scholarly journals Genomic destabilization and its associated mutagenesis increase with senescence‐associated phenotype expression

2020 ◽  
Author(s):  
Ken‐ichi Yoshioka ◽  
Yusuke Matsuno
Keyword(s):  
Phenotype Expression

Variable Phenotype Expression of a Maternally Inherited 16P13.11 Deletion in Twin Brothers with Epilepsy

2018 ◽  
Vol 49 (S 01) ◽  
pp. S1-S12
Author(s):  
M. Sallemi ◽  
S. Gambara ◽  
J. Galli ◽  
E. Fazzi
Keyword(s):  
Variable Phenotype ◽  
Phenotype Expression

scholarly journals A Systematic Framework for Drug Repositioning from Integrated Omics and Drug Phenotype Profiles Using Pathway-Drug Network

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Erkhembayar Jadamba ◽  
Miyoung Shin
Keyword(s):  
Breast Cancer ◽  
Drug Repositioning ◽  
Expression Profiles ◽  
A Priori ◽  
Gene Expression Profiles ◽  
Biological Data ◽  
Genomic Knowledge ◽  
High Level ◽  
Systematic Framework ◽  
Phenotype Expression

Drug repositioning offers new clinical indications for old drugs. Recently, many computational approaches have been developed to repurpose marketed drugs in human diseases by mining various of biological data including disease expression profiles, pathways, drug phenotype expression profiles, and chemical structure data. However, despite encouraging results, a comprehensive and efficient computational drug repositioning approach is needed that includes the high-level integration of available resources. In this study, we propose a systematic framework employing experimental genomic knowledge and pharmaceutical knowledge to reposition drugs for a specific disease. Specifically, we first obtain experimental genomic knowledge from disease gene expression profiles and pharmaceutical knowledge from drug phenotype expression profiles and construct a pathway-drug network representing a priori known associations between drugs and pathways. To discover promising candidates for drug repositioning, we initialize node labels for the pathway-drug network using identified disease pathways and known drugs associated with the phenotype of interest and perform network propagation in a semisupervised manner. To evaluate our method, we conducted some experiments to reposition 1309 drugs based on four different breast cancer datasets and verified the results of promising candidate drugs for breast cancer by a two-step validation procedure. Consequently, our experimental results showed that the proposed framework is quite useful approach to discover promising candidates for breast cancer treatment.

Abstract 1727: Apolipoprotein E (ApoE) Induces an Anti-inflammatory Phenotype in Macrophages

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Daniel Baitsch ◽  
Ralph Telgmann ◽  
Georg Varga ◽  
Carsten Muller-Tidow ◽  
Martine Bot ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Apolipoprotein E ◽  
Kinase Inhibitor ◽  
Plasma Cholesterol ◽  
Macrophage Phenotype ◽  
Anti Inflammatory ◽  
M2 Phenotype ◽  
Functional Phenotype ◽  
Expression And Activity ◽  
Phenotype Expression

Apolipoprotein E (apoE) exerts anti-atherogenic effects by promoting cholesterol efflux and hepatic lipoprotein clearance. However, apoE retains protective effects even under experimental settings, in which its influence on plasma cholesterol is negligible suggesting that this lipoprotein inhibits atherosclerosis independently from cholesterol transport. To gain further insight into mechanisms underlying apoE-mediated atheroprotection, we investigated its effect on the functional phenotype of RAW 264.7 macrophages overexpressing either of two apoE receptors: ApoER2/LRP8 or VLDL-R. Incubation of ApoER2/LRP8- or VLDL-R-expressing macrophages with apoE downregulated markers of pro-inflammatory M1 functional phenotype (expression and activity of iNOS, production of IL-12), whereas markers of anti-inflammatory M2 phenotype (expression and activity of arginase-I, production of IL-1RA) were upregulated. In addition, macrophage responses typical for M1 phenotype (migration, generation of reactive oxygen species, antibody-dependent cell cytotoxicity) were suppressed in ApoER2/LRP8- or VLDL-R-expressing cells in the presence of apoE. Finally, apoE prevented LPS- and IFN-γ-induced activation of ApoER2/LRP8- or VLDL-R-expressing macrophages as documented by reduced production of IL-12, TNF-α and MCP-1, reduced expression and activity of iNOS and COX2, and reduced activation and/or phosphorylation of NF-κB, IκB and STAT1. The modulatory effects of apoE on macrophage phenotype were inhibited by SB220025, a p38MAP kinase inhibitor, and PP1A, a tyrosine kinase inhibitor. Accordingly, apoE induced tyrosine kinase-dependent activation of p38MAP kinase in ApoER2/LRP8- or VLDL-R-expressing macrophages. Under in vivo conditions, apoE −/− mice transplanted with apoE-producing wild-type bone marrow presented with increased plasma IL-1RA levels. In addition, peritoneal macrophages from transplanted animals demonstrated enhanced M2 phenotype (increased IL-1RA production and CD206 expression). We conclude that apoE signalling over ApoER2/LRP8 or VLDL-R promotes macrophage conversion from pro-inflammatory M1 to anti-inflammatory M2 phenotype. This effect may represent a novel anti-atherogenic activity of apoE.

R1-nj expression in parental inbreds as a predictor of amenability of maize hybrids to R1-nj-based doubled haploid development

2020 ◽  
Vol 79 (04) ◽  
Author(s):  
R. K. Khulbe ◽  
A. Pattanayak ◽  
Vivek Panday
Keyword(s):  
Doubled Haploid ◽  
Current Method ◽  
Distinct Pattern ◽  
Complex Nature ◽  
Maize Breeding ◽  
Early Maturity ◽  
Haploid Inducer ◽  
Source Populations ◽  
Phenotype Expression

The current method of doubled haploid (DH) development in maize involves in vivo production of haploids using R1-njbased haploid inducer lines that upon use as male render a small fraction of seed in the pollinated female ears haploid. Identification of haploid seed relies on R1-nj marker expression in the endosperm and embryo, and the degree of its expression determines efficiency of DH development process. In the present study, R1-nj expression in the endosperm was characterized in crosses of CIMMYT’s R1-nj-based haploid inducer TAILP1 with a set comprising 18 early maturity hybrids and their 23 parental inbreds. Kernel colour inhibition was observed only in a small proportion of the hybrids and inbreds. Comparison of R1-nj expression in the hybrids and their parental inbreds revealed a distinct pattern, which may be useful in identifying source populations and/or determining parental constituents for synthesizing source populations with predicted amenability to doubled haploid development using R1-nj-based haploid inducers. However, deviation from the pattern was noted in hybrids involving inbreds with higher degree of colour inhibition, which suggests complex nature of R1-nj phenotype expression and necessitates further investigation involving larger sets of germplasm for dissecting the role of maternal and paternal genetic factors in determining R1-nj phenotype expression. The hybrids found exhibiting complete kernel anthocyanin expression in present study can be used directly as source populations for DH development using R1-nj based haploid inducers. Besides, since the inbreds used in the study have originated from and/or are accessible to CGIAR/NARS maize breeding programmes, the information on their kernel anthocyanin expression can be helpful in selection of source populations or generating new source populations amenable for DH development using R1-nj based haploid inducers.

scholarly journals Effect of FDC-SP on the phenotype expression of cultured periodontal ligament cells

2011 ◽  
Vol 2 ◽  
pp. 235-241 ◽  
Author(s):  
Na Wei ◽  
Haiyang Yu ◽  
Shulin Yang ◽  
Xingmei Yang ◽  
Quan Yuan ◽  
...  
Keyword(s):  
Periodontal Ligament ◽  
Periodontal Ligament Cells ◽  
Phenotype Expression

scholarly journals toxB Gene on pO157 of Enterohemorrhagic EscherichiacoliO157:H7 Is Required for Full Epithelial Cell Adherence Phenotype

2001 ◽  
Vol 69 (11) ◽  
pp. 6660-6669 ◽  
Author(s):  
Ichiro Tatsuno ◽  
Masanori Horie ◽  
Hiroyuki Abe ◽  
Takeyoshi Miki ◽  
Kozo Makino ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Bacterial Infection ◽  
Intestinal Epithelium ◽  
Secreted Proteins ◽  
Cell Adherence ◽  
Full Adherence ◽  
Infection Study ◽  
Phenotype Expression

ABSTRACT Adherence of enterohemorrhagic Escherichia coli (EHEC) to the intestinal epithelium is critical for initiation of a bacterial infection. An in vitro infection study previously indicated that EHEC bacteria initially adhere diffusely and then proliferate to develop MC, a process that is mediated by various secreted proteins, such as EspA, EspB, EspD, Tir, and intimin, as well as other putative adherence factors. In the present study, we investigated the role of a large 93-kb plasmid (pO157) in the adherence of O157:H7 (O157Sakai) and found the toxB gene to be involved in the full adherence phenotype. A pO157-cured strain of O157Sakai (O157Cu) developed microcolonies on Caco-2 cells; however, the number of microcolonies was lower than that of O157Sakai, as were the production and secretion levels of EspA, EspB, and Tir. Introduction of a mini-pO157 plasmid (pIC37) composed of thetoxB and ori regions restored full adherence capacity to O157Cu, including production and secretion of the proteins. In contrast, introduction of a pO157 mutant possessingtoxB::Km into O157Cu could not restore the full adherence phenotype. Expression of truncated versions of His-tagged ToxB also promoted EspB production and/or secretion by O157Cu. These results suggest that ToxB contributes to the adherence of EHEC to epithelial cells through promotion of the production and/or secretion of type III secreted proteins.

scholarly journals Diagnosis of Familial Combined Hyperlipidemia Based on Lipid Phenotype Expression in 32 Families

2002 ◽  
Vol 22 (2) ◽  
pp. 274-282 ◽  
Author(s):  
Mario J. Veerkamp ◽  
Jacqueline de Graaf ◽  
Sebastian J.H. Bredie ◽  
Jan C.M. Hendriks ◽  
Pierre N.M. Demacker ◽  
...  
Keyword(s):  
Familial Combined Hyperlipidemia ◽  
Lipid Phenotype ◽  
Phenotype Expression
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