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Structures
Published in Thomas M. Nordlund, Peter M. Hoffmann, Quantitative Understanding of Biosystems, 2019
Thomas M. Nordlund, Peter M. Hoffmann
The primary carriers of energy, in their ready-to-use form, in biological systems are adenosine triphosphate (ATP) and guanosine triphosphate (GTP). Structures of both are shown in Figure 5.6. Energy is extracted from ATP or GTP by removal of the outermost phosphate group, releasing about 20kBTr ~ 8 × 10–20 J or 50 kJ/mol. We have just noted that independent phosphate groups exist in four forms, with charge ranging from –3 to 0: PO43−,HPO42−,H2PO4−, and H3PO4. In ATP and GTP, two of the phosphates have bonding that prevents ionization of two of the phosphate OH groups. The end phosphate group has two OH groups that can ionize. Thus an ATP or GTP can exist in four forms, with charge ranging from 0 to –4: H4ATP, H3ATP–, H2ATP2–, HATP3–, and ATP4–. Between pH 6.5 and 7.5, the H2ATP2–, HATP3–, and ATP4– species are most numerous. In cells, ATP is often associated with Mg++, MgATP2-, because of stronger binding of Mg++. Mg++ turns out to be an important factor governing the structure of DNA.
Computational modeling of inhibitory signal transduction in urinary bladder PDGFRα+ cells
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Amritanshu Gupta, Rohit Manchanda
In animal models, it has been demonstrated that nitric oxide (NO) induces dSMC relaxation, and the application of nitric oxide synthase (NOS) inhibitors reduced detrusor contractions (Mumtaz et al. 2000; Mamas et al. 2003). NO acts in target tissues via the nitric oxide-soluble guanyl cyclase-cyclic guanosine monophosphate (NO-sGC-cGMP) pathway. However, in isolated guinea pig bladder preparations, the application of the NO donor sodium nitroprusside did not raise cyclic guanosine monophosphate (cGMP) levels in the dSMCs suggesting the involvement of an indirect pathway for mediation of NO-induced relaxation (Gillespie and Drake 2004). This indirect pathway could be via NO action on PDGFRα+ cells, which express the nitric oxide sensitive soluble guanylyl cyclase (NO-sGC) and exhibit intense cGMP immunoreactivity (Blair et al. 2014).
The polymorphisms in cGAS-STING pathway are associated with mitochondrial DNA copy number in coke oven workers
Published in International Journal of Environmental Health Research, 2022
Xiaohua Liu, Xinling Li, Wan Wei, Yahui Fan, Zhifeng Guo, Xiaoran Duan, Xiaoshan Zhou, Yongli Yang, Wei Wang
The cGAS-STING pathway plays an important role in DNA damage response, transcriptional induction of type I interferons, and nuclear factorκBdependent expression of proinflammatory cytokines (Motwani et al. 2019). When PAHs cause damage to mitochondria, mtDNA can be released into the cytoplasm from mitochondria. The cGAS genes, located on chromosome 6, encode DNA-sensing nucleotidyl transferase enzymes, which can detect damaged DNA that was released into the cytosol. Upon DNA binding, cGAS produces cyclic guanosine monophosphate adenosine monophosphate and then activates the adaptor protein STING (Chen et al. 2016), ultimately promote immunity and influence nuclear DNA repair. STING genes, located on chromosome 5, have a cGAS-independent innate immune response activation in response to DNA damage (Unterholzner and Dunphy 2019). Besides, STING also has been confirmed to maintain cell homeostasis by regulating the cell cycle, whereas loss of STING will cause the cells to enter the S phase and mitosis prematurely, leading to smaller cell size and increased chromosome instability (Ranoa et al. 2019). Thus, it is likely that the STING gene affects mtDNAcn by regulating the cell cycle. Therefore, genetic variations in the cGAS-STING pathway may influence mtDNAcn. In this study, we focused on eight single-nucleotide polymorphisms in the cGAS-STING pathway to explore the effects of PAHs exposure and gene variants on mtDNAcn.
A review on state of art and perspectives of Metal-Organic frameworks (MOFs) in the fight against coronavirus SARS-CoV-2
Published in Journal of Coordination Chemistry, 2021
From the biochemically and structurally point of view, SARS-CoV-2 is composed of approximately 29,900 bases, which encode 16 non-structural and 4 structural proteins designed as nsp1 - nsp16, which are essential for the SARS-CoV-2 life cycle [29]. Viral RNA is protected from the innate immunity of cells by a cap that forms a specific arrangement at the 5′ end of the RNA molecule. The arrangement consists of C2'-O-methyl-ribosyladenine and N-methylated guanosine triphosphate, which resembles native host cell mRNA. In human cells, the cap is installed on newly transcribed mRNA already present in the nucleus, to which coronaviruses do not have access. Instead, SARS-CoV-2 possess their own enzymes that synthesize caps, through which they are involved in the cell cycle [30] and subsequently causes COVID-19 disease.