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CREB and ChREBP oppositely regulate SIRT1 expression in response to energy availability 总被引:2,自引:0,他引:2
Noriega LG Feige JN Canto C Yamamoto H Yu J Herman MA Mataki C Kahn BB Auwerx J 《EMBO reports》2011,12(10):1069-1076
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FoxO1 and SIRT1 regulate beta-cell responses to nitric oxide 总被引:1,自引:0,他引:1
Hughes KJ Meares GP Hansen PA Corbett JA 《The Journal of biological chemistry》2011,286(10):8338-8348
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The control of phytochrome A expression at the protein and mRNA levels was investigated in wild-type and phyB-1 mutant sorghum ( Sorghum bicolor [L.] Moench). PHYA mRNA abundance follows a diurnal rhythm in both genotypes, with maximal accumulation near the latter part of the light period. PHYA mRNA is more abundant in the phyB-1 mutant. The level of PHYA message correlates with both R : FR and photon flux density in wild-type, but only with photon flux density in the phyB-1 mutant. The differences in mRNA abundance are reflected in the level of phyA protein, which is elevated in the phyB-1 mutant and accumulates under low photon flux density. During de-etiolation, PHYA message accumulation is initially repressed solely by a very low fluence response (VLFR) presumably mediated by phyA. The phyB-mediated low fluence response maintains the repression of accumulation past the time controlled by the VLFR. With repetitive photoperiods, the transition from the etiolated growth form to autotrophic competency is accompanied by a transition from light-induced reduction of PHYA mRNA abundance to enhanced accumulation during the light period. The loss of phyB function allows partial de-repression of PHYA message accumulation under repetitive photoperiods, resulting in plants deficient in phyB but enriched in phyA. The modification of PHYA mRNA and protein levels in the phyB-1 mutant documented in this study may help clarify the molecular basis of the phyB-1 phenotype. The tailoring of phyA abundance in wild-type to the time of day and shade signals suggests a plastic role for this pigment in controlling development in light-grown plants. 相似文献
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Metabolic adaptations through the PGC-1 alpha and SIRT1 pathways 总被引:6,自引:0,他引:6
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Jeong-Rang Jo Sung-Eun Lee Seungwon An Balachandar Nedumaran Swati Ghosh Keun-Gyu Park Yong Deuk Kim 《BMB reports》2021,54(4):221
Hepcidin (HAMP) is synthesized in the liver. It is a key iron-regulatory hormone that controls systemic iron homeostasis. Cereblon (CRBN) and Kruppel-like factor 15 (KLF15) are known to regulate diverse physiological functions. In this study, we investigated the role of CRBN on hepatic hepcidin gene expression and production under gluconeogenic stimuli. Fasted mice as well as forskolin (FSK)- and glucagon (GLU)-treated mice had reduced serum iron levels but increased expression levels of hepatic Crbn and Klf15 and hepcidin secretion. MicroRNA (miRNA) expression analysis of fasted and Ad-Crbn-infected mice revealed significant reduction of microRNA-639 (miR-639). Hepatic overexpression of Crbn elevated hepcidin expression and production along with Klf15 gene expression, whereas knockdown of Crbn and Klf15 markedly decreased FSK- and fasting-mediated induction of hepcidin gene expression and its biosynthesis in mouse livers and primary hepatocytes. Moreover, expression of KLF15 significantly increased the activity of hepcidin reporter gene. It was exclusively dependent on the KLF15-binding site identified within the hepcidin gene promoter. Overall, this study demonstrates that CRBN and KLF15 are novel mediators of gluconeogenic signal-induced hepcidin gene expression and production. Thus, CRBN and KLF15 might be novel potential therapeutic targets to intervene metabolic dysfunction. 相似文献
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The Wnt signaling pathway is a robust regulator of skeletal homeostasis. Gain-of-function mutations promote high bone mass, whereas loss of Lrp5 or Lrp6 co-receptors decrease bone mass. Similarly, mutations in antagonists of Wnt signaling influence skeletal integrity, in an inverse relation to Lrp receptor mutations. Loss of the Wnt antagonist Sclerostin (Sost) produces the generalized skeletal hyperostotic condition of sclerosteosis, which is characterized by increased bone mass and density due to hyperactive osteoblast function. Here we demonstrate that prostaglandin E(2) (PGE(2)), a paracrine factor with pleiotropic effects on osteoblasts and osteoclasts, decreases Sclerostin expression in osteoblastic UMR106.01 cells. Decreased Sost expression correlates with increased expression of Wnt/TCF target genes Axin2 and Tcf3. We also show that the suppressive effect of PGE(2) is mediated through a cyclic AMP/PKA pathway. Furthermore, selective agonists for the PGE(2) receptor EP2 mimic the effect of PGE(2) upon Sost, and siRNA reduction in Ptger2 prevents PGE(2)-induced Sost repression. These results indicate a functional relationship between prostaglandins and the Wnt/β-catenin signaling pathway in bone. 相似文献
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To investigate the effects of calorie restriction (CR) on behavioral performance and expression of SIRT1 and SIRT5 in rat cerebral tissues. Beginning at 18 months of age, 60 rats were randomly divided into a CR group (n = 30) and a group that remained fed ad libitum (AL; n = 30). CR rats were restricted to a diet of 60% of their daily food consumption. After 6 months of CR, CR rats displayed a maximum 50% reduction in escape latency (AL 20 ± 0.3 s vs. CR 10 ± 0.2 s) and a 3.2 s decrease in time and distance to target when evaluated in Morris water maze tests. The levels of SIRT1 and SIRT5 protein in cerebral tissues of CR rats were elevated compared to AL rats (P < 0.05). CR retarded declines in cognitive ability and enhanced the expression of both SIRT1 and SIRT5 proteins in the cerebral tissue of CR rats compared with AL rats. 相似文献
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Long-distance signals generated in shoots are thought to be associated with the regulation of iron uptake from roots; however,
the signaling mechanism is still unknown. To elucidate whether the signal regulates iron uptake genes in roots positively
or negatively, we analyzed the expressions of two representative iron uptake genes: NtIRT1 and NtFRO1 in tobacco (Nicotiana tabacum L.) roots, after shoots were manipulated in vitro. When iron-deficient leaves were treated with Fe(II)-EDTA, the expressions
of both genes were significantly reduced; nevertheless iron concentration in the roots maintained a similar level to that
in roots grown under iron-deficient conditions. Next, all leaves from tobacco plants grown under the iron-deficient condition
were excised. The expression of two genes were quickly reduced below half within 2 h after the leaf excision and gradually
disappeared by the end of a 24-h period. The NtIRT1 expression was compared among the plants whose leaves were cut off in various patterns. The expression increased in proportion
to the dry weight of iron-deficient leaves, although no relation was observed between the gene expression and the position
of excised leaves. Interestingly, the NtIRT1 expression in hairy roots increased under the iron-deficient condition, suggesting that roots also have the signaling mechanism
of iron status as well as shoots. Taken together, these results indicate that the long-distance signal generated in iron-deficient
tissues including roots is a major factor in positive regulation of the expression of NtIRT1 and NtFRO1 in roots, and that the strength of the signal depends on the size of plants. 相似文献
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Interspecific nematode signals regulate dispersal behavior 总被引:2,自引:0,他引:2
Kaplan F Alborn HT von Reuss SH Ajredini R Ali JG Akyazi F Stelinski LL Edison AS Schroeder FC Teal PE 《PloS one》2012,7(6):e38735
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Abdelmohsen K Pullmann R Lal A Kim HH Galban S Yang X Blethrow JD Walker M Shubert J Gillespie DA Furneaux H Gorospe M 《Molecular cell》2007,25(4):543-557
The RNA binding protein HuR regulates the stability of many target mRNAs. Here, we report that HuR associated with the 3' untranslated region of the mRNA encoding the longevity and stress-response protein SIRT1, stabilized the SIRT1 mRNA, and increased SIRT1 expression levels. Unexpectedly, oxidative stress triggered the dissociation of the [HuR-SIRT1 mRNA] complex, in turn promoting SIRT1 mRNA decay, reducing SIRT1 abundance, and lowering cell survival. The cell cycle checkpoint kinase Chk2 was activated by H(2)O(2), interacted with HuR, and was predicted to phosphorylate HuR at residues S88, S100, and T118. Mutation of these residues revealed a complex pattern of HuR binding, with S100 appearing to be important for [HuR-SIRT1 mRNA] dissociation after H(2)O(2). Our findings demonstrate that HuR regulates SIRT1 expression, underscore functional links between the two stress-response proteins, and implicate Chk2 in these processes. 相似文献
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