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Jyoti J. Watters

Researcher at University of Wisconsin-Madison

Publications -  103
Citations -  5530

Jyoti J. Watters is an academic researcher from University of Wisconsin-Madison. The author has contributed to research in topics: Microglia & Intermittent hypoxia. The author has an hindex of 37, co-authored 87 publications receiving 4971 citations. Previous affiliations of Jyoti J. Watters include University of Washington & Case Western Reserve University.

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Rapid Membrane Effects of Steroids in Neuroblastoma Cells: Effects of Estrogen on Mitogen Activated Protein Kinase Signalling Cascade and c-fos Immediate Early Gene Transcription

TL;DR: It is shown that in the human neuroblastoma cell line SK-N-SH, the membrane impermeable conjugated 17beta-estradiol (E2BSA) activates mitogen activated protein kinase kinase (MAPKK or MEK) and induces the phosphorylation and activation of both ERK-1 and ERK
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BDNF is necessary and sufficient for spinal respiratory plasticity following intermittent hypoxia

TL;DR: It is found that intermittent hypoxia elicited serotonin-dependent increases in BDNF synthesis in ventral spinal segments containing the phrenic nucleus, and the magnitude of these BDNF increases correlated with pLTF magnitude.
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Microglia function in brain tumors.

TL;DR: A better understanding of microglia and macrophage function is essential for the development of immune‐based treatment strategies against malignant brain tumors.
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Microglia express distinct M1 and M2 phenotypic markers in the postnatal and adult central nervous system in male and female mice.

TL;DR: Age‐ and sex‐specific variances in basal gene expression may allow differential microglial responses to the same stimulus at different ages, perhaps contributing to altered CNS vulnerabilities and/or disease courses.
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Estrogen rapidly induces the phosphorylation of the cAMP response element binding protein in rat brain.

TL;DR: These data provide evidence for non-genomic effects of steroid hormones involving protein kinase associated signal transduction pathways traditionally associated with effects at the cell membrane and provide a possible explanation for estrogen's effects on neuronal genes lacking estrogen response elements but which contain cAMP response elements.