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Keri Martinowich

Researcher at Johns Hopkins University

Publications -  98
Citations -  9739

Keri Martinowich is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Neurotrophic factors & Brain-derived neurotrophic factor. The author has an hindex of 32, co-authored 81 publications receiving 8058 citations. Previous affiliations of Keri Martinowich include Johnson & Johnson Pharmaceutical Research and Development & University of California, Los Angeles.

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DNA methylation-related chromatin remodeling in activity-dependent BDNF gene regulation.

TL;DR: It is reported that increased synthesis of brain-derived neurotrophic factor in neurons after depolarization correlates with a decrease in CpG methylation within the regulatory region of the Bdnf gene, suggesting that DNA methylation–related chromatin remodeling is important for activity-dependent gene regulation that may be critical for neural plasticity.
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Direct current stimulation promotes BDNF-dependent synaptic plasticity: potential implications for motor learning.

TL;DR: It is demonstrated in mouse M1 slices that DCS induces a long-lasting synaptic potentiation (DCS-LTP), which is polarity specific, NMDA receptor dependent, and requires coupling of DCS with repetitive low-frequency synaptic activation (LFS).
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New insights into BDNF function in depression and anxiety

TL;DR: BDNF may be a target of antidepressants, but not the sole mediator of depression or anxiety, and as the precursor proBDNF and the mature protein mBDNF can elicit opposite effects on cellular functions, the impact of proBD NF and its cleavage on mood should be considered.
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Interaction between BDNF and Serotonin: Role in Mood Disorders

TL;DR: Brain-derived neurotrophic factor promotes the survival and differentiation of 5-HT neurons and administration of antidepressant selective serotonin reuptake inhibitors (SSRIs) enhances BDNF gene expression.
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DNA methylation controls the timing of astrogliogenesis through regulation of JAK-STAT signaling

TL;DR: This study suggests that during the neurogenic period, DNA methylation inhibits not only astroglial marker genes but also genes that are essential for JAK-STAT signaling, and demethylation of these two groups of genes and subsequent elevation of STAT activity are key mechanisms that control the timing and magnitude of astrocyte differentiation.