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51.
52.
Position effect variegation in Drosophila: towards a genetics of chromatin assembly 总被引:31,自引:0,他引:31
J C Eissenberg 《BioEssays : news and reviews in molecular, cellular and developmental biology》1989,11(1):14-17
The formation of a highly condensed chromosome structure (heterochromatin) in a region of a eukaryotic chromosome can inactivate the genes within that region. Genetic studies using the fruitfly Drosophila melanogaster have identified several essential genes which influence the formation of heterochromatin. My purpose in this review is to summarize some recent work on the genetics of heterochromatin assembly in Drosophila and a recent model for how chromosomal proteins may interact to form a heterochromatic structure. 相似文献
53.
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56.
Recognizing the forest for the trees: testing temporal patterns of cladogenesis using a null model of stochastic diversification 总被引:2,自引:1,他引:1
Computer simulations are developed and employed to examine the expected
temporal distributions of nodes under a null model of stochastic lineage
bifurcation and extinction. These Markovian models of phylogenetic process
were constructed so as to permit direct comparisons against empirical
phylogenetic trees generated from molecular or other information available
solely from extant species. For replicate simulated phylads with n extant
species, cumulative distribution functions (cdf's) of branching times were
calculated, and compared (using the Kolmogorov-Smirnov test statistic D) to
those from three published empirical trees. Molecular phylogenies for
columbine plants and avian cranes showed statistically significant
departures from the null expectations, in directions indicating recent and
ancient species' radiations, respectively, whereas a molecular phylogeny
for the Drosophila virilis species group showed no apparent historical
clustering of branching events. Effects of outgroup choice and phylogenetic
frame of reference were investigated for the columbines and found to have a
predictable influence on the types of conclusions to be drawn from such
analyses. To enable other investigators to statistically test for
nonrandomness in temporal cladogenetic pattern in empirical trees generated
from data on extant species, we present tables of mean cdf's and associated
probabilities under the null model for expected branching times in phylads
of varying size. The approaches developed in this report complement and
extend those of other recent methods for employing null models to assess
the statistical significance of pattern in evolutionary trees.
相似文献
57.
Regulation of the Drosophila melanogaster protein, enhancer of rudimentary, by casein kinase II 下载免费PDF全文
Gelsthorpe ME Tan Z Phillips A Eissenberg JC Miller A Wallace J Tsubota SI 《Genetics》2006,174(1):265-270
The Drosophila melanogaster gene enhancer of rudimentary, e(r), encodes a conserved protein, ER. Most ER homologs share two casein kinase II (CKII) target sites. In D. melanogaster, these sites are T18 and S24. A third CKII site, T63, has been seen only in drosophilids. The conservation of these CKII sites, particularly T18 and S24, suggests a role for these residues in the function of the protein. To test this hypothesis, these positions were mutated either to alanine as a nonphosphorylated mimic or to glutamic acid as a phosphorylated mimic. The mutations were tested individually or in double or triple combinations for their ability to rescue either a wing truncation characteristic of the genotype e(r)(p1) r(hd1-12) or the synthetic lethal interaction between e(r)(p2) and the Notch allele N(nd-p). All of the substitutions as single mutations rescued both mutant phenotypes, arguing that individually the phosphorylation of the three residues does not affect ER activity. The double mutants T18A-S24A and T18E-S24E and the triple mutants T18A-S24A-T63A and T18E-S24E-T63E failed to rescue. Together the data support the following model for the regulation of ER by CKII. ER that is unphosphorylated at both T18A and S24 is inactive. CKII activates ER by phosphorylating either T18 or S24. Further phosphorylation to produce the doubly phosphorylated protein inactivates ER. 相似文献
58.
Eissenberg JC 《BioEssays : news and reviews in molecular, cellular and developmental biology》2006,28(6):574-577
Most tissues contain cells capable of the self-renewal and differentiation necessary to maintain tissue and organ integrity. These somatic stem cells are generally thought to have limited developmental potential. The mechanisms that restrict cell fate decisions in somatic stem cells are only now being understood. This understanding will be important in the clinical exploitation of adult stem cells in tissue repair and replacement. Experiments performed over fifty years ago in Drosophila showed that developmental restriction could be relaxed in the proliferating larval cells that are destined to form the adult fly integument. This phenomenon, called transdetermination, can serve as a model for mechanisms of stem-cell commitment. A recent publication (1) sheds new light on the mechanism of transdetermination by demonstrating that loss of homeotic gene silencing leads to increased frequency of transdetermination. In addition, the authors link a specific signaling pathway induced by tissue regeneration to the relaxation of homeotic gene silencing. The data identify key mechanisms that control developmental homeostasis and cell fate restriction that could be manipulated to make somatic stem-cell engineering possible. 相似文献
59.
JC Biro 《Theoretical biology & medical modelling》2006,3(1):15-12
Background
Prediction of protein folding and specific interactions from only the sequence (ab initio) is a major challenge in bioinformatics. It is believed that such prediction will prove possible if Anfinsen's thermodynamic principle is correct for all kinds of proteins, and all the information necessary to form a concrete 3D structure is indeed present in the sequence. 相似文献60.
The demonstration that interleukin 2 (IL-2) is a lectin specific for
oligomannosides allows to understand a new function for this cytokine: as a
bifunctional molecule when bound to its receptor ss, IL-2 associates the
latter which the CD3/TCR complex, interacting with oligosaccharides of CD3
through its carbohydrate-recognition domain (Zanetta et al. , 1996,
Biochem. J., 318, 49-53). This induces the tyrosine phosphorylation of the
IL-2R beta by ++p56(lck) , the first step of the IL-2-dependent signaling.
Since this specific association is disrupted in vitro by oligomannosides
with five and six mannose residues, we made the hypothesis that pathogenic
cells or microorganisms could bind IL-2, consequently disturbing the IL-2-
dependent response. This study shows that the pathogenic yeast Candida
albicans (in contrast with nonpathogenic yeasts) binds high amounts of IL-2
as did cancer cells. In contrast with cancer cells, yeasts do not bind the
Man6GlcNAc2-specific lectin CSL, an endogenous "amplifier of activation
signals" (Zanetta et al. , 1995, Biochem. J., 311, 629-636).
相似文献