全文获取类型
收费全文 | 233篇 |
免费 | 43篇 |
出版年
2021年 | 3篇 |
2020年 | 4篇 |
2018年 | 3篇 |
2017年 | 2篇 |
2016年 | 7篇 |
2015年 | 12篇 |
2014年 | 8篇 |
2013年 | 12篇 |
2012年 | 10篇 |
2011年 | 16篇 |
2010年 | 8篇 |
2009年 | 2篇 |
2008年 | 6篇 |
2007年 | 11篇 |
2006年 | 10篇 |
2005年 | 5篇 |
2004年 | 12篇 |
2003年 | 10篇 |
2002年 | 9篇 |
2001年 | 9篇 |
2000年 | 11篇 |
1999年 | 8篇 |
1998年 | 3篇 |
1997年 | 4篇 |
1996年 | 5篇 |
1995年 | 4篇 |
1994年 | 5篇 |
1989年 | 2篇 |
1988年 | 2篇 |
1987年 | 2篇 |
1986年 | 4篇 |
1985年 | 5篇 |
1983年 | 2篇 |
1982年 | 2篇 |
1981年 | 2篇 |
1980年 | 4篇 |
1979年 | 10篇 |
1978年 | 3篇 |
1977年 | 5篇 |
1974年 | 3篇 |
1973年 | 6篇 |
1972年 | 3篇 |
1971年 | 2篇 |
1970年 | 3篇 |
1968年 | 1篇 |
1966年 | 4篇 |
1965年 | 2篇 |
1959年 | 1篇 |
1956年 | 1篇 |
1950年 | 1篇 |
排序方式: 共有276条查询结果,搜索用时 31 毫秒
1.
The ability of isolated rat heart mitochondria to take up coenzyme A (CoA) from the incubation medium was studied. Mitochondria accumulated CoA in a time- and concentration-dependent manner. The accumulation process occurred in two phases. Within the first 30 s of incubation, mitochondrial content of CoA increased, and this phase did not plateau in the concentration range studied. Following this initial increase, a second slower phase of CoA accumulation occurred which plateaued around 50 microM CoA. The initial phase was decreased significantly by ATP or by carboxyatractyloside. In contrast, the presence of ATP or carboxyatractyloside did not affect the second phase. Decreasing the temperature from 30 to 0 degrees C did not affect the initial phase, but the second phase was almost abolished. In the presence of metabolic inhibitors (either 2,4-dinitrophenol or a combination of rotenone and antimycin), the initial "binding" phase was not affected; but the second "uptake" phase was abolished. These results suggest that the first phase of mitochondrial CoA accumulation is probably CoA binding to adenine recognizing sites on the mitochondria while the second phase may represent a specific uptake process for CoA which, although not directly ATP-dependent, is energy-dependent. 相似文献
2.
Pantothenate kinase (ATP:D-pantothenate 4'-phosphotransferase, EC 2.7.1.33), the first enzyme in the pathway of CoA synthesis, was partially purified from rat heart. A study of the properties of the kinase showed that it possesses a broad pH optimum between 6 and 9, is activated or inhibited nonspecifically by various anions, and has MgATP as the nucleotide substrate. The Km for MgATP is 0.6 mM and that for pantothenate is 18 microM. CoA and acyl esters of CoA are inhibitors of the kinase with the inhibition by acetyl-CoA being only slightly greater than that by free CoA. The inhibition by free CoA is uncompetitive with respect to pantothenate concentration, with a Ki for inhibition of 0.2 microM. L-Carnitine was found to be a nonessential activator of the kinase. This compound had no effect by itself but specifically reversed the inhibition of the kinase by CoA. The Ka for deinhibition by L-carnitine is 0.27 mM. Free carnitine content was measured in perfused hearts and is found to vary in correlation with perfusion conditions that are known to alter rates of intracellular phosphorylation of pantothenate. These properties of pantothenate kinase provide a potential mechanism for the control of CoA synthesis. The enzyme is regulated by feedback inhibition by CoA and its acyl esters and this inhibition is modified by changes in the concentration of free carnitine. 相似文献
3.
Codon usage in the vertebrate hemoglobins and its implications 总被引:2,自引:0,他引:2
A study of codon usage in vertebrate hemoglobins revealed an evolutionary
trend toward elevated numbers of CpG codon boundary pairs in mammalian
hemoglobin alpha genes. Selection for CpG codon boundaries countering the
generally observed CpG suppression is strongly suggested by these data.
These observations parallel recently published experimental results that
indicate that constitutive expression of the human alpha-globin gene
appears to be determined by regulatory information encoded within the
structural gene. The possibility is raised that, in the absence of
selection, CpG decay can be used to date the evolutionary origin of a
mammalian alpha pseudogene from its active alpha gene.
相似文献
4.
Evolution of crystallins: expression of lens-specific proteins in the blind mammals mole (Talpa europaea) and mole rat (Spalax ehrenbergi) 总被引:3,自引:0,他引:3
Quax-Jeuken Y; Bruisten S; Bloemendal H; de Jong WW; Nevo E 《Molecular biology and evolution》1985,2(4):279-288
The mole (Talpa europaea; Insectivora) and the mole rat (Spalax ehrenbergi;
Rodentia) both have degenerated eyes as a convergent adaptation to
subterranean life. The rudimentary eye lenses of these blind mammals no
longer function in a visual process. The crystallin genes, which display a
lens-specific expression pattern, were studied in these blind mammals and
in related species with normal eyes by hybridizing their genomic DNAs with
probes obtained from cDNA clones for alpha A-, alpha B-, and beta
Bp-crystallins from calf and gamma 3- crystallin from the rat. For all
crystallin genes examined, the hybridization signals of mole and mole rat
genomic DNA were comparable, respectively, with those of shrew and of rat
and mouse, normal-vision representatives of the orders Insectivora and
Rodentia. The expression of the crystallins at the protein level was tested
by using antiserum specific for alpha-crystallin in immunofluorescence
reactions on lens sections of mole and mole rat eyes and by using antisera
against the beta- and gamma-crystallins on sections of the mole eye. All
antisera gave positive fluorescence reactions exclusively with lens tissue
of these blind mammals, indicating that the crystallins are still normally
expressed despite the fact that these lenses have had no function in a
visual process in these mammals for at least many million years. These
findings apparently imply that some unknown selective advantage has
conserved the crystallin genes and their expression after the loss of
normal function of the lenses.
相似文献
5.
Alice N. Neely Paul B. Nelson Gleen E. Mortimore 《Biochimica et Biophysica Acta (BBA)/General Subjects》1974,338(2):458-472
Livers from nonfasted rats were perfused in situ under conditions known from previous studies in this laboratory to increase or decrease overall endogenous proteolysis. At the termination of the experiments, lysosomal alterations were evaluated by the increase in free acid phosphatase or N-acetyl-β-D-glucosaminidase that occurred when tissue homogenates were subjected to osmotic shock in hypotonic sucrose. In control perfusions, osmotic sensitivity increased spontaneously over unperfused values, reaching maximum by 60 min or earlier. Additions of insulin, amino acid mixtures, or cycloheximide in amounts known to suppress proteolysis prevented this spontaneous perfusion effect or, when added at 60 min, rapidly reversed it. Glucagon alone during perfusion did not increase osmotic sensitivity further; however, stimulation with glucagon was observed when the perfusion effect was suppressed by insulin or cycloheximide. Anoxia, induced by gassing with nitrogen instead of oxygen, markedly reduced the perfusion effect and also doubled the amount of free acid phosphatase in the initial isotonic homogenates. Total acid phosphatase activities in the perfusion experiments were not significantly different from unperfused values and, with the exception of the anoxia perfusions, the amounts of free enzyme present in the initial isotonic sucrose homogenates did not change. 相似文献
6.
In Drosophila pseudoobscura, the amylase (Amy) multigene family is
contained within a series of inversions, or gene arrangements, on the third
chromosome. The Standard (ST), Santa Cruz (SC), and Tree Line (TL)
inversions are central to the phylogeny of arrangements, and have clusters
of other arrangements derived from them. The gene arrangements belonging to
each of these three clusters have a characteristic number of Amy genes,
ranging from three in ST to two in SC to one in TL. This distribution
pattern can reflect a history of either duplications or deletions, although
the data available in the past did not permit a decision between these
alternatives. We provide unambiguous evidence that three Amy genes were
present before the divergence of the ST, SC, and TL arrangements. Thus, the
current status of the Amy multigene family is the result of deletions in
the TL and SC arrangements, which created three new pseudogenes: TL
Amy2-psi, TL Amy3-psi, and SC Amy3- psi. Analysis of pseudogene sequences
revealed that, in the SC and ST arrangements, pseudogene evolution has been
retarded, most likely due to the homogenization effect of gene conversion.
Finally, by determining the original copy number, we have reconstructed the
evolutionary history of the Amy multigene family and linked it with the
evolution of the central gene arrangements.
相似文献
7.
The alpha-amylase (Amy) multigene family in Drosophila pseudoobscura is
located on the third chromosome, which is polymorphic for more than 40
inverted gene arrangements. The number of copies in this family ranges from
one to three, depending on the arrangement in question. A previous study of
the three Amy genes from the Standard (ST) arrangement suggested either
that duplicated copies (Amy2 and Amy3) are functionally constrained or that
they are undergoing gene conversion with Amy1. In order to elucidate
further the pattern of molecular evolution in this family, we cloned and
sequenced four additional Amy genes, two from the Santa Cruz (SC) and two
from the Chiricahua (CH) gene arrangement. Of the two alternatives, only
the hypothesis of gene conversion is supported by the sequence analysis.
The homogenization effect of gene conversion has been strongest in SC,
whose copies differ by only two nucleotides, less noticeable in ST, and
negligible in the CH. Furthermore, the action of gene conversion is
apparently localized, occurring only in the coding region. Interestingly,
these results concur with the findings of other workers for the duplicated
Amy genes in the Drosophila melanogaster group. Thus, the occurrence of
gene conversion in the Amy multigene family seems to be a common feature in
the Drosophila species studied so far.
相似文献
8.
Daily injections of 150 units oxytocin administered to 6 mares on Days 4, 5, 6, 7 and 8 after ovulation (Day 0 = ovulation) failed to induced luteolysis as indicated by the maintenance of normal plasma progestagen concentrations and the occurrence of normal ovulatory intervals. Three additional mares were given oestrogen injections 24 h before an injection of oxytocin on Day 7 after ovulation, but this treatment also failed to induce luteolysis since plasma progestagen concentrations were maintained in all three mares. Two mares exhibited normal ovulatory intervals, while the third developed a corpus luteum which persisted for 46 days. 相似文献
9.
Control of fatty acid metabolism in ischemic and hypoxic hearts 总被引:16,自引:0,他引:16
J T Whitmer J A Idell-Wenger M J Rovetto J R Neely 《The Journal of biological chemistry》1978,253(12):4305-4309
The effects of whole heart ischemia on fatty acid metabolism were studied in the isolated, perfused rat heart. A reduction in coronary flow and oxygen consumption resulted in lower rates of palmitate uptake and oxidation to CO2. This decrease in metabolic rate was associated with increased tissue levels of long chain acyl coenzyme A and long chain acylcarnitine. Cellular levels of acetyl-CoA, acetylcarnitine, free CoA, and free carnitine decreased. These changes in CoA and its acyl derivatives indicate that beta oxidation became the limiting step in fatty acid metabolism. The rate of beta oxidation was probably limited by high levels of NADH and FADH2 secondary to a reduced supply of oxygen. Tissue levels of neutral lipids showed a slight increase durning ischemia, but incorporation of [U-14C]palmitate into lipid was not altered significantly. Although both substrates for lipid synthesis were present in higher concentrations during ischemia, compartmentalization of long chain acyl-CoA in the mitochondrial matrix and alpha-glycerol phosphate in the cytosol may have accounted for the relatively low rate of lipid synthesis. 相似文献
10.
Regulation of fatty acid activation was studied in whole tissue homogenates of rat heart. The palmityl-CoA synthestase activity was proportional to the fatty acid to albumin ratio in the incubation medium with maximal activity occurring at a molar ratio of about 5. Fatty acyl-CoA synthetase activity was inhibited by products of the reaction (AMP, pyrophosphate, and palmityl-CoA). The apparent Ki for palmityl-CoA inhibition was 5 muM and this inhibition could be relieved by CoA-SH or albumin. The Km for CoA-SH in the absence of palmityl-CoA was 7 muM and was increased to 24 muM by addition of 8 muM palmityl-CoA. Cytosolic and mitochondrial levels of CoA-SH and carnitine were estimated in whole tissue homogenates of heart and liver. From 90 to 100% of whole tissue CoA was recovered in the mitochondrial fraction of heart muscle and it was estimated that the cytosolic concentration of free CoA-SH probably never exceeds its Km value for fatty acid activation in this tissue. Therefore, the rate of fatty acid activation would be expected to depend on the availability of CoA-SH in the cytosolic space. By adjusting the concentration of CoA-SH in the cytosol to the rate of acetyl-CoA oxidation, carnitineacetyl-CoA transferase may function in cardiac muscle to couple the rate of fatty acid activation in the cytosolic compartment to acetyl-CoA oxidation in the mitochondria. Approximately 30% of whole tissue CoA-SH was located in the cytosolic space in liver. Heart muscle has about twice as much carnitine as liver but in both tissues 100% of whole tissue carintine was located in the cytosolic space. The ratio of carnitine to CoA-SH in the cytosolic space was estimated to be about 100 in heart and 17 in liver. This high ratio in cardiac muscle may function to channel fatty acids toward oxidation rather than toward synthesis of complex lipids. 相似文献