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Translation
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
The functional PP7 homology to the coliphages was further confirmed by the structural alignments (Olsthoorn et al. 1995a). The regulatory RNA secondary structure features that were present in the coliphages were also identified in the PP7 RNA, although the sequences were hard to align. Among such intrinsic elements were the coat protein binding helix at the start of the replicase gene, the replicase binding site, and the structure of the coat protein gene start. Some of these features resembled the MS2-type coliphages but others the Qβ type. These structures will be analyzed in more detail below in the sections devoted to the repressor complexes I and II. The similar functional homology to coliphages was also revealed when the full-length genome of the caulophage φCB5 was sequenced (Kazaks et al. 2011). By analogy to the coliphages, the phage PRR1 coat recognized its RNA and formed the structure similar to the complex I (Persson et al. 2013).
Disease Prediction and Drug Development
Published in Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam, Introduction to Computational Health Informatics, 2019
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam
Gene-to-protein translation involves the use of a specific protein that transcribes the DNA to mRNA that acts as a template for the translation of DNA to the corresponding protein. The gene translation process involves: 1) transcription of DNA → mRNA, 2) mRNA moving through a ribosome, 3) polymerase creating a chain of amino acids brought by tRNA into ribosomes based upon the codons in mRNA and so on 4) maturation of a chain of amino-acids to protein. During transcription, enhancers (or repressors) play a major role. Enhancers increase the transcription-rate. Conversely, repressors suppresses the transcription-rate.
Notes on Genetic and Radiation Control of Senescence
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
DNA, DNA repair, and the enzymes involved show little or no change with age; however, the histone content and binding activity do. In 1962 Benzer and Champe suggested that a “suppressor mutation”, a hereditary alteration of the genetic code, must exist to explain the mutations of phage T4 in several bacterial hosts.264 Ptashne summarized genetic experiments that indicated that a group of genes can be inactivated by a regulator gene or “supressor” gene.265 The postulated mechanism is that an isolated repressor binds with high affinity to DNA — and in doing so blocks transcription from DNA to RNA. A number of investigations indicate that histone binding is the effector of gene suppression.234,246,266–271 Von Hahn suggested that histone blocks DNA by cross-linking with it.246 The degree of histone binding increases with age.269 Supressed genes in normal cells may be active in neoplastic ones.272,273 Gene expression is readily reversible, indicating the existence of an “on-off” switch mechanism.271,273
The involvement of regulatory T cells in amyotrophic lateral sclerosis and their therapeutic potential
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
I. Giovannelli, P. Heath, P. J. Shaw, J. Kirby
Clearly, FOXP3 has a crucial role for Tregs. It is a transcriptional regulator which is fundamental for their development and function. It can act both as a transcriptional activator or repressor because it interacts with several transcription factors and proteins involved in epigenetic regulation (13). In particular, it prevents the transcription of pro-inflammatory cytokines such as IL-2 and IFN-γ and it concomitantly activates immune suppressors including cytotoxic T lymphocyte antigen 4 (CTLA4) (13). Furthermore, other key markers for Tregs are glucocorticoid-induced tumor necrosis factor receptor (GITR) and inducible T cell co-stimulator (ICOS). GITR, also referred to as TNFRSF18, plays a role in Treg suppressive activities, in fact, antibodies against GITR can abrogate Treg immune modulatory functions, and it is also crucial for thymus Tregs differentiation process (14–16). ICOS is a costimulatory molecule which is known to exert various roles within the immune system, participating both to inflammatory and suppressive processes (17). However, ICOS appears to play a role in Treg functions. In fact, the blockage of ICOS interaction with its ligand (ICOSL) causes a decrease in the expression of CTLA4 and ICOS deficiency induces reduction in FOXP3 expression (18,19).
Mechanisms of antimicrobial resistance in Stenotrophomonas maltophilia: a review of current knowledge
Published in Expert Review of Anti-infective Therapy, 2020
Teresa Gil-Gil, José Luis Martínez, Paula Blanco
Besides contributing to intrinsic resistance, the SmeDEF efflux system is also involved in the acquisition of antibiotic resistance through mutations in SmeT [53]. These changes are located in the DNA-binding domain of this repressor, hence impeding its binding to its cognate operator sequence [82]. Under this situation both smeDEF and smeT are overexpressed [53,55]. It is important to highlight that, differing to the situation in other bacteria, it has been reported that the acquisition of resistance to quinolones in S. maltophilia involves mutations leading to the overexpression of this efflux system, and not in the genes encoding the quinolones targets, the bacterial topoisomerases [23,83,84]. Even when changes in gyrA or parC have been found, no significant difference was observed in their prevalence between fluoroquinolone resistant and susceptible isolates, suggesting that they correspond to natural allelic forms of the genes, not to mutations selected by quinolones [85]. More recently, it has been described that exposure to tigecycline also leads to the selection of mutations in SmeT, leading to smeDEF overexpression and acquired resistance against this antibiotic as well as to other drugs [86].
Beyond EZH2: is the polycomb protein CBX2 an emerging target for anti-cancer therapy?
Published in Expert Opinion on Therapeutic Targets, 2019
Maïka Jangal, Benjamin Lebeau, Michael Witcher
Based on the work described above CBX2 is predicted to be an emerging therapeutic target [89]. CBX2 genomic amplification and higher levels of CBX2 mRNA may predict a poor overall survival in multiple cancer types [53]. Emerging data indicates CBX2 may promote metastasis [80]. Importantly, two publications carrying out knockdown of CBX2 found similar phenotypes in that CBX was essential for the proliferation of both prostate cancer and AML cells [89,95]. Understandably, gene regulation by CBX2 has focused on repressive aspects of the PRC1 complex. Unexpectedly, overexpression of CBX2 leads to increased expression of mRNAs involved in stem cell maintenance and tumor initiation such as SOX9 [48] and additional mitogenic factors such as FGF2 [96]. The mechanism for this remains obscure but may be through indirect transcriptional downregulation of a repressor. Further reports will be required to confirm this data, as it appears to contradict a role for CBX2 in promoting differentiation of stem cell populations [52].