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Görkem Garipler

Researcher at New York University

Publications -  10
Citations -  275

Görkem Garipler is an academic researcher from New York University. The author has contributed to research in topics: Mitochondrial DNA & Mitochondrion. The author has an hindex of 7, co-authored 10 publications receiving 208 citations. Previous affiliations of Görkem Garipler include Koç University & University of Tampere.

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A multi-step transcriptional and chromatin state cascade underlies motor neuron programming from embryonic stem cells

TL;DR: This analysis reveals a highly dynamic process in which Ngn2 and the Isl1/Lhx3 pair initially engage distinct regulatory regions, and motor neuron programming is the product of two initially independent transcriptional modules that converge with a feedforward transcriptional logic.
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Proneural factors Ascl1 and Neurog2 contribute to neuronal subtype identities by establishing distinct chromatin landscapes

TL;DR: This study provides a mechanistic understanding of how transcription factors constrain terminal cell fates, and it delineates the importance of choosing the right proneural factor in neuronal reprogramming strategies.
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Mitochondrial Dysfunction Plus High-Sugar Diet Provokes a Metabolic Crisis That Inhibits Growth.

TL;DR: The Drosophila mutant tko25t exhibits a deficiency of mitochondrial protein synthesis, leading to a global insufficiency of respiration and oxidative phosphorylation, which entrains an organismal phenotype of developmental delay and sensitivity to seizures induced by mechanical stress.
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Deletion of conserved protein phosphatases reverses defects associated with mitochondrial DNA damage in Saccharomyces cerevisiae

TL;DR: Deletion of protein phosphatases 2A or PP6 protects cells from the reduced proliferation, mitochondrial protein import defects, lower mitochondrial electrochemical potential, and nuclear transcriptional response associated with mtDNA damage, suggesting a potential therapeutic approach for mitochondrial disease.
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Defects Associated with Mitochondrial DNA Damage Can Be Mitigated by Increased Vacuolar pH in Saccharomyces cerevisiae

TL;DR: It is found that disrupting vacuolar biogenesis permitted survival of a sensitized yeast background after mitochondrial genome loss and elevating vacUolar pH increases proliferation after mtDNA deletion and reverses the protein import defect of mitochondria lacking DNA.