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Nitric Oxide Signaling Pathway01:28

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Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure...
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Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
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Nuclear receptors, or NRs, are unique transcription factors that regulate gene transcription and affect the cellular pathways involved in reproduction, development, or metabolism. Their ability to be stimulated by small lipophilic ligands and control vital cellular processes makes them ideal drug targets. Nearly 10-15% of currently prescribed drugs target these receptors.
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Nuclear Export01:42

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The nucleus restricts several proteins within and allows others to pass. The restricted proteins possess a nuclear retention sequence or NRS, anchoring them to the nuclear lamins and preventing their transport to the cytosol. The non-restricted proteins, after their synthesis, are transported to their site of action, such as the cytosol or other organelles, with the help of nuclear export signals or NES.
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Related Experiment Video

Updated: Jan 13, 2026

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Nuclear eNOS Interacts With and S-Nitrosates ADAR1 to Modulate Type I Interferon Signaling and Endothelial Function.

Xiaozhu Zhou1, Carsten Kuenne2, Stefan Günther2

  • 1Institute for Vascular Signaling, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany (X.Z., B.G., F.D.L., I.F., M.S.).

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Nuclear endothelial nitric oxide synthase (eNOS) regulates RNA editing via ADAR1, maintaining vascular homeostasis. Loss of eNOS function impairs this, activating type I interferon signaling and contributing to atherosclerosis.

Keywords:
ADAR1S-nitrosationdsRNAeNOStype I IFN signaling

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Area of Science:

  • Vascular Biology
  • Molecular Biology
  • Immunology

Background:

  • Endothelial nitric oxide (NO) produced by endothelial NO synthase (eNOS) is crucial for vascular homeostasis and anti-inflammatory responses.
  • While typically membrane-bound, eNOS is also found in the endothelial cell nucleus, prompting investigation into its nuclear role.

Purpose of the Study:

  • To investigate the functional significance of nuclear eNOS and its associated NO signaling in endothelial cells.
  • To elucidate the molecular mechanisms linking nuclear eNOS to endothelial cell function and vascular health.

Main Methods:

  • Utilized eNOS loss-of-function models combined with confocal microscopy, biochemical assays, histology, and multiomics.
  • Assessed pathophysiological relevance in murine models of atherosclerosis and human patient samples.

Main Results:

  • Nuclear eNOS was identified in human and murine endothelial cells, with VEGF stimulation enhancing its nuclear presence.
  • Nuclear eNOS interacts with RNA-binding proteins, including ADAR1, crucial for RNA editing.
  • eNOS deficiency led to impaired ADAR1 editing, increased double-stranded RNA, MAVS aggregation, type I interferon signaling activation, and altered cell cycle gene expression, ultimately reducing proliferation and increasing cell death.
  • Endothelial dysfunction in atherosclerosis correlated with increased double-stranded RNA and type I interferon signaling.

Conclusions:

  • Discovered a novel pathway where nuclear eNOS-derived NO modulates ADAR1 activity to maintain vascular homeostasis.
  • Reduced NO bioavailability triggers a previously unrecognized type I interferon response in the endothelium, promoting atherogenesis.