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31.
Roger J. Mulder Cynthia M. Shafer Doralyn S. Dalisay Tadeusz F. Molinski 《Bioorganic & medicinal chemistry letters》2009,19(11):2928-2930
Analogs of the potent antifungal agent, bengazole A, were prepared and evaluated against Candida spp. in both microbroth dilution and disk diffusion assays. 相似文献
32.
Evan W. Rogers Doralyn S. Dalisay Tadeusz F. Molinski 《Bioorganic & medicinal chemistry letters》2010,20(7):2183-2185
Analogs and diastereomers of the natural product zwittermicin A were prepared. SAR studies of these compounds reveal the antifungal activity to be dependent singularly upon the natural constitution and configuration. 相似文献
33.
Evolutionary relatedness of some primate models of Plasmodium 总被引:1,自引:0,他引:1
Primate--and, specifically, monkey--malaria infections are commonly used
for understanding the pathology of and immune response to the human disease
because they are thought to resemble most closely the host-parasite
relationship found in humans. Plasmodium cynomolgi is used extensively as a
model for the human parasite, P. vivax, and P. knowlesi is used primarily
as a model for the development of erythrocytic-stage vaccines. Both of
these simian parasites can naturally infect man, resulting in mildly
symptomatic episodes of the disease. The phylogenetic relationship between
these two simian parasites and previously characterized Plasmodium species,
including P. vivax, was examined by comparison of the asexually expressed
small- subunit ribosomal RNA genes. Our analysis confirmed that P. vivax is
most closely related to P. cynomolgi and that it remains an appropriate
model of the human pathogen. Furthermore, with P. knowlesi and P. fragile,
these two species form a group of closely related species, distant from
other Plasmodium species. What is considered to be the most ancient of the
human malaria pathogens, P. malariae, was also included in the analysis and
does not group at all with other simian or human parasites.
相似文献
34.
Blaise?TF?Alako Antoine?Veldhoven Sjozef?van Baal Rob?Jelier Stefan?Verhoeven Ton?Rullmann Jan?Polman Guido?JensterEmail author 《BMC bioinformatics》2005,6(1):51
Background
High throughput microarray analyses result in many differentially expressed genes that are potentially responsible for the biological process of interest. In order to identify biological similarities between genes, publications from MEDLINE were identified in which pairs of gene names and combinations of gene name with specific keywords were co-mentioned. 相似文献35.
Comprehensive mapping of cystic fibrosis mutations to CFTR protein identifies mutation clusters and molecular docking predicts corrector binding site
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Steven V. Molinski Vijay M. Shahani Adithya S. Subramanian Stephen S. MacKinnon Geoffrey Woollard Marcon Laforet Onofrio Laselva Leonard D. Morayniss Christine E. Bear Andreas Windemuth 《Proteins》2018,86(8):833-843
Cystic Fibrosis (CF) is caused by mutations in the CFTR gene, of which over 2000 have been reported to date. Mutations have yet to be analyzed in aggregate to assess their distribution across the tertiary structure of the CFTR protein, an approach that could provide valuable insights into the structure‐function relationship of CFTR. In addition, the binding site of Class I correctors (VX‐809, VX‐661, and C18) is not well understood. In this study, exonic CFTR mutations and mutant allele frequencies described in 3 curated databases (ABCMdb, CFTR1, and CFTR2, comprising >130 000 data points) were mapped to 2 different structural models: a homology model of full‐length CFTR protein in the open‐channel state, and a cryo‐electron microscopy core‐structure of CFTR in the closed‐channel state. Accordingly, residue positions of 6 high‐frequency mutant CFTR alleles were found to spatially co‐localize in CFTR protein, and a significant cluster was identified at the NBD1:ICL4 interdomain interface. In addition, immunoblotting confirmed the approximate binding site of Class I correctors, demonstrating that these small molecules act via a similar mechanism in vitro, and in silico molecular docking generated binding poses for their complex with the cryo‐electron microscopy structure to suggest the putative corrector binding site is a multi‐domain pocket near residues F374‐L375. These results confirm the significance of interdomain interfaces as susceptible to disruptive mutation, and identify a putative corrector binding site. The structural pharmacogenomics approach of mapping mutation databases to protein models shows promise for facilitating drug discovery and personalized medicine for monogenetic diseases. 相似文献
36.
The mutation rates of di-, tri- and tetranucleotide repeats in Drosophila melanogaster 总被引:3,自引:1,他引:3
Schug MD; Hutter CM; Wetterstrand KA; Gaudette MS; Mackay TF; Aquadro CF 《Molecular biology and evolution》1998,15(12):1751-1760
In a recent study, we reported that the combined average mutation rate of
10 di-, 6 tri-, and 8 tetranucleotide repeats in Drosophila melanogaster
was 6.3 x 10(-6) mutations per locus per generation, a rate substantially
below that of microsatellite repeat units in mammals studied to date (range
= 10(-2)-10(-5) per locus per generation). To obtain a more precise
estimate of mutation rate for dinucleotide repeat motifs alone, we assayed
39 new dinucleotide repeat microsatellite loci in the mutation accumulation
lines from our earlier study. Our estimate of mutation rate for a total of
49 dinucleotide repeats is 9.3 x 10(-6) per locus per generation, only
slightly higher than the estimate from our earlier study. We also estimated
the relative difference in microsatellite mutation rate among di-, tri-,
and tetranucleotide repeats in the genome of D. melanogaster using a method
based on population variation, and we found that tri- and tetranucleotide
repeats mutate at rates 6.4 and 8.4 times slower than that of dinucleotide
repeats, respectively. The slower mutation rates of tri- and
tetranucleotide repeats appear to be associated with a relatively short
repeat unit length of these repeat motifs in the genome of D. melanogaster.
A positive correlation between repeat unit length and allelic variation
suggests that mutation rate increases as the repeat unit lengths of
microsatellites increase.
相似文献