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Molecular Biology and Gene Therapy
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
Each DNA molecule is packaged into a chromosome by complex folding of the DNA around proteins. Diploid human cells contain 22 pairs and a pair of sex chromosomes (XX or XY) that determines the sex of the organism. One of each pair of chromosomes is maternally inherited and the other is paternally inherited. The ends of the chromosomes are capped by telomeres, which are specialised structures that are involved in cell mortality. During normal cell division, DNA replication is achieved by the separation of the two strands by DNA helicase. Each separated single strand then acts as a template for forming a new complementary strand.
Antibiotics: The Need for Innovation
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
Protein synthesis is orchestrated by the cell’s DNA. An enzyme called DNA helicase separates the strands at a specific region on the DNA molecule; the gene containing the instruction for a specific protein, such as those like β-lactamase, which give rise to resistance. DNA helicase breaks the hydrogen bonds between the DNA bases, enabling another enzyme, called RNA polymerase to move along the template DNA strand and bind the exposed bases to complementary nucleotides that are present in the cell. This process is known as transcription and results in the production of a stand of RNA, which carries a complementary sequence of bases to the template gene on the DNA.
Werner Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Through its magnesium and ATP-dependent DNA-helicase activity (which unwinds and separates double-stranded DNA) and 3′→5′ exonuclease activity (which trims the broken ends of damaged DNA by removing nucleotides) toward double-stranded DNA with a 5′-overhang, WRN contributes to DNA repair (homologous recombination for DSB repair using the intact sister chromatid during late S and G2 phases, non-homologous end joining [NHEJ] for exogenous DSB repair during the G0 and G1 phases, and base excision for single strand DNA repair), replication, transcription, telomere maintenance, and genome stability. Further, WRN interacts with tumor suppressor p53 via its C-terminus [2,11].
Simple and feasible detection of hepatitis a virus using reverse transcription multienzyme isothermal rapid amplification and lateral flow dipsticks without standard PCR laboratory
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Mao-ling Sun, Yang Zhong, Xiao-na Li, Jun Yao, Yu-qing Pan
Several isothermal technologies have been developed for rapid, feasible nucleic detection. Multienzyme isothermal recombinase amplification (MIRA) is a novel nucleic acid amplification method based on recombinase polymerase amplification (RPA) [17]. This technique utilises four core proteins: recombinase-Rec A, DNA helicase-GP41, single-stranded binding (SSB) protein, and DNA pol I [18]. During amplification, helicase-GP41 and SSB form the D-Loop and start the reaction. Recombinase and DNA pol I then allow DNA extension rapidly at isothermal conditions. For RNA template amplification, specific primers can be used to directly synthesise cDNA using reverse transcriptase [19,20]. Simultaneously, the newly generated cDNA is used as a template for MIRA [21]. The whole reaction can be performed at 25 to 42 °C within 5 to 30 min without requiring complex instruments, providing a major advantage over conventional PCR. The lateral flow dipstick (LFD) can produce visually observable results in a relatively short time by hybridising with labelled colloidal gold [22]. Moreover, it provides a convenient, sensitive, and economical assay when combined with RT-MIRA.
Screening and identification of key genes in imatinib-resistant chronic myelogenous leukemia cells: a bioinformatics study
Published in Hematology, 2021
Hong Zhang, Peiran Wang, Ting Song, Uwituze Laura Bonnette, Zhichao Zhang
MCM protein family is a class of highly conserved proteins which were involved in DNA replication, elongation and transcription. MCM4 is a key component of the minichromosome maintenance protein complex that is necessary for the initiation of DNA replication in eukaryotes. The aberrant expression of MCM4 indicates the proliferation of malignant cells and atypical cells including potential malignant cells. Therefore, MCM4 can be used as an effective marker for the diagnosis of tumors and precancerous lesions [43,44]. Overexpression of MCM4 has also been found in lung, breast and other cancers [45,46]. However, MCM4 has not been identified a biomarker in imatinib-resistant CML cells by biological methods and our work is first time to identify MCM4 as a biomarker in imatinib-resistant CML cells by Bioinformatics. In the previous study, DNA helicase activity of MCM4-6-7 complex inhibited by the phosphorylation by CCNE2-CDK2, indicating that the inhibition of DNA replication because of phosphorylation of MCM4 with CCNE2-CDK2 [44]. We speculate that the effect of imatinib treatment in CML cells was upregulating MCM4 related to cell-cycle phase transition and DNA replication to resistant apoptosis. Our results suggest the combination of MCM4 inhibitor and imatinib may show the synergistic effect in imatinib-resistant CML cells and the potential to decrease tumor regression.
Ras-Mediated Activation of NF-κB and DNA Damage Response in Carcinogenesis
Published in Cancer Investigation, 2020
Few other honorable mentions of the vital DNA damage and repair pathways include Bloom syndrome protein (BLM), that in humans is regulated by BLM gene and possess both DNA-stimulated ATPase and ATP-dependent DNA helicase activities. Mutations may delete or modify the helicase motifs and may incapacitate its helicase function and is somatically altered which becomes the hallmark of a number of cancer types including colorectal cancer (195–198). Similarly Checkpoint kinase 2 (CHEK2) is another tumor suppressor gene that gives the protein CHK2 and regulates genome instability. It is needed in homology directed repair by regulating cell cycle checkpoints in such a way that DNA double strand breaks get correctly repaired. The erroneous activity of CHEK2 is linked with cell cycle checkpoint errors and incorrect DNA repair and tumor development (199–201) (Figure 8).