Authentication email has already been sent, please check your email box: and activate it as soon as possible.
You can login to My Profile and manage your email alerts.
If you haven’t received the email, please:
|
|
There are 39 papers published in subject: > since this site started. |
Select Subject |
Select/Unselect all | For Selected Papers |
Saved Papers
Please enter a name for this paper to be shown in your personalized Saved Papers list
|
1. Expression and sub-cellular localization of leucine-rich repeats and immunoglobulin-like domain 1 is related to antioxidant enzymes in human ependymoma and oligodendroglioma | |||
YI Wei,LIU Lin,OKECHI Humphrey,CHEN Qianxue,HUANG Shulan | |||
Biology 27 May 2011 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:The current study investigated correlations between the expression of leucine-rich repeats and immunoglobulin-like domain 1 (LRIG1) and antioxidant enzymes and related proteins, including manganese superoxide dismutase, glutamate cysteine ligase catalytic or regulatory subunit, thioredoxin and thioredoxin reductase, in both human ependymoma and oligodendroglioma. Results revealed that the cytoplasmic expression of LRIG1 was associated with expression of glutamate cysteine ligase catalytic subunit in the human ependymoma, while the nuclear expression of LRIG1 was associated with expression of thioredoxin reductase. In human oligodendroglioma, the cytoplasmic expression of LRIG1 was associated with expression of the glutamate cysteine ligase catalytic subunit. Both the nuclear and perinuclear expressions of LRIG1 were associated with expression of glutamate cysteine ligase regulatory subunit. These results indicated that several antioxidant enzymes and related proteins contributed to LRIG1 expression, and that these may participate in the antioxidation of the cells. | |||
TO cite this article:YI Wei,LIU Lin,OKECHI Humphrey, et al. Expression and sub-cellular localization of leucine-rich repeats and immunoglobulin-like domain 1 is related to antioxidant enzymes in human ependymoma and oligodendroglioma[OL].[27 May 2011] http://en.paper.edu.cn/en_releasepaper/content/4429431 |
2. Colon cancer cell supernatant polarized THP-1 macrophages to a M2 like phenotype | |||
Chen Nanpeng,Qi Caiwa,Chen Ying,Ding Wen,He Qingyu | |||
Biology 22 March 2011 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Tumor associated macrophages(TAMs) are tightly related to carcinogenesis, metastasis and invasion. It has been reported that the phenotype of tumor associated macrophages was rather different from the classical activated macrophages namely M1. TAMs produce anti-inflammtory and immune inhibitory cytokines and chemokines, thus inhibit the anti-tumor immunity within solid tumor. The mechanisms by which the tumor cell polarized macrophages to a pro-tumor state are largely unknown. In this study, we used flow cytometry and ELISA methods to analyze the effect of the condition medium from colon cancer cell line Caoco2 on the THP-1 macrophages. The results showed that the level of M2 markers, CD206 and CD163, were strongly upregulated, the M1 marker CCR7 was significantly downregulated. The cytokines IL-1b, TNF-a, IL-10 were all upregulated. Our research indicated that the tumor supernatant has the ability to induce macrophages to a M2 like phenotype. | |||
TO cite this article:Chen Nanpeng,Qi Caiwa,Chen Ying, et al. Colon cancer cell supernatant polarized THP-1 macrophages to a M2 like phenotype[OL].[22 March 2011] http://en.paper.edu.cn/en_releasepaper/content/4417762 |
3. Expression of dephosphorylated NSSR1 increases during mouse epididymis development and is induced by androgen | |||
Xiao Pingjie,Peng Zhengyu,Huang Lu,Chen Xianhua,Xu Ping | |||
Biology 11 January 2011 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:NSSR1 (Neural salient serine/arginine rich protein 1, alternatively SRp38) is a newly identified RNA splicing factor and predominantly expressed in neural tissues. Although our recent study detected the expression of NSSR1 in mouse testis and uterus, the regulation of its expression during the development of reproduction system has not been reported by far. Here we showed that the expression of dephosphorylated NSSR1 increased significantly, while that of the phosphorylated NSSR1 keep stable during development of the caput epididymis. In adult mice, phosphorylated NSSR1 was mainly expressed in the apical side of epithelial cells, while dephosphorylated NSSR1 was mainly expressed in the principle cells of the epididymis and was regulated by testosterone. These results imply for the first time the potential roles of NSSR1 in the development and function of epididymis. | |||
TO cite this article:Xiao Pingjie,Peng Zhengyu,Huang Lu, et al. Expression of dephosphorylated NSSR1 increases during mouse epididymis development and is induced by androgen[OL].[11 January 2011] http://en.paper.edu.cn/en_releasepaper/content/4405917 |
4. Expression profile analysis of human hemopoietic tissues | |||
Chen Tinggui,Wang Feifei,Jiao Yong | |||
Biology 30 March 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Human have different hemopoietic organs at different times, such as fetal liver, thymus, lymph node and bone marrow, etc. In this study, we analyzed their expression profilings by GO and hierarchical cluster to understand their developmental mechanisms and mutual relations. Results: (1) GO classification showed that they are divided into 1045 categories. (2) The expression activities are: fetal liver > bone marrow > thymus > lymph node. (3) The specific genes of fetal liver, thymus, bone marrow and lymph node are 953, 175, 102 and 52, most of these genes have more relations with their respective physiological functions. (4) Hierarchical clustering analysis illustrated the relations among thymus, lymph node and bone marrow are closer than them with fetal liver. Discusses: GO classification still needs to develop newer methods to improve applicability, and hemopoietic cell are apt to transfer to lymphoid organs, or lymphoid organs and hemopoietic organs essentially come from same ancestor. | |||
TO cite this article:Chen Tinggui,Wang Feifei,Jiao Yong. Expression profile analysis of human hemopoietic tissues[OL].[30 March 2010] http://en.paper.edu.cn/en_releasepaper/content/41346 |
5. Inhibition of cadmium-induced apoptosis by Glutathione S-transferase P1 via mitogen-activated protein kinases (MAPKs) and mitochondria | |||
Chao Zhang,Weiping Mao,Xiuqin Kong,Ling Yue,Yanhong Gao,Zhimin Yin | |||
Biology 04 March 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Cadmium is a well-known toxic compound for the kidney. GSTP1 plays an important role in the detoxification and xenobiotics metabolism. We showed that in HEK 293 cells, hGSTP1-targeting RNAi reinforced apoptosis and the decrease in cell viability induced by Cd2+. Overexpression of GSTP1 diminished loss of mitochondrial membrane potential and cytochrome c release, inhibited MAPKs including ERK, JNK and p38, prevented caspase-3 activation and suppressed apoptosis induced by Cd2+. Oligonucleosomal DNA fragmentation demonstrated that adenovirus-mediated transfer of GSTP1 also prevented Cd2+-induced apoptosis in primary renal tubule cells. Our data suggest that GSTP1 is an inhibitor of Cd2+-induced apoptosis. | |||
TO cite this article:Chao Zhang,Weiping Mao,Xiuqin Kong, et al. Inhibition of cadmium-induced apoptosis by Glutathione S-transferase P1 via mitogen-activated protein kinases (MAPKs) and mitochondria[OL].[ 4 March 2010] http://en.paper.edu.cn/en_releasepaper/content/40427 |
6. Stem cell and the central nervous system regeneration in planarians | |||
Chen Guangwen,Ma Kexue | |||
Biology 04 February 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Planarians are well known for their powerful regenerative capabilities that enable them to form complete organisms from tiny body fragments. Such extraordinary regeneration and renewal of central nervous system (CNS) are depended on a population of totipotent stem cells called “Neoblasts”. Neoblasts are the only mitotically active cells in adult planarians and can differentiate into all cell types, including neurons. Therefore, planarians are ideal model systems for studying the regulation of stem cells and neurogenesis. In the last ten years, due to molecular approaches widely used in the study of planarian regeneration, the biological knowledge of this fascinating animal has been growing rapidly. In this review, we discussed the possible factors that control stem cells self-renewal and differentiation, summarized the genes specifically expressed in stem cells and the CNS, introduced the possible signaling systems in the CNS regeneration, and proposed some aspects of stem cells and neural regeneration that will need to be addressed in order to understand the fundamental principles of biology. | |||
TO cite this article:Chen Guangwen,Ma Kexue. Stem cell and the central nervous system regeneration in planarians[OL].[ 4 February 2010] http://en.paper.edu.cn/en_releasepaper/content/39870 |
7. Interactions between anti-ErbB2 antibody A21 and the ErbB2 extracellular domain provide a basis for improving A21 affinity | |||
Chang Liang ,Zhou Changhai ,Xu Man,Liu Jing | |||
Biology 01 February 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Anti-ErbB2 antibodies are well researched for the therapy of ErbB2-overexpressing tumors. The therapeutic potential and efficacy of these antibodies are closely related to their affinities to ErbB2. Previously we reported that an anti-ErbB2 antibody A21 targeting a conformational epitope comprising several loops in ErbB2 extracellular subdomain I and II could inhibit the proliferation of ErbB2-overexpressing cancer cells in vitro and in vivo. Here we found that another structureless and non-conserved loop in subdomain I of ErbB2 extracellular domain (ECD) was important for binding to A21, and then the antigen-contact sites on A21 were determined by site-directed mutation. The loop was constructed by molecular modeling, and a new model of A21-ErbB2 complex was generated by docking using the crystal structure of the scfv A21 and the model of ErbB2 ECD with the loop built. Based on the complex model, computational design for A21 affinity improvement was performed to enhance its affinity to ErbB2. Two mutants with about 1.7-fold improvement in affinity were obtained. Our study provided a rational molecular basis for affinity improvement and mechanism investigation of A21. | |||
TO cite this article:Chang Liang ,Zhou Changhai ,Xu Man, et al. Interactions between anti-ErbB2 antibody A21 and the ErbB2 extracellular domain provide a basis for improving A21 affinity [OL].[ 1 February 2010] http://en.paper.edu.cn/en_releasepaper/content/39758 |
8. Toxoplasma gondii Profilin Induces Cytokine-mediated Acute Liver Injury through Kupffer Cells and NK Cells in D-Galactosamine-sensitized Mice | |||
Jiang Qun ,Wei Haiming ,Sun Rui ,Tian Zhigang | |||
Biology 01 February 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Accumulating evidence suggests that parasites is inflammatorily active in liver, but the molecular mechanism(s) through which parasites modulates the hepatic innate immune system has not been clearly elucidated. In this study, we found that Toxoplasma gondii profilin, a ligand of toll-like receptor 11 (TLR11), induced the fulminant hepatitis in D-GalN-sensitized mice. The levels of inflammatory cytokine TNFα, IFN-γ and IL-12 in the serum were significantly increased following administration of profilin and D-GalN. Neutralization of these cytokine completely abolished profilin/GalN-induced liver injury. Profilin/GalN treatment could induce recruitment and activation of Kupffer cells and NK cells in liver. TNFα and IFN-γ were produced by Kupffer cells and NK cells, respectively, in profilin/GalN treated mice. Moreover, depletion of Kuppfer cells or NK cells could protect mice from profilin/GalN-induced liver injury, suggesting that these innate immune cells were the major sources of those inflammatory cytokines. This is the first report to show TLR11-induced liver injury, which is helpful to study the liver diseases with parasite infection. | |||
TO cite this article:Jiang Qun ,Wei Haiming ,Sun Rui , et al. Toxoplasma gondii Profilin Induces Cytokine-mediated Acute Liver Injury through Kupffer Cells and NK Cells in D-Galactosamine-sensitized Mice[OL].[ 1 February 2010] http://en.paper.edu.cn/en_releasepaper/content/39741 |
9. Study of IL-12 Cytokine Therapy for OVA-Induced Asthma Model Mice | |||
Xuewei Qu,Fengqi Li,Zhigang Tian,Haiming Wei | |||
Biology 28 January 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:Asthma is the disease of allergic hypersensitivity with airway hyperresponsiveness and airway inflammation. Recent studies have shown that IL-12 has a good role in the treatment of asthma, but the mechanisms are not clearly. Therefore, we construct the OVA-induced mouse asthma to studying the mechanisms of IL-12 treatment. Here we demonstrate that IL-12 treatment ameliorated the pathology of OVA-induced asthma. The roles of IL-12 were to inhibit the increase of NKT cells and promote the increase of NK cells. Furthermore, IL-12 treatment promoted the activation of NK cells and enhanced the expression of IFN-γ in lung NK cells. Our results provide the mechanisms of IL-12 cytokine therapy for OVA-induced asthma model mice. | |||
TO cite this article:Xuewei Qu,Fengqi Li,Zhigang Tian, et al. Study of IL-12 Cytokine Therapy for OVA-Induced Asthma Model Mice[OL].[28 January 2010] http://en.paper.edu.cn/en_releasepaper/content/39596 |
10. Different effects of MEK/ERK and PI3K/Akt signaling pathways in regulating TRAIL sensitivity of human leukemia cells | |||
Fang Fang,Hong Suli,Feng Zhiyong,Yinqiang Xin,Wang Qi,Fu Jin,Xu Yimiao,Luo Lan,Zhimin Yin | |||
Biology 26 January 2010 | |||
Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
Abstract:In order to investigate the role of MEK/ERK and PI3K/Akt signaling pathways in regulating cell sensitivity to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), we have conducted a comparative study regarding the effects of TRAIL on these pathways. We showed that TRAIL-induced apoptosis may be differentially regulated by inhibitors of MEK/ERK (U0126) or PI3K/Akt (LY294002) pathway in TRAIL-sensitive (U937) and TRAIL-resistant (K562) human leukemia cells. U0126 increased, but LY294002 significantly decreased TRAIL-induced apoptosis in U937 cells. We also demonstrated that ERK1/2 phosphorylation upon TRAIL treatment was obviously increased in the presence of LY294002. Overexpression of HA-Akt-WT reduced ERK1/2 phosphorylation and increased cell apoptosis induced by TRAIL. Moreover, we found that MEK/ERK and PI3K/Akt pathways had opposite effects on Bad phosphorylation upon TRAIL treatment. In conclusion, our results suggest that the crosstalk between these two pathways and the activation of ERK1/2 play crucial roles in TRAIL- induced apoptosis. | |||
TO cite this article:Fang Fang,Hong Suli,Feng Zhiyong, et al. Different effects of MEK/ERK and PI3K/Akt signaling pathways in regulating TRAIL sensitivity of human leukemia cells[OL].[26 January 2010] http://en.paper.edu.cn/en_releasepaper/content/39417 |
Select/Unselect all | For Selected Papers |
Saved Papers
Please enter a name for this paper to be shown in your personalized Saved Papers list
|
|
About Sciencepaper Online | Privacy Policy | Terms & Conditions | Contact Us
© 2003-2012 Sciencepaper Online. unless otherwise stated