
Articles
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4 weeks ago |
science.org | Xiaoyong Chen |Alex Luebbers |Leslie K. Ferrarelli
AbstractAn antibody delivered nasally after brain injury induces a neuroprotective, anti-inflammatory response. SIGN UP FOR FIRST RELEASE ALERTS Get the latest First Release papers from Science delivered right to you Neuroinflammation is a major cause of neuropathology after traumatic brain injury (TBI), including neurodegeneration and dementia (see Cairns et al. in the Science Signaling archive). Izzy et al.
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1 month ago |
science.org | Jesús Aguirre-Gutiérrez |Jennifer Hill |Zijian Zhang |Leslie K. Ferrarelli
Neuroinflammation Acetylation to fuel neuroinflammationLeslie K. FerrarelliFluorescence microscopy image of mouse hippocampus area CA3 reveals localization of GCN5 (red) in microglia, but not astrocytes (green). Open in viewerThe acetyltransferase GCN5 promotes inflammation in peripheral tissues. Cho et al. found that GCN5 mediates inflammation in the brain as well, suggesting that it may be a target for treating neuroinflammatory diseases.
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Nov 19, 2024 |
science.org | Eyal Zoler |Matthew Knarr |Leslie K. Ferrarelli |Jamie K. Moon
Editor’s summaryHigh-grade serous ovarian cancer (HGSOC) is aggressive and lacks durably effective treatments. Forskolin can suppress cancer cell proliferation but cannot be used clinically. Knarr et al. found that colforsin daropate, a forskolin derivative, specifically induced cell death in HGSOC cells but not normal fallopian or ovarian cells and inhibited HGSOC invasion in part by attenuating MYC signaling.
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Nov 19, 2024 |
science.org | Eyal Zoler |Matthew Knarr |Leslie K. Ferrarelli |Thomas Meyer
Editor’s summaryType I interferons (IFNs) stimulate antiviral or antiproliferative signaling in a cell type–dependent manner. The Janus kinases TYK2 and JAK1 are recruited to the IFN receptor subunits IFNAR1 and IFNAR2, respectively, cross-phosphorylating each other and STAT proteins to transduce IFN signals. However, in experiments with synthetic IFNARs and JAK-deficient cell lines, Zoler et al.
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Nov 19, 2024 |
science.org | Eyal Zoler |Matthew Knarr |Leslie K. Ferrarelli
AbstractThe kinase TYK2 facilitates pathological tau assembly through protein-stabilizing modifications. SIGN UP FOR THE AWARD-WINNING SCIENCEADVISER NEWSLETTER The latest news, commentary, and research, free to your inbox daily Tauopathies are a diverse group of neurodegenerative diseases caused by the abnormal self-assembly of tau, a protein that promotes cellular function by stabilizing microtubules, the filaments that support cell shape and movement.
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