Browsing by Subject "Codon"

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Open Access
DNA codon recognition by a cubane wire: In silico approach
(DergiPark, 2021) Mirzaei, M.; Hadipour, N.; Gülseren, Oğuz
DNA codons, consisting of triplet nucleotides (NTs), could play important roles for RNA transcription and protein translation in living systems. Therefore, their recognition could be seen important for diagnosis and therapy purposes. Based on triplet sequence formations of Adenine (A), Guanine (G), Cytosine (C) and Thymine (T) NTs, 64 codons were investigated in this work regarding their complexation with a molecular cubane (CUB) wire. To achieve this aim, each of singular 64 codons and CUB were optimized to be prepared for docking processes of complex formations. Hence, 64 complexes of codon-CUB were docked to see the recognition potency of CUB wire versus each of DNA codons. Interestingly, the obtained docking scores indicated that the CUB could work specifically versus the DNA codons, in which G-rich and A-rich triples were seen to be more favorable for complexation with CUB in comparison with other C-rich and T-rich triplet codons. Moreover, the results indicated that not pure G triplet but GAG codon was the most favorable one to be recognized by the CUB wire. However, pure T triplet was the worst one for such complex formations. The results of this work remarkably indicated that the CUB wire could work for recognition process of DNA codons from each other and such recognition could be very much specified for each of G-rich and A-rich codons, in which GAG codon was the best one among all the 64 investigated codons.
Open Access
p53 mutation with frequent novel codons but not a mutator phenotype in BRCA1-and BRCA2-associated breast tumours
(Nature Publishing Group, 1998) Crook, T.; Brooks, L. A.; Crossland, S.; Osin, P.; Barker, K. T.; Waller, J.; Philp, E.; Smith, P. D.; Yulug, I.; Peto, J.; Parker, G.; Allday, M. J.; Crompton, M. R.; Gusterson, B. A.
The status of p53 was investigated in breast tumours arising in germ-line carriers of mutant alleles of BRCA1 and BRCA2 and in a control series of sporadic breast tumours. p53 expression was detected in 20/26 (77%) BRCA1-, 10/22 (45%) BRCA2-associated and 25/72 (35%) grade-matched sporadic tumours. Analysis of p53 sequence revealed that the gene was mutant in 33/50 (66%) BRCA-associated tumours, whereas 7/20 (35%) sporadic grade-matched tumours contained p53 mutation (P < 0.05). A number of the mutations detected in the BRCA-associated tumours have not been previously described in human cancer databases, whilst others occur extremely rarely. Analysis of additional genes, p16(INK4), Ki-ras and β-globin revealed absence or very low incidence of mutations, suggesting that the higher frequency of p53 mutation in the BRCA-associated tumours does not reflect a generalized increase in susceptibility to the acquisition of somatic mutation. Furthermore, absence of frameshift mutations in the polypurine tracts present in the coding sequence of the TGF β type II receptor (TGF β IIR) and Bax implies that loss of function of BRCA1 or BRCA2 does not confer a mutator phenotype such as that found in tumours with microsatellite instability (MSI). p21(Waf1) was expressed in BRCA-associated tumours regardless of p53 status and, furthermore, some tumours expressing wild-type p53 did not express detectable p21(Waf1). These data do not support, therefore, the simple model based on studies of BRCA-/- embryos, in which mutation of p53 in BRCA-associated tumours results in loss of p21(Waf1) expression and deregulated proliferation. Rather, they imply that proliferation of such tumours will be subject to multiple mechanisms of growth regulation.