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The specific mechanism may also be by activating VEGF-A / VEGFR1 -mediated AKT and p38/MAPK signaling pathways to upregulate downstream eNOS expression, which may increase the NO product synthesis, thus promote angiogenesis of gastric mucosa and also interact with endoplasmic reticulum (ER) stress
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Ure2p and Sup35 have been extensively investigated by SSNMR techniques
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