https://transhumanist.ru/index.php?action=history&feed=atom&title=AQR 2026-04-13T03:41:14Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=AQR&diff=5911&oldid=prev 2021-05-12T14:59:49Z

<p>Новая страница: «RNA helicase aquarius (EC 3.6.4.13) (Intron-binding protein of 160 kDa) (IBP160) [KIAA0560] ==Publications== {{medline-entry |title=Synergism between soluble gu...»</p> <p><b>Новая страница</b></p><div>RNA helicase aquarius (EC 3.6.4.13) (Intron-binding protein of 160 kDa) (IBP160) [KIAA0560]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Synergism between soluble guanylate cyclase signaling and neuropeptides extends lifespan in the nematode Caenorhabditis elegans.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28054425<br /> |abstract=Oxygen (O ) homeostasis is important for all aerobic animals. However, the manner by which O sensing and homeostasis contribute to lifespan regulation is poorly understood. Here, we use the nematode Caenorhabditis elegans to address this question. We demonstrate that a loss-of-function mutation in the neuropeptide receptor gene npr-1 and a deletion mutation in the atypical soluble guanylate cyclase gcy-35 O sensor interact synergistically to extend worm lifespan. The function of npr-1 and gcy-35 in the O -sensing neurons [[AQR]], PQR, and URX shortens the lifespan of the worm. By contrast, the activity of the atypical soluble guanylate cyclase O sensor gcy-33 in these neurons is crucial for lifespan extension. In addition to [[AQR]], PQR, and URX, we show that the O -sensing neuron BAG and the interneuron RIA are also important for the lifespan lengthening. Neuropeptide processing by the proprotein convertase EGL-3 is essential for lifespan extension, suggesting that the synergistic effect of joint loss of function of gcy-35 and npr-1 is mediated through neuropeptide signal transduction. The extended lifespan is regulated by hypoxia and insulin signaling pathways, mediated by the transcription factors HIF-1 and DAF-16. Moreover, reactive oxygen species (ROS) appear to play an important function in lifespan lengthening. As HIF-1 and DAF-16 activities are modulated by ROS, we speculate that joint loss of function of gcy-35 and npr-1 extends lifespan through ROS signaling.<br /> |mesh-terms=* Animals<br /> * Caenorhabditis elegans<br /> * Caenorhabditis elegans Proteins<br /> * Food<br /> * Gene Expression Regulation<br /> * Guanylate Cyclase<br /> * Immunity, Innate<br /> * Interneurons<br /> * Longevity<br /> * Mutation<br /> * Neuropeptides<br /> * Neurotransmitter Agents<br /> * Oxidation-Reduction<br /> * Oxygen<br /> * Paraquat<br /> * Reactive Oxygen Species<br /> * Receptors, Neuropeptide Y<br /> * Signal Transduction<br /> * Stress, Physiological<br /> * Temperature<br /> * Transcription, Genetic<br /> |keywords=* <br /> Caenorhabditis elegans<br /> <br /> * NPR-1<br /> * lifespan<br /> * oxygen sensing<br /> * reactive oxygen species<br /> * soluble guanylate cyclase<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5334569<br /> }}</div>

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