SUMMARYNitric oxide (NO) promotes the accumulation of PHYB and thus reduces PIF3. The activity of PIF3 was also regulated by RGL3. PIF3 may lie downstream of PHYB and RGL3, and regulate NO-induced root growth inhibition of Arabidopsis seedlings in light.
Homocysteine (Hcy) is regarded as a risk factor for hypertension, but research on the causal relationship between Hcy and hypertension is limited. In the present study, we prospectively tracked the blood pressure progression of a normotensive population with different Hcy levels over a 2-year period. The incidence of hypertension with increasing Hcy quartiles produced an approximately U-shaped curve, with significance in males. Compared with the third quartile, the risk of hypertension in the first and second quartiles was increased by 1.55 (95% confidence interval [CI] 1.154–2.081) fold and 1.501 (95% CI 1.119–2.013) fold, respectively, with the increase being more significant in males. In conclusion, Hcy is related to hypertension incidence with the results approximating an U-shaped curve. Low Hcy levels might also increase the risk of hypertension.
Acute myeloid leukemia (AML) with mutated nucleophosmin (NPM1) has been defined as a distinct leukemia entity in the 2016 updated WHO classification of myeloid neoplasm. Our previous report showed that autophagic activity was elevated in NPM1-mutated AML, but the underlying molecular mechanisms remain elusive. Mount of study provides evidence that glycometabolic enzymes are implicated in the autophagic process. Pyruvate kinase isoenzyme M2 (PKM2), a key glycolytic enzyme, has been recently reported as a tumor supporter in leukemia. However, little is known about the roles of PKM2 in autophagic activity in NPM1-mutated AML. In this study, PKM2 highly expressed in NPM1-mutated AML, and partially, high levels of PKM2 were upregulated by PTBP1. Further experiments demonstrated that PKM2 mediated autophagic activation and increased the phosphorylation of key autophagy protein Beclin-1. Importantly, functional experiments demonstrated that PKM2 contributed to cell survival via autophagic activation. Ultimately, high PKM2 expression was associated with short overall and event-free survival time in NPM1-mutated AML patients. Our findings indicate for the first time that glycolytic enzyme PKM2 mediates autophagic activation and further contributes to cell survival in NPM1-mutated AML, suggesting that PKM2 may serve as a promising target for treatment of NPM1-mutated AML.
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