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611.
Ultrastructure of initial crystal formation in dentin 总被引:5,自引:0,他引:5
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Both plasmid pPFC4, which contains 10.6 kb, and a derivative of pPFC4—viz., pPFC4-4.6—which contains 4.6 kb ofPseudomonas fluorescens subsp.cellulosa DNA, direct the synthesis of six distinct endoglucanases inEscherichia coli. Two of these enzymes were purified to homogeneity in a single step by means of anion exchange HPLC. One enzyme has a molecular weight of 30.0 ± 1.0 kDa, an isoelectric point of 7.5, and a specific activity of 3470 U of activity/mg of protein, whereas the other has a molecular weight of 38.5 ± 1.0 kDa, an isoelectric point of 6.7, and a specific activity of 18,050 U of activity/mg of protein. On the basis of the amino acid composition, the 38.5 kDa enzyme appears to be a modified version of the 30.0 kDa enzyme. Thus, the multiplicity of endoglucanases produced inE. coli/pPFC4-4.6 cells may be owing to the posttranslational modification of a smaller number of primary translation products. 相似文献
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S D Glick 《Life sciences》1985,36(5):499-503
An attempt was made to breed strains of strongly and weakly rotating rats. A strain difference in rotation parameters was limited to females and developed gradually over eight generations before asymptoting. Unexpectedly, a left-sided population bias developed in both male and female rats bred for weak rotation. It is suggested that testosterone modulates several aspects of the inheritance of cerebral lateralization. 相似文献
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Ian R Mackenzie Stefanie L Butland Rebecca S Devon Emily Dwosh Howard Feldman Caroline Lindholm Scott J Neal Francis BR Ouellette Blair R Leavitt 《BMC neurology》2006,6(1):32-7
Background
Many cases of frontotemporal dementia (FTD) are familial, often with an autosomal dominant pattern of inheritance. Some are due to a mutation in the tau- encoding gene, on chromosome 17, and show an accumulation of abnormal tau in brain tissue (FTDP-17T). Most of the remaining familial cases do not exhibit tau pathology, but display neuropathology similar to patients with dementia and motor neuron disease, characterized by the presence of ubiquitin-immunoreactive (ub-ir), dystrophic neurites and neuronal cytoplasmic inclusions in the neocortex and hippocampus (FTLD-U). Recently, we described a subset of patients with familial FTD with autopsy-proven FTLD-U pathology and with the additional finding of ub-ir neuronal intranuclear inclusions (NII). NII are a characteristic feature of several other neurodegenerative conditions for which the genetic basis is abnormal expansion of a polyglutamine-encoding trinucleotide repeat region. The genetic basis of familial FTLD-U is currently not known, however the presence of NII suggests that a subset of cases may represent a polyglutamine expansion disease. 相似文献620.