全文获取类型
收费全文 | 56篇 |
免费 | 7篇 |
国内免费 | 2篇 |
出版年
2022年 | 1篇 |
2019年 | 2篇 |
2017年 | 2篇 |
2015年 | 5篇 |
2014年 | 1篇 |
2013年 | 2篇 |
2012年 | 7篇 |
2011年 | 3篇 |
2010年 | 1篇 |
2009年 | 2篇 |
2008年 | 1篇 |
2007年 | 3篇 |
2006年 | 2篇 |
2005年 | 1篇 |
2004年 | 5篇 |
2003年 | 2篇 |
2002年 | 2篇 |
2001年 | 1篇 |
2000年 | 1篇 |
1998年 | 3篇 |
1997年 | 2篇 |
1996年 | 1篇 |
1995年 | 1篇 |
1993年 | 2篇 |
1992年 | 1篇 |
1987年 | 1篇 |
1984年 | 1篇 |
1982年 | 1篇 |
1981年 | 1篇 |
1978年 | 1篇 |
1977年 | 2篇 |
1976年 | 1篇 |
1974年 | 1篇 |
1934年 | 1篇 |
1929年 | 1篇 |
排序方式: 共有65条查询结果,搜索用时 14 毫秒
51.
Sheikh SZ Kobayashi T Matsuoka K Onyiah JC Plevy SE 《The Journal of biological chemistry》2011,286(2):1174-1180
We have demonstrated previously that IFN-γ plays a protective role in the initiation of chronic intestinal inflammation through attenuation of Toll-like receptor-mediated IL-23 induction in macrophages. Here, an interferon-stimulated response element (ISRE) is identified in a region of conserved nucleotide sequences in the Il23a promoter. This ISRE mediated, in part, Il23a promoter induction by LPS and inhibition of LPS-induced activity by IFN-γ. LPS and IFN-γ recruit interferon regulatory factors (IRFs) to the Il23a ISRE in murine bone marrow-derived macrophages (BMMs). Functionally, IRF-1 is a negative regulator of Il23a in LPS-stimulated BMMs. IRF-1(-/-) BMMs demonstrated enhanced LPS-induced Il23a expression compared with WT BMMs. Moreover, IRF-1 deficiency resulted in prolonged occupancy of RelA on the Il23a promoter. Consequently, IRF-1(-/-) mice were more susceptible to colonic injury by trinitrobenzenesulfonic acid, and IL-10/IRF-1 double-deficient (IL-10/IRF-1(-/-)) mice demonstrated more severe colonic inflammation compared with IL-10(-/-) mice. The severity of colitis in both models correlated with increased colonic IL-23. CD11b(+) lamina propria mononuclear cells, comprising predominantly macrophages, were identified as the major source of IL-23 in colitis-prone mice. Basal and heat-killed Escherichia coli-stimulated levels of Il23a were increased in IL-10/IRF-1(-/-) compared with WT and IL-10(-/-) colonic CD11b(+) lamina propria mononuclear cells. In conclusion, these experiments characterize IRF-ISRE interactions on the Il23a promoter, which have in vivo relevance as a homeostatic checkpoint in chronic intestinal inflammation. 相似文献
52.
Quezada-Rivera JJ RE Soria-Guerra FS Pérez-Juárez L Martínez-González SE Valdés- Rodríguez NL Vasco-Méndez JF Morales-Domínguez 《Phyton》2019,88(1):25-35
The use of antimicrobial peptides (AMPs) synthesized
by bacteria (bacteriocins) is an alternative for combating multidrug
resistant bacterial strains and their production by recombinant route
is a viable option for their mass production. The bacteriocin E-760
isolated from the genus Enterococcus sp. has been shown to possess
inhibitory activity against Gram-negative and Gram-positive
bacteria. In this study, the expression of a chimeric protein coding
for E-760 in the nucleus of C. reinhardtii was evaluated, as well as,
its antibacterial activity. The synthetic gene E-760S was inserted
into the genome of C. reinhardtii using Agrobacterium tumefaciens.
A transgenic line was identified in TAP medium with hygromycin
and also by PCR. The increment in the culture medium temperature
of the transgenic strain at 35 °C for 10 minutes, increased the
production level of the recombinant protein from 0.14 (Noninduced
culture, NIC) to 0.36% (Induced culture, IC) of total soluble
proteins (TSP); this was quantified by an ELISA assay. Recombinant
E-760 possesses activity against Staphylococcus aureus in 0.34 U
log, Streptococcus agalactiae in 0.48 U log, Enterococcus faecium in
0.36 U log, Pseudomonas aeruginosa in 2 U log and for Klebsiella
pneumoniae, the activity was 0.07 U log. These results demonstrate
that the nucleus transformation of C. reinhardtii can function as
a stable expression platform for the production of the synthetic
gene E-760 and it can potentially be used as an antibacterial agent. 相似文献
53.
54.
55.
Zhu C Rao K Xiong H Gagnidze K Li F Horvath C Plevy S 《The Journal of biological chemistry》2003,278(41):39372-39382
Interleukin (IL)-12 is a heterodimeric cytokine that is critical for the development of a T-helper-1 immune response and immunity against intracellular pathogens. The IL-12 p40 gene product, expressed specifically in macrophages and dendritic cells, heterodimerizes with p35 to form bioactive IL-12, and heterodimerizes with p19 to comprise the cytokine IL-23. Regulation of the murine IL-12 p40 promoter is complex. Multiple cis-acting elements have been characterized that are involved in activation by bacterial products. However, molecular mechanisms through which interferon (IFN)-gamma and bacterial products synergistically activate IL-12 p40 gene expression are less clear. In this study, a composite NFAT/ICSBP binding site at -68 to -54 is identified that is functionally important for p40 promoter activation by lipopolysaccharide (LPS) and LPS plus IFN-gamma. DNA binding of NFAT and ICSBP is demonstrated on the endogenous promoter by chromatin immunoprecipitation. NFAT is required for ICSBP binding to this region. Overexpression of NFAT and ICSBP synergistically activates the p40 promoter. A dominant negative NFAT molecule attenuates LPS- and IFN-gamma-activated endogenous IL-12 p40 mRNA expression. A physical association between NFAT and ICSBP in the absence of DNA is detected by co-immunoprecipitation of endogenous proteins. Three NFAT domains are required for ICSBP interaction. Finally, in LPS- and IFN-gamma-activated RAW-264.7 cells, the association between NFAT and ICSBP is abrogated by IL-10 priming. 相似文献
56.
Xiong H Zhu C Li F Hegazi R He K Babyatsky M Bauer AJ Plevy SE 《The Journal of biological chemistry》2004,279(11):10776-10783
Nitric oxide (NO), an important effector molecule of the innate immune system, can also regulate adaptive immunity. In this study, the molecular effects of NO on the toll-like receptor signaling pathway were determined using interleukin-12 (IL-12) as an immunologically relevant target gene. The principal conclusion of these experiments is that NO inhibits IL-1 receptor-associated kinase (IRAK) activity and attenuates the molecular interaction between tumor necrosis factor receptor-associated factor-6 and IRAK. As a consequence, the NO donor S-nitroso-N-acetylpenicillamine (SNAP) inhibits lipopolysaccharide (LPS)-induced IL-12 p40 mRNA expression, protein production, and promoter activity in murine macrophages, dendritic cells, and the murine macrophage cell line RAW 264.7. Splenocytes from inducible nitric-oxide synthase-deficient mice demonstrate markedly increased IL-12 p40 protein and mRNA expression compared with wild type splenocytes. The inhibitory action of NO on IL-12 p40 is independent of the cytokine IL-10. The effects of NO can be directly attributed to inhibition of NF-kappaB activation through IRAK-dependent pathways. Accordingly, SNAP strongly reduces LPS-induced NF-kappaB DNA binding to the p40 promoter and inhibits LPS-induced IkappaB phosphorylation. Similarly, NO attenuates IL-1beta-induced NF-kappaB activation. These experiments provide another example of how an innate immune molecule may have a profound effect on adaptive immunity. 相似文献
57.
58.
Siân SE Cox Mark van der Giezen Sarah J Tarr Mark R Crompton Jorge Tovar 《BMC microbiology》2006,6(1):45-16
Background
Giardia intestinalis is a parasitic protozoan and major cause of diarrhoeal disease. Disease transmission is dependent on the ability of the parasite to differentiate back and forth between an intestine-colonising trophozoite and an environmentally-resistant infective cyst. Our current understanding of the intracellular signalling mechanisms that regulate parasite replication and differentiation is limited, yet such information could suggest new methods of disease control. Phosphoinositide-3 kinase (PI3K) signalling pathways have a central involvement in many vital eukaryotic processes, such as regulation of cell growth, intracellular membrane trafficking and cell motility. Here we present evidence for the existence of functional PI3K intracellular signalling pathways in G. intestinalis. 相似文献59.
Prenatal maternal psychological distress increases risk for adverse infant outcomes. However, the biological mechanisms underlying this association remain unclear. Prenatal stress can impact fetal epigenetic regulation that could underlie changes in infant stress responses. It has been suggested that maternal glucocorticoids may mediate this epigenetic effect. We examined this hypothesis by determining the impact of maternal cortisol and depressive symptoms during pregnancy on infant NR3C1 and BDNF DNA methylation. Fifty-seven pregnant women were recruited during the second or third trimester. Participants self-reported depressive symptoms and salivary cortisol samples were collected diurnally and in response to a stressor. Buccal swabs for DNA extraction and DNA methylation analysis were collected from each infant at 2 months of age, and mothers were assessed for postnatal depressive symptoms. Prenatal depressive symptoms significantly predicted increased NR3C1 1F DNA methylation in male infants (β = 2.147, P = 0.044). Prenatal depressive symptoms also significantly predicted decreased BDNF IV DNA methylation in both male and female infants (β = −3.244, P = 0.013). No measure of maternal cortisol during pregnancy predicted infant NR3C1 1F or BDNF promoter IV DNA methylation. Our findings highlight the susceptibility of males to changes in NR3C1 DNA methylation and present novel evidence for altered BDNF IV DNA methylation in response to maternal depression during pregnancy. The lack of association between maternal cortisol and infant DNA methylation suggests that effects of maternal depression may not be mediated directly by glucocorticoids. Future studies should consider other potential mediating mechanisms in the link between maternal mood and infant outcomes. 相似文献
60.