Erika Davies
Thomas Jefferson University
5 Papers
Erika Davies is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Calcium signaling & Mitochondrion. The author has an hindex of 5, co-authored 5 publications.
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Papers
Loss of Omi mitochondrial protease activity causes the neuromuscular disorder of mnd2 mutant mice
Julie M. Jones,Pinaki Datta,Srinivasa M. Srinivasula,Weizhen Ji,Sanjeev Gupta,Zhi Jia Zhang,Erika Davies,György Hajnóczky,Thomas L. Saunders,Margaret L. Van Keuren,Teresa Fernandes-Alnemri,Miriam H. Meisler,Emad S. Alnemri +12 more
TL;DR: The mnd2 mutation is identified as the missense mutation Ser276Cys in the protease domain of the nuclear-encoded mitochondrial serine protease Omi (also known as HtrA2 or Prss25), which increases the susceptibility of mitochondria to induction of the permeability transition, and increases the sensitivity of mouse embryonic fibroblasts to stress-induced cell death.
Ca2+-dependent control of the permeability properties of the mitochondrial outer membrane and voltage-dependent anion-selective channel (VDAC).
TL;DR: The VDAC gating is dependent on the physiological concentrations of cations, allowing the OMM to control the passage of ions and some small molecules, and single cell imaging data indicate that Ca2+ may facilitate the cation and ATP transport across the O MM.
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Bad targets the permeability transition pore independent of Bax or Bak to switch between Ca2+-dependent cell survival and death.
Soumya Sinha Roy,Muniswamy Madesh,Erika Davies,Bruno Antonsson,Nika N. Danial,György Hajnóczky +5 more
TL;DR: It is shown that ceramide and staurosporine target PP2A and protein kinases A and C, respectively, in a mitochondria-associated signaling complex to induce dephosphorylation of the BH3-only protein Bad, which switches between the survival and apoptotic functions of mitochondrial calcium signaling.
Bid-induced mitochondrial membrane permeabilization waves propagated by local reactive oxygen species (ROS) signaling
TL;DR: Bid engages a ROS-dependent, local intermitochondrial potentiation mechanism that amplifies the apoptotic signal as a wave, propagating through a cell at a constant velocity without dissipation, reports that Bid-induced permeabilization and cytochrome c release regularly demonstrate a wave-like pattern.
Calcium signaling and apoptosis.
TL;DR: The recent progress of research on the mechanisms mediating the apoptosis-regulating effects of Ca(2+) and the interactions of Bcl-2 family proteins with the Ca( 2+) storage organelles are discussed.