scholarly journals Semantic Mining based on graph theory and ontologies. Case Study: Cell Signaling Pathways

2016 ◽  
Author(s):  
Carlos R. Rangel ◽  
Junior Altamiranda ◽  
Jose Aguilar
Keyword(s):  
Graph Theory ◽  
Cell Signaling ◽  
Signaling Pathway ◽  
Research Area ◽  
Semantic Enrichment ◽  
Semantic Mining ◽  
A Cell ◽  
A New Technique ◽  
Two Phases ◽  
Pathway Networks

In this paper we use concepts from graph theory and cellular biology represented as ontologies, to carry out semantic mining tasks on signaling pathway networks. Specifically, the paper describes the semantic enrichment of signaling pathway networks. A cell signaling network describes the basic cellular activities and their interactions. The main contribution of this paper is in the signaling pathway research area, it proposes a new technique to analyze and understand how changes in these networks may affect the transmission and flow of information, which produce diseases such as cancer and diabetes. Our approach is based on three concepts from graph theory (modularity, clustering and centrality) frequently used on social networks analysis. Our approach consists into two phases: the first uses the graph theory concepts to determine the cellular groups in the network, which we will call them communities; the second uses ontologies for the semantic enrichment of the cellular communities. The measures used from the graph theory allow us to determine the set of cells that are close (for example, in a disease), and the main cells in each community. We analyze our approach in two cases: TGF-ß and the Alzheimer Disease.

scholarly journals Five patterns of cell signaling pathways associated with cell behavior

2020 ◽  
Author(s):  
Yuji Takeda ◽  
Kazuharu Kawano ◽  
Rui Ma ◽  
Shinichi Saitoh ◽  
Hironobu Asao
Keyword(s):  
Cell Signaling ◽  
Signaling Pathways ◽  
Signaling Pathway ◽  
Cell Behavior ◽  
General Strategy ◽  
Signal Transducers ◽  
Cell Signaling Pathway ◽  
Flow Cytometric Data ◽  
Phosphorylation Level ◽  
A Cell

AbstractCell signaling pathway is complex systems. Here, we present a concept for a new approach to analyze cell signaling pathway associated with cell behavior. In theoretically, cell behavior is recognized by energy and fluctuation. In this study, we measured phosphorylation level of signal transducers in a cell and fluctuation of the phosphorylation level in the cell population using flow cytometry. Flow cytometric data of mean fluorescence intensity (MFI) and coefficient variation (CV) were considered to the energy and the fluctuation, respectively. Topologically, the changes of MFI and CV were categorized into five patterns (we tentatively named as attractive, subsequent, passive, counter, and negative arbiter). In this study, we clarified the relationship between the cell behavior and the five patterns. Furthermore, combining the five patterns can define the signaling pathways, such as simple activated signal, oscillating signal, regulatory signal, robust signal, or homeostatic signal. These observations provide a proof of concept for general strategy to use the five patterns for connection between cell signaling pathway and cell behavior.

Toxic hijack of a cell signaling pathway

Science ◽  
2018 ◽  
Vol 360 (6389) ◽  
pp. 615.2-615
Author(s):  
Valda Vinson
Keyword(s):  
Cell Signaling ◽  
Signaling Pathway ◽  
Cell Signaling Pathway ◽  
A Cell

Protein Flexibility Catalyzes a Cell Signaling Reaction of the Ras-GAP Complex

2019 ◽  
Author(s):  
Keiei Kumon ◽  
Masahiro Higashi ◽  
Shinji Saito ◽  
Shigehiko Hayashi
Keyword(s):  
Cell Signaling ◽  
Conformational Changes ◽  
Catalytic Reaction ◽  
Protein Complex ◽  
Enzyme Mechanism ◽  
Activation Free Energy ◽  
Chemical Catalysis ◽  
Simple Chemical ◽  
A Cell ◽  
Enzyme Molecules

Many enzyme molecules exhibit characteristic global and slow dynamics which furnish them with allostery realizing remarkable molecular functionalities more than simple chemical catalysis. However, molecular mechanism of a catalytic reaction associated with the molecular flexibility of enzymes is not well-understood. Here we report a hybrid molecular simulation study on GTPase activity of a Ras-GAP protein complex for cell signaling termination. We unveiled that extensive conformational changes of the protein complex and exclusion of internal water molecules are induced upon the transition state (TS) formation in the catalytic reaction and significantly lower the reaction activation free energy. We also revealed that tumor-related mutations perturb those conformational changes upon the TS formation, leading to reduction of the catalytic activity. The findings of the remarkably dynamic protein conformation directly linking to the catalytic reaction have broad implications for understanding of enzyme mechanism and for developments of allosteric drugs and novel catalysts.

scholarly journals Gambogic acid protects LPS-induced apoptosis and inflammation in a cell model of neonatal pneumonia through the regulation of TrkA/Akt signaling pathway

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xu Gao ◽  
Jingya Dai ◽  
Guifang Li ◽  
Xinya Dai
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Cell Model ◽  
Akt Signaling ◽  
Gambogic Acid ◽  
Akt Signaling Pathway ◽  
Western Blot Assay ◽  
A Cell ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation

Abstract Objective In this work, we investigated the effects of gambogic acid (GA) on lipopolysaccharide (LPS)-induced apoptosis and inflammation in a cell model of neonatal pneumonia. Method Human WI-38 cells were maintained in vitro and incubated with various concentrations of GA to examine WI-38 survival. GA-preincubated WI-38 cells were then treated with LPS to investigate the protective effects of GA on LPS-induced death, apoptosis and inflammation. Western blot assay was utilized to analyze the effect of GA on tropomyosin receptor kinase A (TrkA) signaling pathway in LPS-treated WI-38 cells. In addition, human AKT serine/threonine kinase 1 (Akt) gene was knocked down in WI-38 cells to further investigate the associated genetic mechanisms of GA in protecting LPS-induced inflammation and apoptosis. Results Pre-incubating WI-38 cells with low and medium concentrations GA protected LPS-induced cell death, apoptosis and inflammatory protein productions of IL-6 and MCP-1. Using western blot assay, it was demonstrated that GA promoted TrkA phosphorylation and Akt activation in LPS-treated WI-38 cells. Knocking down Akt gene in WI-38 cells showed that GA-associated protections against LPS-induced apoptosis and inflammation were significantly reduced. Conclusions GA protected LPS-induced apoptosis and inflammation, possibly through the activations of TrkA and Akt signaling pathway. This work may broaden our understanding on the molecular mechanisms of human neonatal pneumonia.

C-factor: A cell-cell signaling protein required for fruiting body morphogenesis of M. Xanthus

Cell ◽  
1990 ◽  
Vol 61 (1) ◽  
pp. 19-26 ◽  
Author(s):  
Seung K. Kim ◽  
Dale Kaiser
Keyword(s):  
Cell Signaling ◽  
Fruiting Body ◽  
Signaling Protein ◽  
A Cell ◽  
Cell Cell

scholarly journals Dysregulation of the IFN-γ-STAT1 signaling pathway in a cell line model of large granular lymphocyte leukemia

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0193429 ◽  
Author(s):  
Paige M. Kulling ◽  
Kristine C. Olson ◽  
Cait E. Hamele ◽  
Mariella F. Toro ◽  
Su-Fern Tan ◽  
...  
Keyword(s):  
Cell Line ◽  
Signaling Pathway ◽  
Large Granular Lymphocyte ◽  
Line Model ◽  
Large Granular Lymphocyte Leukemia ◽  
Cell Line Model ◽  
A Cell ◽  
Stat1 Signaling ◽  
Ifn Γ

scholarly journals Combination therapy using TGF-β1 and STI-571 can induce apoptosis in BCR-ABL oncogene-expressing cells

2021 ◽  
Vol 12 (1) ◽  
pp. 144-155
Author(s):  
Masoome Bakhshayesh ◽  
Ladan Hosseini Gohari ◽  
Mahmood Barati ◽  
Majid Safa
Keyword(s):  
Combination Therapy ◽  
Tyrosine Kinase ◽  
Cell Signaling ◽  
Signaling Pathway ◽  
Kinase Inhibitor ◽  
K562 Cells ◽  
Parp Cleavage ◽  
Kinase Gene ◽  
Sti 571 ◽  
Tgf Β1

Abstract The BCR-ABL oncogene is a tyrosine kinase gene that is over-expressed in CML. It inhibits the TGF-β1 signaling pathway. Due to resistance of cells to the tyrosine kinase inhibitor, STI-571, the combined effect of STI-571 and TGF-β1 on K562 cells was studied in the present research. Results revealed that the TGF-β1 cell signaling pathway, which is activated in K562 cells treated with TGF-β1, activates collective cell signaling pathways involved in survival and apoptosis. It is noteworthy that treating K562 cells with STI-571 triggered apoptotic pathways, accompanied by a reduction in proteins such as Bcl-xL, Bcl-2, p-AKT, p-Stat5, p-FOXO3, and Mcl-1 and an increase in the pro-apoptotic proteins PARP cleavage, and p27, leading to an increase in sub-G1 phase-arrested and Annexin-positive cells. Interestingly, the proliferation behavior of TGF-β1-induced cells was changed with the combination therapy, and STI-571-induced apoptosis was also prompted by this combination. Thus, combination treatment appears to promote sub-G1 cell cycle arrest compared to individually treated cells. Furthermore, it strongly triggered apoptotic signaling. In conclusion, TGF-β1 did not negatively impact the effect of STI-571, based on positive annexin cells, and AKT protein phosphorylation remains effective in apoptosis.

scholarly journals A New Technique to Solve the Instant Insanity Problem

2016 ◽  
Vol 11 (10) ◽  
pp. 5766-5773
Author(s):  
Salar Y Alsardary ◽  
Hwee Jung Kim ◽  
Julie George
Keyword(s):  
Graph Theory ◽  
Programming Language ◽  
New Technique ◽  
New Approach ◽  
A New Technique

Instant Insanity [1] consists of four cubes, each of whose six faces are colored with one of the four colors: red, blue, white, and green. The object is to stack the cubes in such a way that each of the four colors appears on each side of the resulting column. See figure 1 below[2]. Traditionally, this could be solved using graph theory.However, in this article, we introduce a new technique to solve the problem without using graph theory. We also used a Perl programming language to implement the new approach for the Instant Insanity.

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