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We hypothesize that such additional DNA repair capacity results from the temporal induction of expression of various DNA repair genes specifically in GC B cells, and we term this putative tumor suppressive DNA repair mechanism somatic hyperrepair (SHR).
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Interestingly, these miRNAs can control the expression of various epigenetic modifying enzymes such as DNA methyltransferases (DNMTs), histone methyltransferases (HMTs), and histone deacetylases (HDACs) involved in carcinogenesis processes (Guil and Esteller 2009; Saito and Jones 2006).
This decrease in turn affects the functions of several cellular enzymes involved in pathways that lead to the replication of cellular DNA and the expression of various genes.
Cell lines were acquired between 2004 and 2010; HLA genotype and/or phenotype and expression of various cancer-associated antigens were confirmed by DNA sequencing, RT-PCR, and antibody staining, and lines displayed phenotypic characteristics of the tumor of origin.
An increasing body of evidence suggests a role for epigenetic regulation in the process of AKI and kidney repair, involving remarkable changes in histone modifications, DNA methylation and the expression of various non-coding RNAs.
Some response regulators control bacterial chemotaxis and sporulation, while others serve as DNA-binding transcriptional regulators, controlling expression of various genes.
To better understand the hypersensitivity of germline tumour cells to DNA-damaging drug, we analysed expression of various proteins that are involved in the drug sensitivity of cells.
Further, it is emerging from various studies that DNA methylation has a role in regulating the expression of various bacterial genes related to virulence in several pathogens [34], and methyltransferase genes have been found on pathogenicity islands [35].
Several investigators have demonstrated that DNA methylation plays a major role in the expression of various cancer tissue antigens and immunomodulatory checkpoints [ 19- 21].
These phenotypic changes were accompanied by a significant increase in p16, p21 and p53 expression, as well as a decreased expression of key proteins in various DNA repair pathways such as xrcc2, xrcc3 and ku70.
The combination of high-throughput expression profiling technology and treatment of cells with various DNA methylation inhibitors has been widely used to discover genome-wide effects of these drugs or to identify specific genes involved in the related pathways.
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