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Signal transduction and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Brendan Egan, Adam P. Sharples
The six steps described occur in a temporal manner, such that homeostatic perturbations due to the exercise stimulus produce molecular signals (Step 1) that are sensed by sensor proteins (Step 2), and which, in turn, induce signal transduction (Step 3) and pre-transcriptional/translational regulation via effector proteins (Step 4) occurs during exercise and in the early phase of recovery (minutes to hours). Changes in messenger RNA (mRNA) and protein abundance (Steps 5 and 6) then occur in the hours and day(s) that follow (Figure 7.1). Changes that ultimately result in functional improvements in exercise capacity and performance occur in the following days, weeks and months consequent to cumulative effect of frequent, repeated sessions of exercise (15, 16). Hence, while each individual session of exercise is necessary as a stimulus for adaptation, the long-term adaptation to exercise (i.e. exercise training) is the result of the progressive and cumulative effects of each acute exercise session, thereby leading to a new functional threshold.
Nucleic Acids as Therapeutic Targets and Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
The recently discovered functions of ribonucleic acid suggest that it can no longer be viewed as a passive structure acting only as an intermediary between genomic information and the primary sequence of proteins. It is now recognized that RNA plays much broader roles in cells and is essential for transcriptional and translational regulation, protein function, and catalysis, roles that have previously been reserved for proteins. Therefore, it is regarded as a useful drug target across a number of disease areas including oncology. Although there has been significant progress in targeting RNA with antisense and RNAi-type approaches, there has been less success with discovering small molecules that can selectively bind to RNA with high affinity as genetics probes or potential therapeutic agents. This contrasts sharply with duplex and quadruplex deoxyribonucleic acid structures for which there is an extensive literature on small-molecule binders that can modulate the biological function of DNA and resulting proteins, many of which are well-known anticancer agents (e.g., Sections 5.2–5.6).
The Acute Phase Response: An Overview
Published in Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, Acute Phase Proteins, 2020
Irving Kushner, Andrzej Mackiewicz
In addition to transcriptional control, posttranscriptional events participate in APP regulation. Both in vivo and in vitro studies have suggested that processing or stabilization of mRNAs for various APP may play a role in inducing some APP changes.84-87 In addition, translational regulation has been implicated.63,88
Scleral Remolding-Related Gene Expression After Scleral Collagen Cross-Linking Using Ultraviolet A and Riboflavin in Myopic Guinea Pig Model
Published in Current Eye Research, 2023
Yushan Xu, Lingbo Lai, Zhe Chen, Yuqian Jia, Dengxin Gao, Xiaotong Lv, Yanzheng Song, Mingshen Sun, Yu Li, Fengju Zhang
In addition to the critical role of scleral ECM in determining scleral biomechanics, the scleral fibroblasts were also of primary importance by cellular contraction.26 When responding to mechanical stimuli or signaling factors, fibroblasts differentiated to myofibroblasts, a highly contractile cell typically expressing α-SMA to limit the expansion of surrounding ECM.14,27 Consistent with previous studies,14,28 the present study showed an increased ACTA2 mRNA level of myopic sclera due to the stress of fibroblasts induced by axial elongation. In the myopic sclera after SCXL, ACTA2 mRNA levels lowered; this alteration indicated that SCXL strengthened scleral biomechanics and then prevented axial elongation, and thus the stress on the fibroblasts reduced and fewer fibroblasts differentiated to myofibroblasts. However, there was no significant difference in ACTA2 protein levels between the five groups. One possible explanation for the differences between mRNA and protein levels is attributed to complex post-transcriptional and translational regulation.
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).
6-Gingerols (6G) reduces hypoxia-induced PC-12 cells apoptosis and autophagy through regulation of miR-103/BNIP3
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Chunyang Kang, Mingyang Kang, Yingying Han, Tuo Zhang, Wei Quan, Jian Gao
miRNAs are responsible for the post-translational regulation of mRNA expression through targeting them [24]. BNIP3 belongs to the BH3 subfamily of the Bcl-2 superfamily and is a proapoptotic protein [25]. It has been reported that BNIP3 is increased by the treatment of hypoxia through the activation of hypoxia inducing factor 1 (HIF1) and it is closely related with autophagic and apoptotic cell deaths in response to hypoxia [26–28]. Combined with the roles of 6G on hypoxia-induced apoptosis and autophagy, we inferred that BNIP3 might exert crucial roles in the regulatory mechanism of 6G. Results demonstrated that hypoxia increased BNIP3 expression while 6G had the opposite effect. BNIP3 expression was negatively modulated by miR-103. Furthermore, results from dual luciferase activity assay indicated that BNIP3 was a target of miR-103. BNIP3 upregulation was observed to counteract the neuroprotective effects of 6G on hypoxia-injured PC-12 cells, suggesting that 6G reduced hypoxia-induced PC-12 cells apoptosis and autophagy through up-regulating miR-103 and down-regulating BNIP3.