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排序方式: 共有99条查询结果,搜索用时 281 毫秒
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2.
Membrane attachment of recombinant G-protein alpha-subunits in excess of beta gamma subunits in a eukaryotic expression system 总被引:4,自引:0,他引:4
W F Simonds R M Collins A M Spiegel M R Brann 《Biochemical and biophysical research communications》1989,164(1):46-53
Recombinant cDNAs encoding the alpha-subunits of Gi1, Gi2, Gi3, Go and Gs were transfected into COS cells with the pCD-PS mammalian expression vector. Expression of each G alpha was verified using subtype-specific peptide antisera on immunoblots. Quantitative immunoblotting of alpha and beta subunits indicated: i) that there was no change in expression of endogenous beta subunits, and ii) overexpression of alpha subunits could achieve a ratio of alpha:beta greater than 25:1. Despite the excess of alpha over beta, the G alpha subunits were found predominantly in the membrane fraction. The results demonstrate that G alpha subunits can attach to the membrane independently of beta gamma subunits. 相似文献
3.
Gordon Y. K. Ng †Brian F. O'Dowd ‡Mirelle Caron ‡Michael Dennis §Mark R. Brann † Susan R. George 《Journal of neurochemistry》1994,63(5):1589-1595
Abstract: We have expressed and biochemically characterized the human D2long (D2L ) dopamine receptor isoform using the baculovirus/Sf9 cell system. The expressed receptor bound ligands with a pharmacological profile similar to that reported for neuronal and cloned D2L receptors expressed in mammalian cell lines. Dopamine binding to D2L receptor was sensitive to guanine nucleotides, indicating receptor coupling to endogenous G proteins. A D2L receptor-specific antibody identified two major protein species at ∼44 kDa and at ∼93 kDa in immunoblots, suggesting the presence of D2L receptor monomers and dimers. Both species were purified by immunoprecipitation from digitonin-solubilized preparation of cells expressing D2L receptor prelabeled with 32 Pi or [3 H]-palmitate. These results constitute the first direct evidence for D2L receptor phosphorylation and palmitoylation. 相似文献
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5.
Expression of GTP-binding proteins and prostaglandin E2 receptors during human T cell activation. 总被引:1,自引:0,他引:1
GTP-binding proteins (G-proteins) are a family of closely related, yet structurally distinct signal transducing proteins. In this study the presence and relative abundance of several G-proteins and of their corresponding mRNAs were measured in resting and activated human T lymphocytes. We found that T lymphocytes contain RNA coding for Gs, Gi2, and Gi3. No Gi1- and Go-specific RNA could be detected. Membrane fractions of resting and activated lymphocytes were studied in immunoblot experiments. Again, Gs, Gi2, and Gi3, but not Gi1 and Go, were detected. Upon mitogenic activation, a relative increase in mRNA for Gs and Gi3, but not for Gi2 could be demonstrated in Northern blot experiments. Immunoblotting indicated an increase in Gs and Gi3 density in membrane fractions of T cells as well. Paralleling the increase in Gs, we found that activated T cells produce five to seven times more cAMP per cell in response to prostaglandin E2 (PGE2) than resting lymphocytes. Finally, PGE2 binding studies showed that the number of receptors for this hormone increased from 435 +/- 322 to 1035 +/- 357 per cell following in vitro stimulation. We propose that in vitro T cell activation is paralleled by an increase in sensitivity to PGE2-induced cAMP generation. This sensitization is accompanied by both an increase in cell surface PGE2 receptor numbers as well as by increased expression of the signal transducing protein Gs and may physiologically be important for limiting an immune response. 相似文献
6.
Progesterone and several progesterone metabolites are capable of inhibiting uterine contractility. Some progesterone metabolites have shown little or no affinity for the progesterone receptor but have been found to be potent modulators of the GABAA receptor system. This study examined whether the inhibition of uterine contraction by progesterone and its metabolites was progesterone receptor-mediated or gamma amino butyric acidA (GABAA) receptor-mediated. Uterine contractions were measured in annular rings of uterine tissue, 5 mm in length, from diestrous II rats, under a fixed tension of 1 gram. The steroids tested were 3 beta-hydroxy-5 beta-pregnan-20-one (6 micrograms/ml), 5 beta-pregnane-3,20-dione (10 micrograms/ml), 3 alpha-hydroxy-5 alpha-pregnan- 20-one (3 alpha,5 alpha-THP, 27.5 micrograms/ml), and progesterone (40 micrograms/ml). All compounds significantly inhibited spontaneous uterine contractions when compared to controls. No effect was seen by either 16 micrograms/ml of the progesterone antagonist, RU486, or 32 micrograms/ml of the GABAA antagonist, pictrotoxin, when administered alone. However, when uterine tissues were exposed to a combination of the steroid and the antagonist, the effect of 3 beta-hydroxy-5 beta-pregnan-20-one and 3 alpha,5 alpha-THP was blocked by picrotoxin but not by RU486, indicating that the action of these steroids was mediated through the GABAA system. The effect of 5 beta-pregnane-3,20-dione and progesterone was effectively blocked by RU486 but not by picrotoxin, suggesting that their actions were mediated through the progesterone receptor system. These results indicate that multiple mechanisms exist in the uterus for inhibiting uterine contractility by progesterone and its metabolites. 相似文献
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Transforming growth factor-β (TGF-β) has diverse and multiple roles throughout the body. This review focuses on the evidence
supporting its functions in the central nervous system, with a particular emphasis on its purported role in cerebral ischemia.
Numerous studies have documented that TGF-β1 levels are enhanced in the brain following cerebral ischemia. As evidence that
such an upregulation is beneficial, agonist studies have demonstrated that TGF-β1 reduces neuronal cell death and infarct
size following middle cerebral artery occlusion (MCAO), while conversely, antagonist studies have shown increased neuronal
cell death and infarct size after MCAO. These studies suggest that TGF-β1 has a neuroprotective role in cerebral ischemia.
Recent work with adenoviral-mediated overexpression of TGF-β1 in vivo in mice has further implicated a neuroprotective role
for TGF-β1 in cerebral ischemia, as evidenced by a reduction in neuronal cell death, infarct size, and neurological outcome.
Additionally, numerous in vitro studies have documented the neuroprotective ability of TGF-β1 in neurons from a variety of
species, including rats, mice, chicks, and humans. Of significant interest, TGF-β1 was shown to be protective against a wide
variety of death-inducing agents/insults, including hypoxia/ischemia, glutamate excitotoxicity, β-amyloid, oxidative damage,
and human immunodeficiency virus. The mechanism of TGF-β1-mediated neuroprotection remains to be resolved, but early evidence
suggests that TGF-β1 regulates the expression and ratio of apoptotic (Bad) and antiapoptotic proteins (Bcl-2, Bcl-x1), creating an environment favorable for cell survival of death-inducing insults. Taken as a whole, these results suggest
that TGF-β1 is an important neuroprotective factor that can reduce damage from a wide-array of death-inducing agents/insults
in vitro, as well as exert protection of the brain during cerebral ischemia.
The authors’ research is supported by research grants (HD-28964 and AG-17186 to DWB) from the National Institutes of Health,
NICHD, and NIA. 相似文献
9.
Current status of antisense DNA methods in behavioral studies 总被引:4,自引:0,他引:4
The antisense DNA method has been used successfully to block the expression
of specific genes in vivo in neuronal systems. An increasing number of
studies in the last few years have shown that antisense DNA administered
directly into the brain can modify various kinds of behaviors. These
findings strongly suggest that the antisense DNA method can be used as a
powerful tool to study causal relationships between molecular processes in
the brain and behavior. In this article we review the current status of the
antisense method in behavioral studies and discuss its potentials and
problems by focusing on the following four aspects; (i) optimal application
paradigms of antisense DNA methods in behavioral studies; (ii) efficiencies
of different administration methods of antisense DNA used in behavioral
studies; (iii) determination of specificity of behavioral effects of
antisense DNA; and (iv) discrepancies between antisense DNA effects on
behaviors and those on protein levels of the targeted gene.
相似文献
10.
Paul DW Kirk Aviva Witkover Alan Courtney Alexandra M Lewin Robin Wait Michael PH Stumpf Sylvia Richardson Graham P Taylor Charles RM Bangham 《Retrovirology》2011,8(1):1-9