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Nitric oxide (·NO) is one of the toxic metabolites that bacteria can be exposed to within phagosomes. Gre factors, which are also known as transcript cleavage factors or transcription elongation factors, relieve back-tracked transcription elongation complexes by cleaving nascent RNAs, which allows transcription to resume after stalling. Here we discovered that loss of both Gre factors in , GreA and GreB, significantly compromised ·NO detoxification due to ·NO-induced phenotypic heterogeneity in ΔΔ populations, which did not occur in wild-type cultures.

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S-nitrosylation of the transcription factor MYB30 facilitates nitric oxide-promoted seed germination in Arabidopsis.

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State Key Laboratory of Crop Stress Adaptation and Improvement, Key Laboratory of Plant Stress Biology, School of Life Sciences, Henan University, Kaifeng 475001, China.

The gaseous signaling molecule nitric oxide (NO) plays an important role in breaking seed dormancy. NO induces a decrease in abscisic acid (ABA) content by transcriptionally activating its catabolic enzyme, the ABA 8'-hydroxylase CYP707A2. However, the underlying mechanism of this process remains unclear.

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The mediating role of inflammation in the association between pregnancy loss history and gestational diabetes mellitus.

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Department of Maternal, Child and Adolescent Health, School of Public Health, Anhui Medical University, Hefei, China.

Background: To assess the association of pregnancy loss history with an elevated risk of Gestational diabetes mellitus (GDM) and to investigate whether this association was mediated by high-sensitivity C-reactive protein (hs-CRP).

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New Phytol

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State Key Laboratory of Crop Biology, College of Horticulture Science and Engineering, Shandong Agricultural University, Tai'an, 271018, China.

Crop loss due to soil salinization is a global threat to agriculture. Nitric oxide (NO) and ethylene involve in multiple plant tolerance. However, their interaction in salt resistance remains largely elusive.

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Near micromolar concentrations of nitric oxide (NO) induce tumor cells death. However, an appropriate NO load has to be delivered selectively to the tumor site in order to avoid NO loss and secondary NO-induced effects. The encapsulation of millimolar concentrations of a NO source and an appropriate trigger of NO release within phospatidylcholine-based liposomes should provide an efficient tool for the selective release of the needed NO payload.

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