全文获取类型
收费全文 | 124篇 |
免费 | 16篇 |
出版年
2021年 | 2篇 |
2019年 | 1篇 |
2018年 | 2篇 |
2017年 | 3篇 |
2016年 | 2篇 |
2015年 | 6篇 |
2014年 | 3篇 |
2013年 | 2篇 |
2012年 | 4篇 |
2011年 | 3篇 |
2010年 | 4篇 |
2009年 | 8篇 |
2008年 | 2篇 |
2007年 | 2篇 |
2004年 | 1篇 |
2003年 | 1篇 |
2002年 | 1篇 |
2001年 | 3篇 |
2000年 | 1篇 |
1999年 | 8篇 |
1998年 | 8篇 |
1997年 | 3篇 |
1996年 | 5篇 |
1995年 | 4篇 |
1994年 | 2篇 |
1993年 | 3篇 |
1992年 | 2篇 |
1991年 | 6篇 |
1990年 | 5篇 |
1989年 | 2篇 |
1988年 | 2篇 |
1987年 | 5篇 |
1986年 | 4篇 |
1985年 | 4篇 |
1984年 | 1篇 |
1983年 | 2篇 |
1982年 | 2篇 |
1981年 | 2篇 |
1980年 | 2篇 |
1979年 | 2篇 |
1978年 | 3篇 |
1977年 | 5篇 |
1976年 | 1篇 |
1975年 | 2篇 |
1974年 | 2篇 |
1973年 | 1篇 |
1971年 | 1篇 |
排序方式: 共有140条查询结果,搜索用时 46 毫秒
91.
Asensio JL; Canada FJ; Bruix M; Gonzalez C; Khiar N; Rodriguez-Romero A; Jimenez-Barbero J 《Glycobiology》1998,8(6):569-577
The specific interaction of hevein with GlcNAc-containing oligosaccharides
has been analyzed by1H-NMR spectroscopy. The association constants for the
binding of hevein to a variety of ligands have been estimated from1H-NMR
titration experiments. The association constants increase in the order
GlcNAc-alpha(1-->6)-Man < GlcNAc < benzyl-beta-GlcNAc <
p-nitrophenyl-beta-GlcNAc < chitobiose < p-
nitrophenyl-beta-chitobioside < methyl-beta-chitobioside <
chitotriose. Entropy and enthalpy of binding for different complexes have
been obtained from van't Hoff analysis. The driving force for the binding
process is provided by a negative DeltaH0which is partially compensated by
negative DeltaS0. These negative signs indicate that hydrogen bonding and
van der Waals forces are the major interactions stabilizing the complex.
NOESY NMR experiments in water solution provided 475 accurate protein
proton-proton distance constraints after employing the MARDIGRAS program.
In addition, 15 unambiguous protein/carbohydrate NOEs were detected. All
the experimental constraints were used in a refinement protocol including
restrained molecular dynamics in order to determine the highly refined
solution conformation of this protein- carbohydrate complex. With regard to
the NMR structure of the free protein, no important changes in the protein
nOe's were observed, indicating that carbohydrate-induced conformational
changes are small. The average backbone rmsd of the 20 refined structures
was 0.055 nm, while the heavy atom rmsd was 0.116 nm. It can be deduced
that both hydrogen bonds and van der Waals contacts confer stability to the
complex. A comparison of the three-dimensional structure of hevein in
solution to those reported for wheat germ agglutinin (WGA) and hevein
itself in the solid state has also been performed. The polypeptide
conformation has also been compared to the NMR-derived structure of a
smaller antifungical peptide, Ac-AMP2.
相似文献
92.
93.
94.
95.
96.
Rapid, sequential changes in surface morphology of PC12 pheochromocytoma cells in response to nerve growth factor 总被引:37,自引:17,他引:20
下载免费PDF全文
![点击此处可从《The Journal of cell biology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
The effect of nerve growth factor (NGF), a substance that promotes the differentiation and maintenance of certain neurons, was studied via scanning electron microscopy utilizing the PC12 clonal NGF-responsive pheochromocytoma cell line. After 2-4 d of exposure to NGF, these cells acquire many of the properties of normal sympathic neurons. However, by phase microscopy, no changes are discernible within the first 12-18 h. Since the primary NGF receptor appears to be a membrane receptor, it seemed likely that some of the initial responses to the factor may be surface related. PC12 cells maintained without NGF are round to ovoid and have numerous microvilli and small blebs. After the addition of NGF, there is a rapidly initiated sequential change in the cell surface. Ruffles appear over the dorsal surface of the cells with 1 min, become prominent by 3 min, and almost disappear by 7 min. Microvilli, conversely, disappear as the dorsal ruffles become prominent. Ruffles are seen at the the periphery of cell at 3 min, are prominent on most of the cells by 7 min and are gone by 15 min. The surface remains smooth from 15 min until 45 min when large blebs appear. The large blebs are present on most cells at 2 h and are gone by 4 h. The surface remains relatively smooth until 6-7 h of NGF treatment, when microvilli reappear as small knobs. These microvilli increase in both number and length to cover the cell surface by 10 h. These changes were not observed with other basic proteins, with α-bungarotoxin (which binds specifically to PC12 membranes), and were not affected by an RNA synthesis inhibitor that blocks initiation of neurite outgrowth. Changes in the cell surface architecture appear to be among the earlist NGF responses yet detected and may represent or reflect primary events in the mechanism of the factor’s action. 相似文献
97.
98.
Regulation is a significant developmental event because successful cell proliferation and migration are critical to shaping young embryos. Regulation -- the replacement of undifferentiated embryonic cells by other cells in response to signals received from the environment -- is distinct from wound healing and regeneration. Investigations on regulation of neural crest cells span all vertebrates and have revealed that regulative ability varies both among classes (even species), and spatially and temporally within individuals. In general, there is greatest regulation for cranial neural crest cells, less for trunk, and virtually none forcardiac. Regulation also appears to be more complete at early embryonic stages. Fate-mapping studies have demonstrated that large regions of neural crest cells must be removed to generate missing or morphologically reduced structures. Recent studies reveal that less extensive neural crest cell extirpations result in normal morphology of cartilaginous and neuronal elements in the head, and normal development of pigmentation in the trunk. Ablation of cardiac neural crest cells frequently generates abnormalities of the heart, great vessels and parasympathetic nerve innervation. Decreased cell death, increased division, change in fate and altered migration are possible cellular mechanisms of regulation. In mostcases, the specific mechanisms of regulation are unknown, but a major premise underlying regulation is that cell potential is greater than cell fate. This concept was born from studies which demonstrated that some cells were able to express alternative fates if transplanted to a new environment. Among the potential cellular mechanisms for regulation, cell migration has received the most attention. Following ablation of neural crest cells, replacement neural crest cells migrate into gaps, most frequently from anterior/posterior locations. Cells from surrounding epidermal and neural ectoderm may have limited regulative ability, while compensation by cells from the ventral neural tube has been demonstrated to an even lesser extent. Regulation by such non-crest cells would require their transformation into neural crest cells. The potential for regulation of neural crest by placodal cells supports a closer relationship between neural crest and placodal ectoderm than previously recognized. Decreased cell death has been discussed primarily with reference to (1) cranial ganglia that have dual contributions from neural crest and placodal cells and (2) programmed cell death in rhombomeres three and five. Increased cell division in response to neural crest ablation is likely more common than has been reported, but this mechanism is difficult to interpret without a 3-D context for viewing how patterns of division differ from normal. Lastly, changes in cell fate may be the driving factor in regulation of embryonic cells. It has been repeatedly demonstrated thatcell potential is greaterthan cell fate. Once reliable mechanisms for assessing cell potential are established, we may find that fates are commonly altered in response to environmental signals. Regulation is therefore significant both as a basic developmental mechanism and as a mechanism for evolutionary change. The more labile the fate of embryonic cells, the more potential there is for maintaining existing characters and for generating new ones. According to Ettensohn (1992, p. 50), further analysis of such systems might . With regard to the neural crest, studies on regulation of this vital population of cells provide insight to the origin of the neural crest, to embryonic repair, and to the source of many craniofacial malformations, heart and other embryonic defects. (ABSTRACT TRUNCATED) 相似文献
99.
RNA polymerase II primes Polycomb‐repressed developmental genes throughout terminal neuronal differentiation
下载免费PDF全文
![点击此处可从《Molecular systems biology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
100.
Previous investigations on the monkey kidney COS cell line demonstrated the
weak expression of fucosylated cell surface antigens and presence of
endogenous fucosyltransferase activities in cell extracts. RT-PCR analyses
have now revealed expression of five homologs of human fucosyltransferase
genes, FUT1, FUT4, FUT5, FUT7, and FUT8, in COS cell mRNA. The enzyme in
COS cell extracts acting on unsialylated Type 2 structures is closely
similar in its properties to the alpha1,3- fucosyltransferase encoded by
human FUT4 gene and does not resemble the product of the FUT5 gene.
Although FUT1 is expressed in the COS cell mRNA, it has not been possible
to demonstrate alpha1,2- fucosyltransferase activity in cell extracts but
the presence of Le(y) and blood-group A antigenic determinants on the cell
surface imply the formation of H-precursor structures at some stage. The
most strongly expressed fucosyltransferase in the COS cells is the
alpha1,6-enzyme transferring fucose to the innermost N -acetylglucosamine
unit in N - glycan chains; this enzyme is similar in its properties to the
product of the human FUT8 gene. The enzymes resembling the human FUT4 and
FUT8 gene products both had pH optima of 7.0 and were resistant to 10 mM
NEM. The incorporation of fucose into asialo-fetuin was optimal at 5.5 and
was inhibited by 10 mM NEM. This result initially suggested the presence of
a third fucosyltransferase expressed in the COS cells but we have now shown
that triantennary N- glycans with terminal nonreducing galactose units,
similar to those present in asialo-fetuin, are modified by a weak
endogenous beta-galactosidase in the COS cell extracts and thereby rendered
suitable substrates for the alpha1,6- fucosyltransferase.
相似文献