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To understand the evolution of duplicate genes, we compared rates of
nucleotide substitution between 17 pairs of nonallelic duplicated genes in
the tetraploid frog Xenopus laevis with rates between the orthologous loci
of human and rodent. For all duplicated X. laevis genes, the number of
synonymous substitutions per site (dS) was greater than the number of
nonsynonymous substitutions per site (dN), indicating that these genes are
subject to purifying selection. There was also a significant positive
correlation (r = 0.915) between dN for the X. laevis genes and dN for the
mammalian genes, suggesting that, at the amino acid level, the X. laevis
genes and the mammalian genes are under similar constraints. Results of
relative-rate tests showed nearly equal rates of nonsynonymous substitution
in each copy of the X. laevis genes; apparently there are similar
constraints on both copies. No correlation was found between dS for the X.
laevis genes and dS for the mammalian genes. There was a significant
positive correlation both between members of pairs of duplicated X. laevis
genes (r = 0.951) and between human and rodent orthologues (r = 0.854) with
respect to third- position G+C content but no such relationship between the
X. laevis genes and either of their mammalian orthologues. The results
indicate that both copies of a duplicate gene can be subject to purifying
selection and thus support the hypothesis of selection against all
genotypes containing a null allele at either of two duplicate loci.
相似文献
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Immunochemical identity of peroxisomal enoyl-CoA hydratase with the peroxisome-proliferation -associated 80,000 mol wt polypeptide in rat liver 总被引:6,自引:1,他引:5 下载免费PDF全文
Peroxisome proliferators, which induce proliferation of hepatic peroxisomes, have been shown previously to cause a marked increase in an 80,000 mol wt polypeptide predominantly in the light mitochondrial and microsomal fractions of liver of rodents. We now present evidence to show that this hepatic peroxisome-proliferation-associated polypeptide, referred to as polypeptide PPA-80, is immunochemically identical with the multifunctional peroxisome protein displaying heat-labile enoyl-CoA hydratase activity. This conclusion is based on the following observations: (a) the purified polypeptide PPA-80 and the heat- labile enoyl-CoA hydratase from livers of rats treated with the peroxisome proliferators Wy-14,643 {[4-chloro-6(2,3-xylidino)-2-pyrimidinylthio]acetic acid} exhibit identical minimum molecular weights of approximately 80,000 on SDS polyacrylamide gel electrophoresis; (b) these two proteins are immunochemically identical on the basis of ouchterlony double diffusion, immunotitration, rocket immunoelectrophoresis, and crossed immunoelectrophoresis analysis; and (c) the immunoprecipitates formed by antibodies to polypeptide PPA-80 when dissociated on a sephadex G-200 column yield enoyl-CoA hydratase activity. Whether the polypeptide PPA-80 exhibits the activity of other enzyme(s) of the peroxisomal β-oxidation system such as fatty acyl-CoA oxidase activity or displays immunochemical identity with such enzymes remains to be determined. The availability of antibodies to polypeptide PPA-80 and enoyl-CoA hydratase facilitated immunofluorescent and immunocytochemical localization of the polypeptide PPA- 80 and enoyl-CoA hydratase in the rat liver. The indirect immunofluorescent studies with these antibodies provided direct visual evidence for the marked induction of polypeptide PPA-80 and enoyl-CoA hydratase in the livers of rats treated with Wy-14,643. The present studies also provide immunocytochemical evidence for the localization of polypeptide PPA- 80 and the heat-labile enoyl-CoA hydratase in the peroxisome, but not in the mitochondria, of hepatic parenchymal cells. These studies, therefore, provide morphological evidence for the existence of fatty acyl-CoA oxidizing system in peroxisomes. An increase of polypeptide PPA-80 on SDS polyacrylamide gel electrophoretic analysis of the subcellular fractions of liver of rodents treated with lipid-lowering drugs should serve as a reliable and sensitive indicator of enhanced peroxisomal β- oxidation system. 相似文献
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We have isolated two genomic clones from the murine dystrophin locus, containing single exons encoding protein sequence from the putative actin-binding domain of the amino-terminus and the terminal portion of the triple helical domain. Using interspecific backcross progeny mice, both clones were shown to be X-linked. Sequence analysis indicated that the amino-terminal clone contains a 173 bp exon exhibiting 90% nucleotide sequence identity to human dystrophin exon 6, whilst the C-terminal clone contains a 61 bp exon with 93% nucleotide sequence identity to the human cDNA sequence.The nucleotide sequence data reported in this paper will appear in the EMBL, GenBank and DDBJ nucleotide sequence databases under the accession numbers X58153 and X57745. 相似文献
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Wells DJ Playle LC Enser WE Flecknell PA Gardiner MA Holland J Howard BR Hubrecht R Humphreys KR Jackson IJ Lane N Maconochie M Mason G Morton DB Raymond R Robinson V Smith JA Watt N 《Laboratory animals》2006,40(2):111-114
In 2003, under the auspices of the main UK funders of biological and biomedical research, a working group was established with a remit to review potential welfare issues for genetically altered (GA) mice, to summarize current practice, and to recommend contemporary best practice for welfare assessments. The working group has produced a report which makes practical recommendations for GA mouse welfare assessment and dissemination of welfare information between establishments using a 'mouse passport'. The report can be found at www.nc3rs.org.uk/GAmice and www.lal.org.uk/gaa and includes templates for the recommended welfare assessment scheme and the mouse passport. An overview is provided below. 相似文献
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Sheran HW Law Rudolf SS Wu Patrick KS Ng Richard MK Yu Richard YC Kong 《BMC molecular biology》2006,7(1):15-13
Background
Hypoxia-inducible factors (HIFs) are involved in adaptive and survival responses to hypoxic stress in mammals. In fish, very little is known about the functions of HIFs. 相似文献39.
Nelly Ninis Claire Phillips Linda Bailey Jon I Pollock Simon Nadel Joseph Britto Ian Maconochie Andrew Winrow Pietro G Coen Robert Booy Michael Levin 《BMJ (Clinical research ed.)》2005,330(7506):1475
Objective To determine whether suboptimal management in hospital could contribute to poor outcome in children admitted with meningococcal disease.Design Case-control study of childhood deaths from meningococcal disease, comparing hospital care in fatal and non-fatal cases.Setting National statistics and hospital records.Subjects All children under 17 years who died from meningococcal disease (cases) matched by age with three survivors (controls) from the same region of the country.Main outcome measures Predefined criteria defined optimal management. A panel of paediatricians blinded to the outcome assessed case records using a standardised form and scored patients for suboptimal management.Results We identified 143 cases and 355 controls. Departures from optimal (per protocol) management occurred more frequently in the fatal cases than in the survivors. Multivariate analysis identified three factors independently associated with an increased risk of death: failure to be looked after by a paediatrician, failure of sufficient supervision of junior staff, and failure of staff to administer adequate inotropes. Failure to recognise complications of the disease was a significant risk factor for death, although not independently of absence of paediatric care (P = 0.002). The odds ratio for death was 8.7 (95% confidence interval 2.3 to 33) with two failures, increasing with multiple failures.Conclusions Suboptimal healthcare delivery significantly reduces the likelihood of survival in children with meningococcal disease. Improved training of medical and nursing staff, adherence to published protocols, and increased supervision by consultants may improve the outcome for these children and also those with other life threatening illnesses. 相似文献
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Jigme M Sethi Augustine MK Choi William J Calhoun Bill T Ameredes 《Respiratory research》2008,9(1):45