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The Scientific Basis of Medicine
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Chris O'Callaghan, Rachel Allen
Gene activation can occur in response to various internal or external stimuli through the action of receptor proteins and signalling pathways. The end point of these pathways is usually the expression or activation of one or more DNA-binding proteins that, in turn, stimulates gene expression. In addition to the regulation of transcription, factors such as mRNA stability, transcriptional regulation and differential splicing may influence protein expression.
Cross Talk Between Heat Shock and Oxidative Stress Inducible Genes During Myocardial Adaptation to Ischemia
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Dipak K. Das, Nilanjana Maulik
Although the aforementioned adaptation techniques have been proven beneficial against ischemia reperfusion, the precise mechanism of adaptation remains unknown. Many questions remain unanswered. Are these adaptations interrelated? Most of the stress adaptations cause synthesis of heat shock proteins and/or oxidative stress-inducible proteins. Is there a common link? Stress adaptation also results in the induction of genes. How does the post-transcriptional regulation occur? To answer some of these questions, the heart was adapted to stress by three different methods, ischemic stress, oxidative stress, and heat shock. The results of myocardial adaptation to ischemia were compared by examining the induction of the gene expression and by studying the antioxidant status of the heart and myocardial performance during ischemia and reperfusion following adaptation.
Homeostasis of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
Long-term regulation of TH operates both at the transcriptional and translational levels and includes transcriptional regulation, alternative RNA splicing, changes in RNA stability, translational regulation, and altered enzyme stability. TH expression increases in response to environmental challenges such as stress (which is often mediated by increased glucocorticoid release), hypoxia, and certain drugs (e.g., reserpine, nicotine, and cocaine). Chronic or repeated exposures to stressors, including cold exposure or immobilization, result in increased TH mRNA and protein levels in the brain [7] as well as in the sympathoadrenal system [8]. Several putative transcriptional regulatory elements have been identified within the promoter region of the TH gene. Among these are a glucocorticoid response element (GRE), a cAMP response element (CRE), and an activator protein-1 (AP-1) element. In PC12 cells, both cAMP and phorbol ester increase the transcription rate of the TH gene via CRE through distinct signaling pathways.
Protective effect of Qingluotongbi formula against Tripterygium wilfordii induced liver injury in mice by improving fatty acid β-oxidation and mitochondrial biosynthesis
Published in Pharmaceutical Biology, 2023
Jie Zhou, Ming Li, Zhichao Yu, Changqing Li, Lingling Zhou, Xueping Zhou
Transcriptional regulation is an important way to regulate metabolic processes (Desvergne et al. 2006). Peroxisome proliferator-activated receptor alpha (PPARα), a member of nuclear receptor superfamily, is the master regulator of energy metabolism and lipid catabolism in the liver (Kersten and Stienstra 2017). Previous studies showed that the suppression of PPARα is linked to the hepatotoxic mechanisms of Tripterygium glycosides tablets and Tripterygium wilfordii tablets, two preparations of TW (Dai et al. 2022). PPARα activation can alleviate triptolide-induced liver injury in mice (Hu et al. 2019). The transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) controls multiple hepatic metabolic pathways (Duan et al. 2022), and acts as a coactivator of PPARα to coordinately regulate the transcription of genes related to fatty acid oxidation and mitochondrial biogenesis (Vega et al. 2000). PPARα/PGC-1α pathway plays a central role in the regulation of cellular metabolism (Cheng et al. 2018). The activation of PPARα/PGC-1α can improve mitochondrial function (Kelly and Scarpulla 2004) and reduce lipotoxicity by enhancing lipid metabolism (Kim et al. 2022). We therefore speculate that the hepatic protective effect of QLT is probably related to the PPARα/PGC-1α pathway.
Regulation of flagellar motility and biosynthesis in enterohemorrhagic Escherichia coli O157:H7
Published in Gut Microbes, 2022
Hongmin Sun, Min Wang, Yutao Liu, Pan Wu, Ting Yao, Wen Yang, Qian Yang, Jun Yan, Bin Yang
In addition to transcriptional regulation, post-transcriptional and post-translational regulation play a key role in coordinating flagellar gene expression networks.72 Post-transcriptional regulation is highly versatile and adaptable; it controls RNA availability in cellular time and space.90 Messenger RNA stability, transport, storage, and translation are largely determined by the interaction of mRNA with post-transcriptional regulatory proteins and sRNAs.91,92 Post-translational regulation controls the biochemical alteration of proteins involving generally reversible covalent modification or irreversible processing to regulate their activity, location, or stability.93,94 Post-transcriptional and post-translational regulatory proteins known to regulate EHEC O157:H7 motility and flagellar biosynthesis include CsrA, ClpXP, and Hfq (Figure 6 and Table 1).
Risk of vaso-occlusive episodes in patients with sickle cell disease exposed to systemic corticosteroids: a comprehensive review
Published in Expert Review of Hematology, 2022
Christophe Ferreira de Matos, Thibault Comont, Marie-Pierre Castex, Margaux Lafaurie, Ondine Walter, Guillaume Moulis, Jérémie Dion, Pierre Cougoul
More precisely, in terms of pharmacodynamics, 90% of cortisol is bound to corticosteroid-binding globulins in the blood stream. Free cortisol is the active form of the hormone. In cytoplasm, cortisol bounds with the glucocorticoid receptor (GCR). The GCR is a member of the nuclear receptor superfamily. It has three mechanisms. First, the cortisol–GCR complex activates specific DNA sequences (Glucocorticoid Response Element), allowing the synthesis of anti-inflammatory mediators (annexin-1 and interleukin [IL]-10). The second, the mechanism is an indirect transcription regulation. The complex inhibits the expression of the nuclear factor-κB (NF-κB) pro-inflammatory pathway by binding to NF-κB DNA sequences. In the third mechanism, called the non-genomic pathway, it interacts with membrane-associated pro-inflammatory receptors and second messengers.