scispace - formally typeset
I

Isabella Derler

Researcher at Johannes Kepler University of Linz

Publications -  27
Citations -  2739

Isabella Derler is an academic researcher from Johannes Kepler University of Linz. The author has contributed to research in topics: ORAI1 & STIM1. The author has an hindex of 20, co-authored 20 publications receiving 2541 citations.

Papers
More filters
Journal ArticleDOI

Dynamic coupling of the putative coiled-coil domain of ORAI1 with STIM1 mediates ORAI1 channel activation.

TL;DR: Förster resonance energy transfer microscopy demonstrates a dynamic coupling of STIM1 and ORAI1 that culminates in the activation of Ca2+ entry and represents a key domain for dynamic coupling toSTIM1.
Journal ArticleDOI

A Cytosolic Homomerization and a Modulatory Domain within STIM1 C Terminus Determine Coupling to ORAI1 Channels

TL;DR: Two cytosolic key regions within STIM1 C terminus are identified that control ORAI1/CRAC activation: a homomerization domain indispensable for coupling to ORAi1 and a modulatory domain that controls the extent of coupling to SOTA1.
Journal ArticleDOI

TRPC3 and TRPC4 Associate to Form a Redox-sensitive Cation Channel EVIDENCE FOR EXPRESSION OF NATIVE TRPC3-TRPC4 HETEROMERIC CHANNELS IN ENDOTHELIAL CELLS

TL;DR: This work proposes TRPC3 and TRPC4 as subunits of native endothelial cation channels that are governed by the cellular redox state and proposes a redox-sensitive TRPC-TRPC4 channel complex.
Journal ArticleDOI

STIM1 couples to ORAI1 via an intramolecular transition into an extended conformation

TL;DR: It is suggested that these mutant STIM1 proteins imitate a physiological activated state, which mimics the intramolecular transition that occurs in native STIM2 upon store depletion, even in the absence of store depletion.
Journal ArticleDOI

Novel pyrazole compounds for pharmacological discrimination between receptor‐operated and store‐operated Ca2+ entry pathways

TL;DR: A series of pyrazole derivatives are characterized in terms of TRPC/Orai selectivity and consequences of selective suppression of these pathways for mast cell activation are delineated.