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71.
Chiu-Chung Young Ta-Chen Lin Mao-Song Yeh Fo-Ting Shen Jo-Shu Chang 《World journal of microbiology & biotechnology》2005,21(8-9):1409-1414
Summary An indigenous strain Gordonia alkanivorans CC-JG39 was isolated from oil-contaminated sludge of a local gas station located in central Taiwan. The bacterial isolate
was able to grow on diesel-containing Bushnell–Haas medium and also tolerate various chemical additives frequently used in
petroleum products (e.g. BETX, methyl-tert-butyl ether, and naphthalene). Kinetics of diesel-limited cell growth and biodegradation
of diesel followed a Monod-type model. The kinetic constants for cell growth (μmax and KS,G) were 0.158 h−1 and 3196 mg/l, respectively, while those for biodegradation of diesel (vmax, diesel and KS,D) were 3.59 mg/h/mg cell and 2874 mg/l, respectively. G. alkanivorans CC-JG39 produced extracellular surface-active material, leading to a low surface tension of nearly 33 mN/m. The CC-JG39 strain
also possessed the ability to float towards the oil/water interface. These features might play some roles in enhancing the
mass transfer efficiency between oil substrate and the bacterial cells. Therefore, G. alkanivorans CC-JG39 may have potential applications in bioremediation of oil pollution sites. 相似文献
72.
73.
Molecular cloning and characterization of human AOS1 and UBA2, components of the sentrin-activating enzyme complex 总被引:10,自引:0,他引:10
Sentrin-1/SUMO-1 is a novel ubiquitin-like protein, which can covalently modify a limited number of cellular proteins. Here we report the identification of the sentrin-activating enzyme complex, which consists of two proteins AOS1 and UBA2. Human AOS1 is homologous to the N-terminal half of E1, whereas human UBA2 is homologous to the C-terminal half of E1. The human UBA2 gene is located on chromosome 19q12. Human UBA2 could form a beta-mercaptoethanol-sensitive conjugate with members of the sentrin family, but not with ubiquitin of NEDD8, in the presence of AOS1. Identification of human UBA2 and AOS1 should allow a more detailed analysis of the enzymology of the activation of ubiquitin-like proteins. 相似文献
74.
75.
Chen GS Chen CS Chien TC Yeh JY Kuo CC Talekar RS Chern JW 《Nucleosides, nucleotides & nucleic acids》2004,23(1-2):347-359
The Mitsunobu reaction was applied to prepare, in one step, purine N(3),5'-cyclonucleosides 10a-d. A subsequent ring opening in the ribose moiety of the resultant N(3),5'-nucleosides by sodium periodate led to the corresponding N(3),5'-cyclo-2',3'-seconucleosides. These products consist of 5-, 6-, and 7-membered tricyclic system which is the basic skeleton of TIBO derivatives, known antiviral agents. 相似文献
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77.
Our recent study indicated that polyglutamine-expanded ataxin-7-Q75 induced apoptotic death of cultured cerebellar neurons by downregulating Bcl-x(L) expression and activating mitochondrial apoptotic cascade. Mutant polyglutamine-expanded proteins are believed to impair the proteolytic function of ubiquitin-proteasome system by sequestering components of proteasomes. Proteasome degradation of IkappaBalpha permits nuclear translocation of NF-kappaB and is required for continuous NF-kappaB activity, which supports the survival of cultured cerebellar neurons by inducing Bcl-x(L) expression. Thus, we tested the hypothesis that mutant ataxin-7-Q75 causes proteasome dysfunction and impairs NF-kappaB activity, leading to reduced Bcl-x(L) expression, caspase activation and cerebellar neuronal death. EMSA assays indicate that DNA-binding activity of NF-kappaB was significantly decreased in cerebellar neurons expressing ataxin-7-Q75. Similar to mutant ataxin-7-Q75, NF-kappaB inhibitor APEQ induced cerebellar neuronal death by decreasing Bcl-x(L) expression and activating caspase-9. Mutant ataxin-7-Q75 inhibited the proteolytic activity of proteasomes in cerebellar neurons. Proteasome inhibitor MG132 also caused cerebellar neuronal death by decreasing Bcl-x(L) expression and activating caspase-9. Both ataxin-7-Q75 and MG132 caused the cytosolic accumulation of IkappaBalpha in cerebellar neurons. Mutant ataxin-7-Q75 or MG132 increased the cytosolic level of NF-kappaB p65 and decreased the nuclear NF-kappaB p65 level. Our study provides the evidence that polyglutamine-expanded ataxin-7-Q75 decreases nuclear translocation of NF-kappaB p65 and impairs NF-kappaB activity by inhibiting proteasome activity of cerebellar neurons. 相似文献
78.
Loss of transferrin receptors following induced differentiation of HL-60 promyelocytic leukemia cells 总被引:8,自引:0,他引:8
Human promyelocytic leukemia (HL-60) and lymphoblastoid (Daudi) cells were studied: for transferrin receptors before and after induced differentiation with dimethyl sulfoxide (DMSO), sodium butyrate or retinoic acid. None of these reagents affected the morphology or presentation of receptors in Daudi cells, but many HL-60 morphologically matured to banded neutrophils and demonstrated a concomitant loss of transferrin binding, suggesting an important role for transferrin receptors in cellular differentiation. 相似文献
79.
OBJECTIVE: We examined the effect of vitamin D supplementation on bone growth in young rats fed a normal or low calcium diet. METHODS: Fifty female Sprague-Dawley rats, 6 weeks of age, were randomized by stratified weight method into five groups with 10 rats in each group: baseline control, 0.5% (normal) or 0.1% (low) calcium diet, and 0.5 or 0.1% calcium diet + vitamin D (25 microg/100 g, food intake). Duration of the experiment was 10 weeks. RESULTS: Vitamin D supplementation stimulated intestinal calcium absorption and increased urinary calcium excretion in rats fed a low or normal calcium diet. Vitamin D supplementation prevented the reduction in periosteal bone gain but enhanced enlargement of the marrow cavity and reduced the maturation-related cancellous bone gain in rats fed a low calcium diet, and increased the maturation-related cancellous and cortical bone gains in rats fed a normal calcium diet. CONCLUSION: This study shows the differential effects of vitamin D supplementation on born growth in young rats fed a normal or low calcium diet. 相似文献
80.
SP Yeh YM Liao WJ Lo CL Lin LY Bai CY Lin CY Hsieh YC Chang YT Huang CF Chiu 《PloS one》2012,7(9):e44416