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Loredana Stoica

Researcher at Baylor College of Medicine

Publications -  9
Citations -  941

Loredana Stoica is an academic researcher from Baylor College of Medicine. The author has contributed to research in topics: mTORC2 & Long-term potentiation. The author has an hindex of 8, co-authored 9 publications receiving 771 citations. Previous affiliations of Loredana Stoica include Pierre-and-Marie-Curie University & French Institute of Health and Medical Research.

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mTORC2 controls actin polymerization required for consolidation of long-term memory

TL;DR: It is found that conditional deletion of Rictor in the postnatal murine forebrain greatly reduced mTORC2 activity and selectively impaired both long-term memory (LTM) and the late phase of hippocampal long- term potentiation (L-LTP).
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Selective pharmacogenetic inhibition of mammalian target of Rapamycin complex I (mTORC1) blocks long-term synaptic plasticity and memory storage

TL;DR: Direct genetic evidence supporting the role of mTORC1 in L-LTP and behavioral memory is provided and it is found that m TORC1-mediated translational control is required for memory reconsolidation.
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Suppression of PKR promotes network excitability and enhanced cognition by interferon-γ-mediated disinhibition.

TL;DR: It is reported that the lack of PKR enhances learning and memory in several behavioral tasks while increasing network excitability and increases the late phase of long-lasting synaptic potentiation in hippocampal slices.
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A Versatile Method for Cell-Specific Profiling of Translated mRNAs in Drosophila

TL;DR: The TRAP method is adapted for use in the versatile GAL4/UAS system of Drosophila allowing profiling of almost any tissue/cell-type with a single genetic cross to determine the unique translatome profiles in different cell-types under varied physiological, pharmacological and pathological conditions.
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Therapeutic inhibition of mTORC2 rescues the behavioral and neurophysiological abnormalities associated with Pten -deficiency

TL;DR: It is indicated that mTORC2 is the major driver underlying the neuropathophysiology associated with Pten-deficiency, and its therapeutic reduction could represent a promising and broadly effective translational therapy for neurological disorders where mTOR signaling is dysregulated.