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2 weeks ago | 
science.org | Hannah Ferris |Scott Earley |Leslie K. Ferrarelli |Danielle Jeffrey
Editor’s summaryIncreased intraluminal pressure in the brain elicits the constriction of arterioles, which is usually mediated by smooth muscle cells situated in arteriole walls. However, Ferris et al. found that, in the mouse brain, this role was extended to mural cells called pericytes that reside on the transitional blood vessel segments between arterioles and capillaries (see also the Focus by Earley).
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2 weeks ago | 
science.org | Hannah Ferris |Scott Earley |Leslie K. Ferrarelli
AbstractThe innate immunity mediator STING senses and repairs lysosomal dysfunction. SIGN UP FOR THE AWARD-WINNING SCIENCEADVISER NEWSLETTER The latest news, commentary, and research, free to your inbox daily Inflammation in the brain contributes to the pathology and progression of various neurological and neurodegenerative diseases. The innate immunity mediator STING is implicated in driving this inflammation (see Wang et al. in the Science Signaling Archive). However, Tang et al.
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2 weeks ago | 
science.org | Hannah Ferris |Scott Earley |Leslie K. Ferrarelli
AbstractIntrinsic control of cerebral blood flow in response to intravascular pressure is traditionally attributed to smooth muscle cells in arterioles. However, in this issue of Science Signaling, Ferris et al. demonstrate that capillary constriction is caused by pressure-induced depolarization of pericytes, mural cells that encircle capillaries, and is mediated by TRPC3 cation channels, identifying the channel as critical for fine-tuning brain perfusion.
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1 month 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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2 months 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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Oct 15, 2024 | 
science.org | Alba de Juan |Leslie K. Ferrarelli |Alice Coillard |Darawan Tabtim-On
Editor’s summaryThe aryl hydrocarbon receptor (AhR), a transcription factor activated by various metabolites and xenobiotics, influences how immune cells respond to the cytokines that direct their differentiation and function. de Juan et al. found that activation of the AhR was required for the induction of a subset of transcripts by the cytokine interleukin-4 (IL-4) in human and mouse monocytes.
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Oct 15, 2024 | 
science.org | Alba de Juan |Leslie K. Ferrarelli
AbstractToo much or too little tau in glial cells enables the accumulation of neurotoxic oxidative stress. SIGN UP FOR THE SCIENCEADVISER NEWSLETTER The latest news, commentary, and research, free to your inbox daily Tau gets a bad rap. Its aggregation in the brain causes the neurofibrillary tangles that underlie cognitive decline and brain atrophy in various neurodegenerative diseases.
