排序方式: 共有43条查询结果,搜索用时 15 毫秒
31.
LI Ming ZHANG Weilun LIU Shilian LIU Yanxin ZHENG Dexian 《科学通报(英文版)》2006,51(1):38-47
The CD2 molecule, an adhesive and co-stimulating molecule, expresses virtually on all T lymphocytes, thymocytes, as well as natural killer cells, playing an important role in thymus development, T cell activation and apoptosis[1―3]. CD2 molecule consists of an ex- tracellular region with two Ig-like domains, a single membrane-spanning domain, and a positively charged proline-rich cytoplasmic tail, which is highly conserved between different species[1,4―7]. The functions of CD2 in signal t… 相似文献
32.
To explore cell malignant phenotype correlated changes of cell surface adhesion molecules and cell-cell communication in carcinogenesis, human stomach transformed and cancer cell lines were investigated. Expressions of E-cadherin, N-cadherin,α-catenin, β-catenin as well as gap junction (GJ) protein Cx32 were studied by utilization of immunoblotting, immunocytochemical and fluorescent dye transfer methods. Mammalian normal stomach mucosal cells expressed E-cadherin but not N-cadherin. E-cadherin im-munofluorescence was detected at cell membranous adher-ens junctions (AJ) where colocalization with immunofluo-rescent staining of inner surface adhesion plaque proteins αnd β-catenins was observed. The existence of E-cadherin/ catenin (α-, β-) protein complexes as AJ was suggested. In transformed and stomach cancer cells E-cadherin was inhibited, instead, N-cadherin was expressed and localized at membranous AJ where co-staining with α- and β-catenin fluorescence was observed. Formation of N-cadherin/catenin (α-, β-) protein complex at AJs of transformed and cancer cells was suggested. The above observations were further supported by immunoblotting results. Normal stomach muscosal and transformed cells expressed Cx32 at membranous GJ and were competent of gap junction communication (GJIC). In stomach cancer cells, Cx32 was inhibited and GJIC was defective. The results suggested that changes of signal pathways mediated by both cell adhesion and cell communication systems are associated intracellular events of stomach carcinogenesis. The alteration of cadherin isoform from E- to N-cadherin in transformed and stomach cancer cells is the first report. 相似文献
33.
Silberman DM Zorrilla-Zubilete M Cremaschi GA Genaro AM 《Cellular and molecular life sciences : CMLS》2005,62(15):1744-1754
Chronic stress has been associated with impaired immune function. In this work we studied the effect of chronic mild stress (CMS) exposure on the early intracellular pathways involved in T cells after stimulation with mitogen. We found that mitogen stimulation of T lymphocytes from CMS-exposed mice resulted in a reduction of the intracellular [Ca2+] rise, an impairment of growth-promoting protein kinase C (PKC) activation, a lower NF-κB activation and an increase in the inhibitory cAMP-protein kinase A (PKA) pathway activity with respect to those found in control lymphocytes. However, T cell activation with the direct PKC activator phorbol 12-myristate 13-acetate plus calcium ionophore led to a similar proliferative response in both CMS and control lymphocytes, indicating that signals downstream of PKC would not be affected by stress. In summary, our results show that chronic stress induced an alteration in T cell early transduction signals that result in an impairment of the proliferative response.Received 11 February 2005; received after revision 20 May 2005; accepted 6 June 2005 相似文献
34.
Moreau P Rousseau P Rouas-Freiss N Le Discorde M Dausset J Carosella ED 《Cellular and molecular life sciences : CMLS》2002,59(9):1460-1466
Data are presented on the intracellular trafficking of HLA-G protein, taking the unique features of this non-classical molecule
into consideration: the existence of seven isoforms resulting from alternative splicing (HLA-G1 to G7), and reduced tail length
compared with HLA class I antigens. Biochemical studies and analysis of viral strategies for escaping the host immune system
led to the demonstration that (i) both the membrane-bound (HLA-G1) and the soluble (HLA-G5) forms of the molecule require
peptide association for cell surface expression, using TAP-dependent or TAP-independent pathways; (ii) peptide loading onto
the HLA-G protein plays a critical role in controlling the quality of the molecule reaching the cell surface; (iii) surface
expression of truncated HLA-G molecules is possible, and (iv) HLA-G expression may be restricted to soluble HLA-G5. These
data reveal that HLA-G presents specific cell trafficking pathways and strongly support the contention that the primary function
of HLA-G is as of an inhibitor ligand for immune-competent cells.
Received 4 June 2002; accepted 2 July 2002
RID="*"
ID="*"Corresponding author. 相似文献
35.
The effect of isoforms of the cell polarity protein, human ASIP, on the cell cycle and Fas/FasL-mediated apoptosis in human hepatoma cells 总被引:3,自引:0,他引:3
Human ASIP (hASIP) is expressed as numerous alternative splicing isoforms and there is an atypical protein kinease C (aPKC) phosphorylation site in exon 17b of the encoded sequence. We have identified an important role for exon 17b in cancer cells. Our results showed that hASIP-sa and sb had different effects on cell growth and Fas/FasL-mediated apoptosis in BEL-7404 human hepatoma cells. Human ASIP-sa modified the S phase of the cell cycle and might stimulate cell proliferation. Growth inhibition by hASIP-a antisense oligonucleotide-confirmed the positive action of hASIP-sa. Compared with hASIP-sa, hASIP-sb accelerated Fas/FasL-induced apoptosis, examined by sub-G1 accumulation, chromatin condensation, nuclear fragmentation, PARP cleavage, caspase-8 degradation and mitochondria- regulated cell death. Treatment with aPKC inhibitor could enhance Fas/FasL-mediated apoptosis in hASIP-sa-overexpressing cells, suggesting that hASIP-sa and its interaction with aPKC might contribute to the malignant growth and the blocking of Fas/FasL-mediated apoptosis, while hASIP-sb might function as an antagonist of hASIP-sa.Received 24 March 2005; received after revision 31 May 2005; accepted 21 June 2005 相似文献
36.
Protein kinases: which one is the memory molecule? 总被引:12,自引:0,他引:12
Encoding of new experiences is likely to induce activity-dependent modifications in the brain. Studies in organisms far apart
on the phylogenetic scale have shown that similar, sometimes identical, signal transduction pathways subserve plasticity in
neuronal systems, and they may play pivotal roles in the formation of long-term memories. It has become evident that phosphorylation/dephosphorylation
reactions are critical for the initiation of cellular mechanisms that embody, retain and modify information in neural circuits.
Although physiological investigations on synaptic plasticity have had a major impact, we have concentrated our review on behavioural
studies that provide direct or indirect evidence for a role of kinases in mechanisms underlying memory formation. From these,
it appears that the learning event induces activation of a variety of kinases with specific time courses. For instance, the
calcium/calmodulin-dependent protein kinase II seems to participate in an early phase of memory formation. Apparently, activation
of both protein tyrosine kinases and mitogen-activated protein kinases is required for much longer and may thus have a particular
function during transformation from short-term into long-term memory. Quite different time courses appear for protein kinase
C (PKC) and protein kinase A (PKA), which may function at two different time points, shortly after training and again much
later. This suggests that PKC and PKA might play a role at early and late stages of memory formation. However, we have considered
some examples showing that these signalling pathways do not function in isolation but rather interact in an intricate intracellular
network. This is indicative of a more complex contribution of each kinase to the fine tuning of encoding and information processing.
To decipher this complexity, pharmacological, biochemical and genetic investigations are more than ever necessary to unravel
the role of each kinase in the syntax of learning and memory formation. 相似文献
37.
中国剩余定理在RSA解密中的应用 总被引:1,自引:0,他引:1
在分析RSA密码算法实现原理的基础上,着重论述了利用单基数转换法(SRC)和混合基数转换法(MRC)计算中国剩余定理惟一解的方法以及利用这两种方法快速实现RSA的解密算法。 相似文献
38.
《科学通报(英文版)》1999,44(12):1110-1110
The role of PKCα in human breast cancer cell proliferation and expression of cyclinD1 and CDK4 has been investigated using inhibition of PKCα expression by its antisense RNA. When PKCα expression was inhibited the rate of cell proliferation decreased apparently and the levels of cyclinD1 and CDK4 mRNA were lower than the control. The results showed that PKCα, a key member of signal transduction system, played an important role in human breast cancer cell proliferation and had a close relationship with expression of cyclinD1 and CDK4 which control start of cell cycle. 相似文献
39.
探讨PKCβ抑制剂(LY333531)对高糖高脂环境下系膜细胞分泌细胞外基质(ECM)的影响,单独培养人肾小球系膜细胞,实验分为对照组、LY333531组、高糖高脂组、高糖高脂+LY333531组.首先采用qRTPCR检测PKCβI的表达,然后通过ELISA法检测细胞上清液Col IV、Fn的含量.结果显示,高糖高脂组相较于对照组,PKCβI mRNA的表达水平明显增加(P0.05),LY333531可以明显抑制PKCβI的表达(P0.05);高糖高脂组相较于对照组,细胞上清液Col IV、Fn含量明显增加(P0.05),而这种作用可被LY333531所抑制(P0.05).表明高糖高脂可通过促进系膜细胞PKCβI表达从而诱导ECM的分泌,增加肾纤维化发生的风险,而LY333531可明显抑制这种作用. 相似文献
40.
为了研究PKA和PKC对HeLa细胞G2 →M期和M→G1期进程的影响 ,用PKA和PKC抑制剂分别处理同步的G2 期和M期的HeLa细胞后 ,测定了细胞有丝分裂指数和PKA ,PKC与CDC2激酶的活性 .结果表明 ,PKAⅢ型抑制剂在促进HeLa细胞G2 /M /G1进程的同时 ,刺激了PKC的活性 ,反之 ,PKC的抑制剂GF 10 92 0 3X在阻抑HeLa细胞G2 /M /G1进程的同时 ,激活了PKA的活性 ,与其相关的CDC2激酶活性也发生了相应的变化 .实验表明 ,PKA和PKC分别负调和正调HeLa细胞G2 /M/G1进程 ,两者表现出拮抗关系 . 相似文献