence for LRRC8 proteins forming the VRAC pore and their heteromeric assembly are discussed and first major insights on the role of LR RC8 proteins in cancer drug resistance and apoptosis and the role in cisplatin and taurine transport are summarized.
Journal ArticleDOI

Inactivation and Anion Selectivity of Volume-regulated Anion Channels (VRACs) Depend on C-terminal Residues of the First Extracellular Loop

TL;DR: A highly conserved extracellular region preceding the second LRRC8 transmembrane domain as a major determinant of ICl,vol inactivation is uncovered and it is suggested that the C-terminal part of the firstextracellular loop not only determines VRAC inactivation but might also participate in forming its outer pore.
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Epithelial coxsackievirus adenovirus receptor promotes house dust mite-induced lung inflammation

TL;DR: In this article , the authors investigated the mechanistic contribution of CAR in mediating responses to the common aeroallergen, House Dust Mite (HDM), and demonstrated that administration of HDM in mice lacking CAR in the respiratory epithelium leads to loss of peri-bronchial inflammatory cell infiltration, fewer goblet-cells and decreased pro-inflammatory cytokine release.